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Endocrinology Flashcards

1
Q

Regular Insulin

A
  • onset: 30-60 minutes
  • peak effect: 2-4 hrs
  • duration: 5-8 hrs
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2
Q

Short acting insulin

A

Lispro
Aspart
Glulisine

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3
Q

Short acting insulin

A
  • onset: 5 - 20 minutes
  • peak effect: 0.5 - 5 hrs
  • duration: 3-8 hrs
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4
Q

NPH

A
  • onset: 2-4 hrs
  • peak effect: 6-10 hrs
  • duration: 18 - 28 hrs
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5
Q

Diabetes Type II

A
  • dysfunction in glucose metabolism due to varying degrees of insulin resistance in peripheral tissue that lead to B-cell failure and insulin dependence
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6
Q

DM II: Hx

A
  • presents with hyperglycemia (polyuria, polydipsia, polyphagia, blurred vision, fatigue)
  • nonketotic hyperosmolar hyperglycemia
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7
Q

DM II: Dx

A

One of the following:

  • fasting glucose > 126 on at least 2 occasions
  • random glucose > 200 mg/dL plus sx
  • 2 hr postprandial glucose test > 200 mg/dL after oral glucose test
  • Hemoglobin A1C > 6.5%
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8
Q

Are anti-islet cell and anti GAD antibodies negative or positive in DM II

A

NEGATIVE

- only positive in DM type 1

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9
Q

Dawn phenomenon

A
  • morning hyperglycemia due to normal nocturanal relase of counterregulatory hormones (e..g glucagon, epinepherine, cortisol) whihc increase insulin resistence and blood glucose levels
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10
Q

DM1

A

autoimmune pancreatic B-cell destruction, leading to insulin deficiency and abnormal glucose metabolism

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11
Q

History and PE: Diabetes Mellitus 1

A
  • classically presents as POLYURIA, POLYDIPSIA, POLYPHAGIA and unexplained weightloss
  • usually affects nonobese children or young adults
  • associated w/ HLA-DR3 and DR4
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12
Q

DM Type 1: Dx

A

anti-islet cell and anti-glutamic acid decarboxylase antibodiies
+ glucose levels under the required diagnoses

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13
Q

DM Type 1: Glucose Diagnosese

A

Need one of the following:

  • Fasting glucose (> 8hr) plasma glucose > 126 mg/dL
  • random plasma glucose > 200 mg/dL plus symptoms
  • 2hr postprandial glucose level > 200 mg/dL following glucose tolerance test on 2 separate occasions
  • Hemoglobin A1C > 6.5%
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14
Q

DM Type 1: Treatment

A
  • insulin injections to maintain normal levels (80 - 120)

- consider insulin pump which provides continuous short actin insulin infusion

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15
Q

Treatment Complications of DM

A
  • Dawn phenomenon (caused by too little pm insuliN)

- Somogyi effect (caused by too much pm insulin)

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16
Q

Dawn phenomenon

A
  • caused by too little pm NPH insulin
  • morning hyperglucemia due to nocturnal release of counterregulatory hormones (epi, cortisol) which increase insulin resistance and blood glucose
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17
Q

Somogyi effect

A
  • caused by too much pm NPH insulin
  • REBOUND HYPERGLYCEMIA
  • excess insulin causes hypoglucemia which stimulates counterregulatory hormones that increase blood glucose levels
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18
Q

Acute Complications of DM

A

DKA (diabetic ketoacidois)

Hyperosmoler hyperglycemic state

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19
Q

DKA

A
  • hyperglycemia induced crisis that commonly occurs in type 1 DM.
  • often precipitated by infections, MI, trauma, or alcohol or insulin non-compliance
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20
Q

DKA: Sx

A

abdominal pain, vomiting, Kussmaul’s respirations (short rapid breathing)

  • fruity acetone breath order
  • pts are severely dehydrated w/ electrolyte abnormalities and may develop mental retardation
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21
Q

DKA: Treatment

A
  • Fluids, potassium, insulin, bicarb (if pH < 7), and treatment of initiating disease process
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22
Q

Hyperosmolar hyperglycemic states

A
  • presents with profound dehydration, mental status changes, hyperosmolality, and extremely high glucose (> 600mg/dL)
  • NO ACIDOSIS AND WITH SMALL/NO KETONES
  • occurs in Type 2 DM
  • precipitated by dehydration and can be fatal
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23
Q

