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Heme/Onc/Endo > Endocrinology Exam 1 Cards > Flashcards

Endocrinology Exam 1 Cards Flashcards

1
Q

P3 Zones of the Adrenal Cortex and what they secrete

A

Glomerulosa - Salt
Fasciculata - Sugar
Reticularis - Sex

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2
Q

3 effects of aldosterone on the body

A

Water and sodium retention
Potassium Excretion
Increased BP

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3
Q

Renin-Angiotensin-Aldosterone-System

A

Kidney detects low perfusion pressure
JG cells release Renin
Renin cleaves Angiotensinogen to Angiotensin I
ACE in lungs cleaves AT I to AT II
AT II stimulates release of Aldosterone

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4
Q

Trigger for release of Cortisol

A

Stress

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5
Q

3 functions of cortisol

A

Gluconeogenesis
Immune system suppression
Decreased inflammation

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6
Q

When is cortisol the highest? and why?

A

In the morning because it needs to wake you up

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7
Q

Main sex hormone secreted by the Zona reticularis

A

DHEA

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8
Q

Role of DHEA

A

Stimulates, controls and maintains the development of sex characteristics

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9
Q

2 secretions of the adrenal medulla

A

Epinephrine and Norepinephrine

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10
Q

What inhibits CRH release

A

Cortisol

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11
Q

Desmolase

A

CYP11A1

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12
Q

17 alpha hydroxylase

A

CYP21A2

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13
Q

21 hydroxylase

A

CYP21A2

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14
Q

Aromatase

A

CYP19

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15
Q

Aldosterone Synthase

A

CYP11B2

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16
Q

11 beta hydroxylase

A

CYP11B1

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17
Q

4 possible cholesterol products from the adrenal cortex

A

DHEA
5-Dihydrotestosterone
Cortisone
Aldosterone

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18
Q

Role of desmolase

A

Kicks off the process, without it no products are made

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19
Q

Role of 3 beta HSD

A

Moves steroids away from becoming DHEA, without it only DHEA can be produced

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20
Q

Role of 17 alpha hydroxylase

A

Moves steroids towards becoming DHEA, without it only aldosterone can be produced

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21
Q

Role of 11 betahydroxylase

A

Required to synthesize cortisol only

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22
Q

Role of CYP11B2

A

Aldosterone synthase, not needed for cortisol synthesis

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23
Q

Role of aromatase

A

Converts androgens to estrogens

(women smell good)

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24
Q

Primary gland

A

Last gland in the line (ie. the adrenal glands)

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25
Q

Addison’s disease

A

Usually autoimmune destruction of the adrenal cortex - results in a loss of glucocorticoids AND mineral corticoids

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26
Q

Most commonly affected enzyme in Addison’s disease

A

21-hydroxylase

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27
Q

Adrenoleukodystrophy

A

Accumulation of long chain fatty acids in the adrenal cortex which blunt the effect of ACTH

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28
Q

Drug that diminishes cortisol synthesis

A

Mitotane

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29
Q

3 drugs that accelerate the metabolism of cortisol

A

Phenytoin, Barbituates, Rifampin

(Notice 2 of them are CYP inducers)

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30
Q

Drug that inhibits cortisol biosynthesis

A

Ketoconazole

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31
Q

2 causes of acute addisons disease

A

Adrenal hemmorhage
Adrenal Crisis

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32
Q

Adrenal Crisis

A

When a patient with addison’s disease is stimulated by a stressor that requires additional adrenal hormones beyond what they are regularaly receiving

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33
Q

Cause of hyperpigmentation in addison’s disease

A

ACTH attaches to the melanotic receptors

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34
Q

Cause of vitiligo in Addison’s disease

A

Antibodies that destroy adrenal cortex, also destroy melanocytes

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35
Q

4 hallmarks of an adrenal crisis

A

Severe fever - Not in adrenal hemmorhage
Severe abdominal pain
Confusion
Hypotensive shock

(Looks a lot like sepsis)

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36
Q

Adrenoleukodystrophy

A

Accumulation of long chain fatty acids in the adrenal cortex which blunt the effect of ACTH

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37
Q

2 CBC findings for Addison’s disease

A

Eosinophilia and Lymphocytosis

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38
Q

Why would you want a blood sputum or urine culture in a suspected adrenal crisis

A

Because you may be able to find a precipitating cause

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39
Q

Diagnostic and rule out levels of cortisol for Addision’s disease

A

Under 3 with high ACTH, Over 25 mcg/dL

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40
Q

Plasma ACTH indicative of Addison’s disease

A

Over 200 pg/mL

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41
Q

Cause of hidden hyperkalemia in Addison’s disease

A

Vomiting leading to potassium loss

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42
Q

Plasma Renin Activity

A

Can help diagnose the need for mineralcorticoid replacement but is also very finicky

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43
Q

ACTH stimulation test indication for addisons

A

administer ACTH and check cortisol in increase
Increase less than 20mc/dL is indicative of Addison’s (not a great test)

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44
Q

When might you use an ACTH stimulation test?

A

When serum cortisol or serum ACTH are non-diagnostic

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45
Q

How might imaging help in an adrenal crisis and what would you order?

A

Identification of an underlying etiology
Order a CXR or Abdominal CT

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46
Q

Standard Treatment for Addison’s disease

A

Hydrocortison PO 15-30mg daily with 2/3rds in the morning and 1/3rd at night

Can also use 3-6 mg prednisone the same way

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47
Q

Cortisone dose adjustment for Addison’s patients with chronic disease

A

Increase up to 50%
Return to baseline upon stressor resolution

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48
Q

Mineralcorticoid therapy for Addison’s disease

A

Covered by a “stress” dose of cortisone
If not on a stress dose - use fludracortison .05-3mg daily
Monitor PRA

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49
Q

4 Steps in managing an adrenal crisis

A

Order serum cortisol and ACTH (don’t wait for results) if undiagnosed
Give an IV hydrocortisone loading dose
Give IV cortisone for 24 hours and then taper
Switch to oral once the patient can tolerate it (isn’t vomiting)

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50
Q

Non-cortisol management of an adrenal crisis

A

Give broad spectrum antibiotics and adjust with cultures
Treat electrolyte and volume abnormalities

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51
Q

3 things to monitor for in an Addison’s patient

A

Development of Cushing syndrome
CBC/CMP normality
DEXA scan for osteoporosis (from steroid use)

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52
Q

2 things you might give an Addison’s patient to help them manage emergencies

A

Emergency injection kit and Zophran for nausea

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53
Q

Cushing Syndrome

A

Excessive administration of corticosteroids
(ACTH independent)

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54
Q

Cushing disease

A

Excessive secretion of cortisol due to excess ACTH
(ACTH dependant)

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55
Q

3 less obvious presentations of cushing’s disease

A

Easy bruising
Proximal muscle weakness
Immune system suppression

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56
Q

3 s/s assocaited with high ACTH

A

Hyperpigmentation
High BP
Hirsutism/Hair loss

3 H’s

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57
Q

What do NEW stretch marks look like?

A

Purple not Gray/Brown

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58
Q

2 CBC findings for cushings

A

Decreased leukocytes and eosinophils

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59
Q

3 CMP findings for Cushing’s

A

Elevated glucose, hypernatremia and hypokalemia (if Aldosterone is effected

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60
Q

MCC of Cushing’s

A

Pituitary tumor

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61
Q

3 steps in a cushings diagnostic workup

A

Establish endogenous or exogenous source
Establish presence of hypercortisolism
Determine cause of hypercortisolism

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62
Q

3 first line tests for hypercortisolism

A

Dexamethasone, 24 Hour Urine free cortisol, Late night salivary cortisol

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63
Q

Number of positive tests needed for hypercortisolism diagnosis

A

2

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64
Q

Low-dose dexamethasone suppression test

A

Give 1 mg PO at 11PM test serum cortisol at 8 AM

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65
Q

Result for dexamethasone suppression test that likely excludes cushing disease

A

Less than 5mcg/dL

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66
Q

24 Hour urine free cortisol test

A

Begin collection AFTER first morning void and continue through first void of the next day

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67
Q

Positive 24 hour urine free cortisol result

A

3x upper limit on two occasions points to Cushing disease

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68
Q

6 interfering factors for a late night salivary cortisol test

A

Bleeding, brushed teeth, oral intake, steroid use, pregnancy, erratic schedule

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69
Q

When to take a late night salivary cortisol test

A

11 PM

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70
Q

Positive salivary cortisol test

A

Elevated cortisol found on TWO separate occasions

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71
Q

Assay to determine cause of hypercortisolism

A

Serum ACTH

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72
Q

Values for serum ACTH and next step for each

A

Under 20 = low = Adrenal CT
Over 20 = high = Pituitary MRI

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73
Q

3 red flags for a malignant adrenal adenoma

A

Over 4 cm
Growing nodule
Density over 10 Housfield Units (HU)

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74
Q

HU

A

Hounsfield unit - measurement of radiographic density (water is 0)

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75
Q

Findings for pituitary MRI and interpretation thereof

A

Under 5mm - Inferior petrosal sinus sampling
Over 5mm - Begin treatment

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76
Q

Search for ectopic source of cushings

A

Chest/Abdomen CT first
Full body PET scan second

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77
Q

Management for exogenous Cushing’s

A

Slowly reduce exogenous glucocorticoid ACTH therapy

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78
Q

Short acting glucocorticoid that can help with recovery of HPA axis

A

Hydrocortisone

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79
Q

First line treatment tumor precipitated cushings

A

Surgical removal or radiation - can result in a need for glucocorticoid replacement

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80
Q

Medications that can manage an adrenal adenoma (3)

A

11b hydroxylase inhibitors such as:
Metyrapone
Osilodrostat
Ketoconazole

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81
Q

Medication that can manage ACTH tumor

A

Pasireotide - somatostatin analog

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82
Q

Two first line and one second line medication to manage mineralocorticoid HTN

A

K sparing diuretics
Spironolactone or Eplerenone

Second line - ACEI

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83
Q

1 drug for hyperandrogenism in women

A

Flutamide

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84
Q

Role of the StAR protein

A

Regulates steroid biosynthesis by allowing cholesterol into the mitochondria

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85
Q

Congenital Adrenal Hyperplasia w/ inheritance pattern

A

Autosomal recessive deficiency in steroid producing enzymes

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86
Q

MC deficiency in CAH

A

21 alpha hydroxylase

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87
Q

2 classic presentations for CAH

A

Salt wasting due to aldosterone deficiency
Virializing due to androgen excess

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88
Q

5 signs of salt wasting

A

vomiting, dehydration, hyponatremia, hyperkalemia, hypotensive shock

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89
Q

3 protein deficiencies that can lead to ambiguous genitalia

A

StAR protein
3 beta hydroxysteroid deficiency
17 alpha hydroxylase deficiency

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90
Q

2 things that are increased in a 21 hydroxylase deficiency

A

17-hydroxyprogesterone
Serum DHEA

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91
Q

workup for CAH suspicion

A

Get electrolytes
Use imaging if needed to rule out other disorders (abdomen CT and Pelvic US)

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92
Q

Goal of CAH treatment

A

Give just enough Aldosterone and Cortisol to keep things normal

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93
Q

Hydrocortisone administration for CAH

A

Initially 1-2 mg/kg/day (suprephysiologic
Maintainance .3-.5 mg/kg/day

TID - even doses as a baby, 2/3 1/3 as an adult

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94
Q

Fludrocortisone administration for CAH

A

Aldosterone substitute
.05-.15 mg daily while monitoring BP and plasma renin activity

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95
Q

What to watch for in CAH hydrocortisone administration in order to ensure that is is working

A

17-hydroxyprogesterone level normalization

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96
Q

Primary hyperaldosteroneism

A

Hypersecretion of aldosterone that cannot be suppressed by giving sodium

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97
Q

Clinical presentation of Primary Hyperaldosteroneism

A

Refractory hypertension
Headaches
Hypokalemia (weakness, paresthesia, fatigue)

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98
Q

2 BMP findings that could indicate hyperaldosteroneism

A

Hypernatremia, Increased CO2 (represents Bicarb)

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99
Q

PAC/PRA

A

Plasma renin activity/Plasma aldosterone concentration

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100
Q

Timing for PAC/PRA

A

Do in the AM while seated

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101
Q

Normal aldosterone/renin ratio

A

Under 10

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102
Q

4 BP meds that do not effect PAC/PRA ratio

A

Slow release verapamil, Hydralazine, terazosin, doxazosin

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103
Q

Oral and IV methods for sodium loading

A

Oral - 3 days of unrestricted salt (over 5g/day)
IV - 2L NS over 4 Hours

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104
Q

Determination of adequate oral sodium loading and next steps

A

Urine sodium over 250 and normal urine creatinine - begin 24 hour urine collection

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105
Q

Confirmatory result for oral sodium loading

A

24 hour urine aldosterone concentration of over 12

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106
Q

Confirmatory result for IV sodium loading

A

Plasma aldosterone concentration of over 10ng/dL

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107
Q

Conn syndrome

A

Adrenal mass smaller than 4cm

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108
Q

Likely adrenal carcinoma

A

Adrenal mass larger than 4 cm

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109
Q

Adrenal vein sampling

A

LAST resort if considering an adenectomy and HTN is severely uncontrolled

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110
Q

2 potassium sparing diuretics for primary hyperaldosteroneism

A

Spironolactone or eplerenone (more expensive with fewer SEs)

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111
Q

2 Additional BP meds for primary hyperaldosteronism

A

ACEI, HCTZ

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112
Q

incidentaloma

A

A tumor that we were not looking for but found

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113
Q

Rule of 10s for pheochromocytoma

A

10% bilateral
10% extra-adrenal
10% malignant

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114
Q

Classic pheochromocytoma triad

A

Episodic palpitations, diaphoresis, sweating - combined with HTN

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115
Q

3 things that can precipitate a pheochromocytoma

A

Stress, Position change, Urination

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116
Q

How long do pheochromocytoma episodes last?

A

Usually under an hour

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117
Q

Workup for Pheochromocytoma

A

Plasma free metanephrines
Sitting, then laying down, then urine - 24 hour preferred

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118
Q

Metanephrine threshold diagnostic for pheochromocytoma

A

3x the upper limit

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119
Q

Imaging for Pheochromocytoma

A

CT/MRI - chest, abdomen, pelvis
PET scan for malignancy rule-out

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120
Q

Management of pheochromocytoma

A

Refer to surgery, assess ACTH level post-op

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121
Q

Pre-surgery management of Pheochromocytoma

A

Alpha adrenergic blockers with high salt and water diet started 3 days later

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122
Q

3 Alpha blockers for pheochromocytoma management

A

Doxazosin, Prasosin, Terzosin

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123
Q

Functional v Nonfunctional adrenal adenoma demographic

A

Functional - Younger pts
Non-functional - Older pts

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124
Q

4 History findings pointing to an adrenal carcinoma

A

Fever, weight loss, abdominal fullness, back pain

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125
Q

Physical exam findings for adrenal carcinoma

A

Palpable, firm, adherent mass of the abdomen

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126
Q

When should fine needle aspiration be done for an adrenal carcinoma

A

ONLY when there is known metastasis already and pt does not have pheochromocytoma

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127
Q

Management of adrenal carcinoma

A

Stage and refer to surgery

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128
Q

Only glucocorticoid offered as a syrup

A

Prednisolone

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129
Q

Indication for glucocorticoid titration

A

Therapy longer than 7-10 days

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130
Q

3 things to monitor in patients on glucocorticoids

A

Glucose, Na retention, K+ loss

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131
Q

5 side effects of glucocorticoids

A

Gastric irritation/Peptic ulcer
Hypertension
CHF
Osteoporosis
Glaucoma

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132
Q

How can thyroid gland growth cause horseness

A

It can impinge the recurrent laryngeal nerve

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133
Q

Thyroglobulin

A

Large protein from which thyroid hormones are cleaved

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134
Q

Difference between T3 and T4

A

T3 is active, T4 is stable

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135
Q

Reverse T3

A

Non-functional form of T3 which is made in the tissues in stressful circumstances and cannot be used

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136
Q

Taking directions for thyroid hormone

A

MUST be taken on an empty stomach

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137
Q

Primary thyroid hormone binding protein

A

Thyroxine binding globulin

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138
Q

Which thyroid hormone is converted in the tissues

A

T4 to T3

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139
Q

Action of thyroid hormone

A

Increases functional activity in the tissues

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140
Q

Thyroid hormone effect on heart strength

A

Helps with a small increase but pathologic with a large increase

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141
Q

4 things usually on a thyroid panel

A

TSH, Total T3, Total T4, Free T4

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142
Q

Peak and trough for TSH levels

A

Peak at 10pm, Trough at 10am

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143
Q

What does an abnormal Total T3 or T4 level indicate

A

An increase or decrease in Thyroid Binding Globulin

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144
Q

Why might a patient only have T3 and no T4

A

They are on a T3 only medication

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145
Q

Binding protein for thyroid hormone

A

TBG - Thyroid Binding Globulin

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146
Q

2 things that can increase TBG levels

A

Estrogen, Infectious hepatitis

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147
Q

Result of maternal hypothyroidism

A

Significant decrease in fetal IQ

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148
Q

MCC of hypothyroidism in developed and underdeveloped countries

A

Developed - Hashimotos
Worldwide - Iodine deficiency

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149
Q

4 facial signs of hypothyroidism

A

Dry coarse hair, thinning of lateral eyebrows, Periorbital edema, puffy dull face (myxedema)

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150
Q

2 antibodies to screen for in hashimoto’s thyroiditis with chances of a positive result

A

Anti-Thyroid peroxidase (90-95%)
Antithyroglobulin (70%)

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151
Q

When might thyroid imaging be useful

A

Detection of thyromegaly or thyroid nodule

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152
Q

What will an ultrasound of a hashimoto’s thyroid look like compared to a normal one

A

Lack of smoothness - the thyroid should have a very uniform texture

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153
Q

Myxedema crisis

A

Triggered most often in elderly women who have a stroke or stop taking meds:

Hypo - thermia, tension, ventilation, glycemia, natremia

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154
Q

Medication for myxedema crisis

A

IV Levothyroxine (L4)

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155
Q

Liothyronine

A

T3 medication - remember T4 levels will be zero

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156
Q

Subclinical hypothyroidism

A

Normal FT4 with High TSH
Observe for s/s

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157
Q

Goal of thyroid hormone therapy

A

Normalize TSH levels

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158
Q

4 things that increase need for thyroid hormone therapy

A

Medications that interact
Increased estrogen
GI disorders
Weight gain over 10%

159
Q

3 things that decrease the need for thyroid hormone therapy

A

Decreased estrogen
Increased androgen
Weight loss over 10%

160
Q

Desiccated thyroid

A

Ground animal thyroid - not recommended and from beef or pork products

161
Q

1 grain of dessicated thyroid

A

100mcg

162
Q

3 Contraindications for thyroid replacement therapy

A

Acute MI, Thyrotoxicosis, uncorrected adrenal insufficiency

163
Q

Black box warning of all thyroid replacement drugs

A

Not for treatment of obesity

164
Q

2 groups at higher risk for thyrotoxicosis

A

Women and smokers

165
Q

Mechanism of grave disease

A

Autoantibodies bind to the thyroid and cause stimulation and excessive function

166
Q

Detection of graves disease

A

Look for TSH receptor antibodies, may treat for graves even if they are not found

167
Q

3 things that can cause thyrotoxicosis

A

Excessive consumption of seaweed products, Amiodarone (contains iodine), Thyroiditis

168
Q

Thyrotoxicosis factitia

A

Thyrotoxicosis caused by ingestion of thyroid hormone

169
Q

3 manifestations of Graves disease

A

Bulging eyes, Digital clubbing, Erythematous rough plaques in the lower legs

170
Q

Cardiopulmonary manifestations of thyrotoxicosis

A

Forceful heartbeat, Exertional dyspnea,Atrial fibrilation, Can lead to cardiomyopathy

171
Q

Thyrotoxicosis in pregnancy - 3 things it can lead to

A

Can lead to eclampsia, preterm delivery and neonatal thyrotoxicosis

172
Q

4 non-thyroid lab abnormalities seen in thyrotoxicosis

A

Hypercalcemia, Increased alkaline phosphatase, Anemia, Decreased granulocytes

173
Q

3 markers for graves disease

A

Thyroid stimulating Immunoglobulin
Anti-Thyroid Peroxidase
Anti-Thyroglobulin

174
Q

2 markers for thyroiditis

A

No antithyroid antibodies
Increased erythrocyte sedimentation rate

175
Q

1 marker for thyrotoxicosis factitia

A

Low serum thyroglobulin levels

176
Q

What might increased uptake of radioactive iodine point to (3)

A

Graves disease, Toxic nodules, Type I amiodarone thyrotoxicosis

177
Q

What might decreased uptake of radioactive iodine point to

A

Thyroiditis, Iodine induced thyrotoxicosis, Type II amiodarone thyrotoxicosis

178
Q

Cold nodule

A

Less active than the rest of the thyroid but more likely to be cancer

179
Q

Hot nodule

A

More active than the rest of the thyroid which usually shuts down to compensate for its overproduction

180
Q

How can doppler US help us detect thyroid cancer

A

By detecting increased/abnormal blood flow to the thyroid gland

181
Q

Treatment for thyrotoxicosis opthalmopathy

A

Steroids for trapped intraocular muscles, radiation or surgery if severe

182
Q

Thyroid storm

A

Severe, life threatening thyrotoxicosis triggered by radioactive iodine, surgery, or illness

183
Q

6 treatment parts for a thyroid storm

A

Thiourea drug to prevent hormone formation
Iodinated contrast agent to prevent T4 to T3 conversion
Beta blocker
Hydrocortisone
Avoid ASA
SUrgery/RAI = Definitive

184
Q

Subclinical hyperthyroidism

A

Low TSH with normal FT4 and T3

185
Q

Is a cystic or solid mass more likely to be cancerous

A

SOLID

186
Q

2 opthalmic signs of thyrotoxicosis/hyperthyroidism

A

Bulging eyes and Double vision from extraoccular muscle impingement

187
Q

2 beta blockers for graves disease

A

Propranolol and Atenolol

188
Q

2 iodonated contrast agents used for thyrotoxicosis and what they do

A

Iopanoic acid and Ipodate sodium
Block conversion of T3 to T4

189
Q

Action of thiourea drugs

A

Inhibit production of thyroid hormone

190
Q

2 thiourea drugs for graves disease

A

Methimazole - Preferred in most patients
Propylthiouracil - For first trimester or breast feeding

191
Q

3 side effects of methimazole

A

Pruritis, abnormal taste, agranulocytosis

192
Q

Black box warning for propylthiouracil

A

Hepatotoxicity

193
Q

Definitive treatment for graves disease

A

Use radioactive iodine or surgery for pregnant patients

194
Q

How long before radiation treatment should methimazole be stopped

A

4 days

195
Q

Thyroiditis

A

Thyroid is not producing hormone, however it is leaking out of the gland causing hyperthyroidism

196
Q

Treatment for thyroiditis

A

Thioureas NOT effective
Use beta blockers and contrast agents if severe

197
Q

NSAID effect on thyroid hormones

A

They knock T3 and T4 off of Thyroid binding globulins

198
Q

Hashimoto thyroiditis

A

Autoimmune thyroiditis common in women
Anti TPO and anti Tg antibodies
May have a tight feeling in neck and complain of hypothyroid symptoms

199
Q

Painless postapartum thyroiditis

A

Sets in 1-6 months after delivery
High recurrence and followed by hypothyroidism
Anti TPO antibodies

200
Q

Painless sporadic thyroiditis

A

Hyper and then hypothyroidism
Not associated with pregnancy
Thyroid “bipolar” disorder

201
Q

Subacute thyroiditis

A

Often associated with pain/dysphagia and low grade fever, often accompanies an upper respiratory tract infection

202
Q

Suppurative thyroiditis

A

Nonviral thyroid gland infection usually in the immune compromised
Severe pain and tenderness with fever

203
Q

Riedel thyroiditis

A

Asymmetric, stony adherent thyroid gland
Due to fibrosis
May have associated dysphagia, dyspnea, pain and hoarseness

204
Q

Diagnostic labs for hashimotothyroiditis

A

Anti TPO/Tg antibodies

205
Q

Diagnostic labs for subacute thyroiditis

A

Elevated ESR with low antibody titers with signs of hypo/hyper thyroidism

206
Q

Suppurative thyroiditis labs

A

Elevated ESR and leukocytes with other labs normal

207
Q

2 differentials for high Anti-TPO antibodies

A

Hashimoto’s or Grave’s disease

208
Q

Difference between graves and thyroiditis on a US

A

Graves has increased vascularity, thyroiditis does not

209
Q

RAI uptake for graves vs. thyroiditis

A

Graves has increased uptake
Thyroiditis has decreased uptake

210
Q

Ultrasound finding for hashimoto’s thyroiditis

A

Non smooth texture

211
Q

Complication of hashimoto’s thyroiditis

A

Can cause 1st trimester miscarriage

212
Q

Management of hashimoto’s thyroiditis

A

Levothyroxine for replacement for suppressive therapy

213
Q

Treatment for subacute thyroiditis

A

High dose aspirin or NSAID - may need contrast agents if severe

214
Q

Treatment for reidel thyroiditis (3)

A

Tamoxifen, Steroids, and decompression surgery if needed

215
Q

Complaint for thyroid vs, Complaint for pharyngeal infection

A

Sore neck = thyroid
Sore throat = Pharyngeal

216
Q

Sick euthyroid syndrome

A

State of abnormal thyroid function in the presence of a non-thyroidal illness

217
Q

Cytokine thought to be especially involved in sick euthyroid syndrome

A

IL-6

218
Q

Management of sick euthyroid syndrome

A

Observe and treat underlying cause

219
Q

Percent of thyroid nodules that care cancerous

A

10%

220
Q

3 associated s/s that can be found with a large multinodular goiter

A

Swelling, hoarseness, dysphagia

221
Q

Diagnostic testing for nodules and goiters of the thyroid

A

TSH +/- FT4
Thyroid ultrasound - larger, more solid, nodules with unclear borders are red flags for cancer

222
Q

Evaluation of thyroid nodule for cancer

A

US guided biopsy - low danger of seeding

223
Q

Cold nodule

A

Nodule with little RAI uptake - high cancer risk

224
Q

Hot nodule

A

Nodule with high RAI uptake - Low cancer risk

225
Q

Warm nodule

A

Nodule with the same metabolic activity as the surrounding tissue

226
Q

4 characteristics of thyroid nodules that warrant a biopsy

A

Over 1 cm with suspicious appearance
Any nodule over 2cm
Associated lymphadenopathy
Nodule growth

227
Q

Management for thyroid nodule

A

Follow up Q6 months, LT4 suppression may be necessary, ethanol injection for shrinkage, RAI therapy, Surgery

228
Q

MC thyroid cancer

A

Papillary thyroid carcinoma - slow growing and autosomal dominant with some iodine uptake

229
Q

Follicular thyroid cancer

A

Higher iodine uptake and more likelihood of distant metastasis

230
Q

Medullary thyroid cancer

A

Secretes calcitonin and prostaglandins, poor iodine uptake and local metastasis

231
Q

Anaplastic thyroid cancer

A

Most aggressive, poor iodine uptake with rapid growth

232
Q

Common sites for thyroid cancer metastasis

A

Lymph nodes, Lungs, Bone

233
Q

2 s/s commonly associated with medullary thyroid cancer

A

Flushing and diarrhea

234
Q

Which thyroid cancers might present with hyperthyroidism?

A

Follicular thyroid cancer

235
Q

Which cancers might present with high thyroglobulin

A

Metastatic papillary and follicular cancer -invalid if anti-Tg also present

236
Q

Thyroid cancers in which calcitonin may be elevated

A

medullary thyroid cancer - have to rule out other conditions such as pregnancy or thyroiditis

237
Q

Thyroid cancer in which carcinoembryonic antigen may be elevated

A

Medullary thyroid cancer - must r/o other cancers

238
Q

Surgical decision making for known thyroid cancer

A

Excise whole thyroid if over 1 cm
Single lobe if not

239
Q

Surgical decision making for indeterminate thyroid lesion (may be cancer)

A

Excise whole thyroid if over 4cm
Single lobe if not

240
Q

2 potential management options for differentiated thyroid cancers

A

Thyroxine suppression (monitor thyroid labs and bone density)
RAI therapy (CI in pregnancy)

241
Q

Screening for thyroid cancers

A

At least yearly US screening recommended

242
Q

Effect of parathyroid hormone on Bone, Kidneys

A

Bone - Osteoclast activity stimulated to release calcium
Kidney - Resorbs calcium and excreted phosphorus

243
Q

Vitamin required for phosphorus absorption

A

Vitamin D

244
Q

3 hormones that regulate calcium/phosphate balance

A

Parathyroid hormone
Vitamin D - 1,25
Calcitonin

245
Q

Normal function of kidney with regards to calcium and phosphate

A

Keep calcium in, let phosphate out

246
Q

Effect of the kidney on vitamin D

A

Changes D25 (inactive) to D1,25 (active)

247
Q

Effect of vitamin D on GI tract

A

promotes absorption of Calcium and phosphorus

248
Q

Calcitonin

A

Released by special cells in the thyroid and works in opposition to PTH

249
Q

Total serum calcium

A

Both bound and free calcium

250
Q

Ionized calcium

A

Unbound/Free calcium

251
Q

Correction equation for serum calcium and when we use it (don’t actually need to memorize the equation)

A

Serum Ca + [.8 x (4.0-Albumin)]
Use when ionized calcium level is not available, when calcium and protein are off

252
Q

Current standard diagnosis for hyperparathyroidism

A

Serum PTH

253
Q

D3 vitamin D

A

Cholecalciferol - synthesized in the epidermis

254
Q

D2 vitamin D

A

Ergocalciferol derived from plant sources

255
Q

1 drug that can lead to decreased active vitamin D

A

HIV protease inhibitors

256
Q

Parathyroid Hormone Related Protein (PTHrP)

A

Protein released by cancer cells that acts like PTH at PTH receptors

257
Q

Clinical presentation of hypercalcemia

A

Bones, Stones, Groans, Moans

258
Q

2 medications for hypercalcemia and what they do

A

Furosemide - Calcium removing diuretic
Corticosteroids - Decrease vitamin D activation in the kidneys

259
Q

2 signs for hypocalcemia

A

Chvosteks and Trousseaus signs

260
Q

Chvostek’s sign

A

Facial twitching when touching the ipsilateral facial nerve just anterior to the ear

261
Q

Trousseu’s sign

A

Carpal spasm induced by inflating a BP cuff on the arm to 20mmHg above obliteration point

262
Q

Primary hyperparathyroidism

A

Excessive PTH secretion leading to hypercalcemia and hypophosphatemia

263
Q

Clinical presentation of hyperparathyroidism

A

Often asymptomatic but may present with hypercalcemia

264
Q

Physical exam findings for primary hyperparathyroidism

A

May have a neck mass if it is cancerous - not definitive

265
Q

Magnesium and PTH secretion

A

Low or high levels stimulate secretion
VERY low levels decrease secretion

266
Q

Caution when diuresing patients with hyperparathyroidism

A

Too much could increase PTH secretion
Loop diuretics are safer if you don’t want to interfere with calcium

267
Q

24 hour urine calcium interpretation

A

Over 200-300 is likely PHPT and excludes FHH
Under 200 is likely FHH or PHPT with vitamin D deficiency

268
Q

What needs to be done prior to urine calcium testing?

A

Stop thiazide and loop diuretics

269
Q

Serum phosphate interpretation

A

Low - likely primary hyperparathyroidism
High - Likely secondary hyperparathyroidism due to CKD

270
Q

Serum vitmin D-25 in hyperparathyroidism

A

Reduced because so much is being converted

271
Q

Imaging for hyperparathyroid syndrome

A

Used only when surgery is going to be done
CT for ectopic sources
Nuclear tracker Technetium-99m-sestamibi also available

272
Q

Procedure for Technetium parathyroid scan

A

Wait for normal thyroid function to fade so that delayed fade of abnormal parathyroid can be visualized

273
Q

Management for asymptomatic primary hyperparathyroidism
1 thing to do
3 things to avoid

A

Weight bearing exercise avoiding thiazide diuretics, Large doses of vitamin a, calcium containing antiacids/supplements

274
Q

Routine monitoring for asymptomatic primary hyperparathyroidism

A

Serum calcium and albumin 2x/year
Yearly renal function and urine calcium
DEXA scan every 2 years for osteoporosis

275
Q

Management for symptomatic hyperparathyroidism patients

A

Surgical removal often recommended
Cinacalcet also increases parathyroid gland affinity for calcium thus reducing secretion

276
Q

Temporary measures for primary hyperparathyroidism

A

Oral or IV bisphosphonates can improve bone density and can temporarily treat the condition, Patient must remain upright for 30 minutes after bisphosphonate ingestion

277
Q

Management of primary hyperparathyroidism for postmenopausal women

A

Estrogen replacement or Raloxifene (estrogen agonist/antagonist)

278
Q

3 common causes of secondary hyperparathyroidism

A

CKD, VItamin D deficiency, and Hypocalcemia

279
Q

Effect of hypermagnesemia of PTH release

A

Suppresses it through unknown mechanism

280
Q

Clinical findings for hypoparathyroidism

A

Tetany, Chvostek and trousseu signs, Prolonged QT interval

281
Q

Acute management for hypoparathyroidism

A

Airway, IV calcium gluconate, Oral calcium later on. Treatm hypomagnesemia as well if present

282
Q

Magnesium supplementation for hypomagnesemia

A

Magnesium sulfate IV and then magnesium oxide PO (can cause gastric acid secretion)

283
Q

Goal for calcium mainainance therapy

A

Keep calcium levels just below normal range to avoid renal stones

284
Q

Recombinant PTH medication and indication

A

Teriparatide - for those with refractory conditions

285
Q

Vitamin D deficiency drug and dose

A

D2, 1500-2000 units PO with calcium

286
Q

Hypoparathyroidism drug and dose

A

D2, 50,000-100,000 units PO with calcium

287
Q

Calcitriol

A

Active Vitamin D - for patients with renal failure

288
Q

Hypocalcemia drug and dose

A

Calcium carbonate PO 1-2g/day

289
Q

Calcium gluconate dosing

A

Give more 100-300 mg booster if there is tetany/seizure
give .5-2 mg/kg/hr after

290
Q

Side effects of magnesium supplemetation

A

Diarrhea and GI irritation

291
Q

Somat-

A

Root for growth

292
Q

Troph

A

Root for a specific cell type

293
Q

Sign of congenital hypopituaitarism

A

Decreased muscle tone, more feminine physique, short stature

294
Q

Inhibitor of prolactin

A

Dopamine

295
Q

Peak time for serum prolactin levels

A

4-6 AM

296
Q

PRL during pregnancy

A

Increase 10x during pregnancy and rapidly decline IF breastfeeding is not initiated

297
Q

How does suckling cause prolactin release

A

By inhibiting dopamine release

298
Q

2 other things that increase prolactin levels

A

TRH secretion and Kidney failure

299
Q

2 things that PRL inhibits

A

Sex drive and reproductive function

300
Q

Causes of Hyperprolactinemia

A

PROLACTINS

Pregnancy
Renal failure
Oral contraceptives
Liver failure
Adenoma
Chest wall disease
Thyroid disease (Hyper)
Infiltrative pituitary disease
Nursing/nipple stimulation
Stalk effect

301
Q

3 clinical presentations of hyperprolactinemia in women

A

Amenorrhea, galactorrhea, and infertility

302
Q

4 clinical presentations of hyperprolactinemia in men

A

Decreased libido, Infertility, Erectile dysfunction, gyencomastia

303
Q

5 things to ask about when prolactin is high

A

Pregnancy
Medications
Renal failure
Thyroid disease
Headache or vision changes

304
Q

What vision change do you expect with a pituitary tumor

A

Bitemporal hemianopia - loose peripheries

305
Q

Serum prolactin evaluation

A

Get basal fasting morning PRL level repeat if slightly high

306
Q

3 things to rule out in hyperprolactinemia

A

Liver/Kidney disease (CMP), Thyroid problems (TSH), Hypogonadism (Testosterone, FSH, LH)

307
Q

Imaging for hyperprolacintemia

A

Brain MRI

308
Q

Treatment for hyperprolactinemia

A

Treat microadenomas (under 1cm) with sex hormone therapy, dopamine antagonists can also help with any cause

309
Q

Long and short acting dopamine agonists for hyperprolactinemia

A

Cabergoline - long acting
Bromocriptine - short acting

310
Q

Side effects of dopamine agonists

A

Constipation, nasal congestion, dry mouth, nightmares, insomnia, vertigo

311
Q

Dopamine agonists and pregnancy

A

May stop for microadenoma, but should stop and closely monitor with macroadenoma

312
Q

Hypoprolactinemia

A

Leads to inability to lactate after pregnancy - often a result of Sheehan syndrome (hypotension after hemorrhage during birth that causes pituitary necrosis)

313
Q

3 direct effects of growth hormone

A

Lipolysis in adipose tissue
Gluconeogenesis in the liver
Insulin resistance in the tissues

314
Q

2 indirect effects of growth hormone via IGF

A

Stimulates Amino Acid uptake to the muscles

315
Q

Role of IGF-1 - (2)

A

Made by the liver in response to GH, stimulates muscle and skeletal growth, also stimulates release of Growth Hormone inhibiting hormone

316
Q

5 signs of GH deficiency in children

A

Short stature, Micropenis, increased fat, high pitched voice, can be x-linked

317
Q

Signs of growth hormone insensitivity

A

Normal or high GH levels with low growth hormone binding protein and IGF-1

318
Q

When are growth hormone levels the highest?

A

At night during stages 3 and 4 of sleep

319
Q

Best way to evaluate height

A

Plot points on a chart to look at overall pattern

320
Q

Children that need a growth evaluation

A

More than 2.5 SDs below the mean
Height velocity below 25th percentile
Less severe short stature combined with growth failure, other evidence suggesting hypothalamic-pituitary dysfunction

321
Q

Diagnostic evaluation for growth failure

A

Evaluate for systemic disease, hypothyroidism, and turner syndrome
Then investigate for Growth hormone deficiency

TL/DR - Rule out other things before working up for Growth hormone issues

322
Q

GH stimulation test

A

Needs to be done twice to be diagnostic, use pharmacological or physiological stimuli

323
Q

2 potential treatments for growth hormone deficiency

A

Recombinant GH and Somatotropin
Use IGF for GH insensitivity

324
Q

Common cause of adult GH deficiency

A

Hypothalamic or pituitary somatotroph damage

325
Q

Sequence of hormone loss in hypothalamic or pituitary somatotroph damage

A

GH then FSH/LH then TSH then ACTH

326
Q

Clinical presentation of adult growth hormone dysfunction

A

Increased fat mass
Hyperlipidemia
Cardiovascular disease
Increased fractures
Depression and fatigue

327
Q

3 contraindications for recombinant growth hormone therapy in adults

A

Active neoplasm
Intercranial hypertension
Uncontrolled diabetes

328
Q

5 things to watch for in patients on Growth hormone therapy

A

Fluid retention
Joint pain
Paresthesias
Diabetes
Carpal tunnel (CTS)

329
Q

Somatomedin

A

Another name for IGF-1

330
Q

4 Associated risk factors of acromegaly

A

Cardiomyopathy
Sleep apnea
Diabetes
Colon polyps

331
Q

Diagnostic confirmation of acromegaly

A

GH suppression to under 0.4mcg/L within 1-2 hours of a 75 g oral glucose load

332
Q

Surgery of choice for tumor related acromegaly

A

Transsphenoidal surgical resection for both micro and macroadenomas

333
Q

Treatment for acromegaly in non-surgical candidates

A

Treat with a somatostatin analog
Dopamine agonists also work (bromocriptine and cabergoline)

334
Q

somatostatin analogs (4)

A

End in TIDE
End in STATIN
Signifor
Somatuline Depot

335
Q

Somatostatin analog that suppresses the gall bladder

A

Octreotide

336
Q

Presentation of hypogonadism in women

A

Oligomennorhea, infertility, decreased libido, osteoporosis

337
Q

Clinical presentation of hypogonadism in men

A

Decreased libido, impotency, Decreased muscle mass, decreased beard and body hair growth

338
Q

Hypogonadism lab workup for males

A

Check testosterone levels (free and serum) verify with LH and PRL levels

339
Q

Hypogonadism workup for females

A

Check hCG to rule out pregnancy, check serum PRL, FSH, LH and TSH

340
Q

4 treatments for men with hypogonadism

A

Testosterone replacement to help with normal sex characteristics
hCG given for men with oligospermia
Leuprolidine (GnRH equivalent) if pituitary is intact
Clomiphene can also stimulate pituitary if intact

341
Q

Treatment for female hypogonadism

A

Estrogen and progesterone replacement or GnRH is secondary

342
Q

Peak cortisol secretion time

A

6 AM

343
Q

Synthetic oxytocin

A

Ptosin

344
Q

2 things that stimulate oxytocin release

A

Cervix dilation, suckling

345
Q

2 actions of ADH

A

Permeability of the collecting duct
Clotting factors from the endothelium

346
Q

3 things that rigger ADH secretion and 1 thing that inhibits it

A

Nausea, Hyperosmolarity and Decreased Volume
Inhibited by Cortisol

347
Q

Water is reabsorbed when the collecting duct is ______________ to water

A

Permeable

348
Q

Electrolyte imbalance caused by SIADH

A

Euvolemic hyponatremia - because the RAAS is suppressed

349
Q

2 most common causes of SIADH

A

Ectopic production of ADH or inappropriate secretion

350
Q

How pulmonary disorders stimulate ADH

A

Increased CO2 stimulates increased ADH

351
Q

Clinical presentation of SIADH

A

Euvolemic and Normotensive with severe hyponatremia leading to cerebral edema

352
Q

3 signs of mild to moderate hyponatremia

A

Headache, Muscle Cramps, Depressed reflexes

353
Q

3 signs of advanced hyponatremia

A

Vomiting, Somnolence, Acute psychosis

354
Q

3 signs of grave hyponatremia

A

Seizures, Coma, Respiratory insufficiency

355
Q

Diagnostic criteria for SIADH

A

Hyponatremia with continued excretion of Sodium at an abnormally high concentration, normal BP, skin turgor, absence of adrenal insufficiency

356
Q

What should correct symptoms in SIADH

A

Fluid restriction

357
Q

Acute SIADH

A

Less than 48 hours

358
Q

Chronic SIADH

A

More than 48 hours

359
Q

Disease resulting in overly rapid correction of hyponatremia and what to monitor

A

Central Pontine Myelinolysis - monitor daily plasma sodium rise

360
Q

Treatment of emergent hyponatremia

A

Raise serum sodium by no more than 10-12 mEq in the first 24 hours and aim for a max of 125-130 mEq/L
Can also use furosemide

361
Q

Treatment of acute hyponatremia

A

3% hypertonic saline
Loop diuretics (furosemide)
Vesopressin-2 receptor antagonists (conivaptan)
Water restriction to 500-1500 mL/d

362
Q

2 vasopressin receptor antagonists

A

Conivaptan
Tolvaptan

END in VAPTAN

363
Q

Risks of vasopressin receptor antagonists

A

Can correct sodium levels too quickly, avoid in hypovolemic hyponatremia - should be given by a provider with experience

364
Q

Treatment for chronic hyponatremia

A

Fluid restriction and V2 receptor antagonists

365
Q

Diabetes insipidus

A

Large quantities of urine with low specific gravity

366
Q

Primary central diabetes insipidus

A

No identifiable lesion of the pituitary or hypothalamus - may be autoimmune or genetic

367
Q

Secondary central diabetes insipidus

A

Damage to hypothalamus or pituitary stock that could be from tumor, infarction, or trauma

368
Q

Nephrogenic diabetes insipidus

A

Kidneys unresponsive to ADH, can be an X-linked trait

369
Q

Vasopressaine-induced diabetes insipidus

A

Last trimester of pregnancy, vasopressin is destroyed by a circulating enzyme but synthetic desmopressin is unaffected

370
Q

Clinical presentation of diabetes insipidus

A

Intense thirst with large urine volume - aggravated by corticosteroid administration

371
Q

1 diagnostic test to run for diabetes insipidus

A

24 hour urine collection for volume and creatinine

372
Q

6 serum levels to check for suspected diabetes insipidus

A

Serum glucose, urea nitrogen, calcium, potassium, sodium, uric acid levels

373
Q

Vasopressin challenge test

A

Give desmopressin acetate IN, SQ, or IV and measure urine volume for 12 hours

374
Q

Vasopressin in nephrogenic DI

A

High

375
Q

Central DI

A

Neurogenic DI

376
Q

Pituitary microadenoma

A

Under 10mm in diameter

377
Q

Pituitary macroadenoma

A

Over 10mm in diameter

378
Q

Mammosomatotrope

A

Pituitary cell that secretes PRL and GH

379
Q

4 familial pituitary tumor causes

A

Multiple Endocrine Neoplasia 1 & 4
Carney complex
Familial Pituitary adenomas (GH secreting)

380
Q

Most common pituitary tumor secretion

A

Prolactin

381
Q

Visual signs of pituitary tumor

A

Bitemporal hemianopia (loose peripheries)

382
Q

How could a pituitary tumor cause a headache

A

Stretching of the dura

383
Q

Rare symptom of a pituitary tumor

A

Hydrocephalus

384
Q

3 diagnostics for a pituitary tumor

A

MRI of brain
Ophthalmologic exam
Lab studies focused on: Acromegaly, Hyperprolactinemia, Cushings

385
Q

3 goals of pituitary tumor treatment

A

Normalize secretions, Relieve systemic symptoms, Shrink tumor to alleviate compression of structures

386
Q

Surgical approach for pituitary tumors

A

Transsphenoidal

387
Q

4 complications of transphenoidal resection surgery and their frequencies

A

Death - 1%
Transient hypopituitarism - 20%
Permanent diabetes insipidus - 10%
CSF leak - 4%

388
Q

Radiation for pituitary adenomas

A

Usually used as a post surgical adjunt - can help ablate nonfunctioning left over tumor tissue

389
Q

Prolactinoma pharm treatment

A

Dopamine agonists

390
Q

Acromegaly pharm treatment

A

Somatostatin analogs

391
Q

TSH secereting tumor treatment

A

Somatostatin analogs, maybe dopamine agonists

392
Q

ACTH secreting tumor treatment

A

Surgery or radiation - generally NOT responsive to treatment

393
Q

Non-functioning pituitary tumor treatment

A

Surgery or radiation - generally NOT responsive to treatment

Heme/Onc/Endo (5 decks)

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