Hypersomolar hyperglycemic state: Treatment

A

Aggressive fluid
Electrolyte replacement
Insulin
Treat initiating event

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24
Q

Chronic Complications

A

Retinopathy (nonproliferative, preliferative)
Diabetic nephropathy
Neuropathy
MAcrovascular complications

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25
Q

DM retinopathy

A

appears when diabetes present for at lease 3-5 years

  • preventative measures include glycemic and BP control, annual eye exams
  • Laser photocoagulation therapy for neovascularization
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26
Q

Diabetic nephropathy

A

characterized by glomerular hyperfiltration followed by microalbuminuria
- preventative measures include ACEis/ARBs and BP/glucose control

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27
Q

DM Neuropathy

A

peripheral, symmetric sensorimotor neuropathy leading to burning pain, foot trauma, infections, and diabetic ulcers
- treat w/ preventative foot care and analgesics

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28
Q

Late complications of neuropathy

A

autonomic dysfunction include delayed gastric emptying, esophageal dysmotility, impotence and orthostatic hypotension

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29
Q

Macrovascular complications 2/2 DM

A

cardiovascular, cerebrovascular disease and PVD

  • Goal is SBP < 130 and SDP < 80
  • LDL < 100
  • Triglycerides < 120
  • patients should be on lose ASA
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30
Q

MC cause of death in diabetic patients

A

CV disease

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31
Q

Type 2 DM

A

dysfunction in glucose metabolism due to degrees of insulin resistance in peripheral tissues that ultimately lead to B-cell failure and complete insulin dependence

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32
Q

Type 2 DM: History and PE

A
  • present w/ hyperglycemia (polyuria, polydipsia, polyphagia, blurred vision, fatigue)
  • more insidious onset than Type 1
  • occurs in older adults with often truncal obseisty and has strong genetic disposition
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33
Q

Diagnosis of Type DM 2

A
  • same as DM 1

- negative anti-islet cell and anti-GAD antibodies

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34
Q

Screening recs for DM 2

A

Patient w/ no risk factors: HbA1C at 45 y/o retest every 3 years

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35
Q

Treatment of DM2

A

Tight glucose control (80 - 120 mg/dl) and H1Ac < 7%

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36
Q

Metabolic Syndrome

A
  • AKA insulin resistance syndrome or syndrome X

- associated w/ increased risk of CAD and CV mortality from CV event

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37
Q

Metabolic Syndrome: PE and HX

A

presents w/ abdominal obesity, high BP, impaired glycemic control and dyslipidemia

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38
Q

Metabolic Syndrome: Diagnosis

A

3 out of 5 following criteria:

  • abdominal obesity: > 40 inches in men or > 35 in in women
  • triglycerides > 150 mg/dL
  • HDL < 40 mg/dl in men and < 50 mg/dl in women
  • BP > 130/85 mm Hg or a requirement for BP meds
  • fasting glucose > 100 mg/dL
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39
Q

Metabolic Syndrome: Treatment

A

Intensive weight loss
Aggressive cholesterol management
BP control
- metformin shown to slow onset of diabetes in high risk populations

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40
Q

Nonproliferative DM retinopathy

A
  • presents w/ exudates, dot-blot hemorrhages, and microaneurysms
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41
Q

Proliferative DM retinopathy

A
  • presents w/ macular edema, vitreous traction and neovascularizaion of retinal vasculature
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42
Q

Lifestyle mods with DM2 treatment

A
  • low fat, low carb, low cal diet
  • 5 - 10% body weight loss w/ combo of diet and exercize
  • moderate intensity exercise for 30 mini
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43
Q

Sulfonylureas (e.g. glipizide, glyburide, glimepriride)

A
  • increased endogenous insulin secretion from B-cells
    Reduce serum glucagon
  • increase binding of insulin to tisse receptors
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44
Q

Sulfoylyureas: side effects

A

hypoglycemia

weight gain

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45
Q

Metformin (giguanides)

A

inhibits hepatic gluconeogenesis and increased peripheral sensitivity to insulin

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46
Q

Metformin: side effects

A

Weight loss
GI upset
Lactic acidosis (rarely)

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47
Q

Metformin contraindicated in which patients

A

Elderly (> 80 y/o)
Renal insufficiency
Hepatic failure
Heart Failure

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48
Q

Thiazolidinediones (e.g. rosiglitazone, pioglitazone)

A
  • decreases hepatic gluconeogenesis,

- increases tissue uptake of glucose

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49
Q

Thiazolidinediones (e.g. rosiglitazone, pioglitazone)

A
  • weight gain
  • edema
  • hepatotoxicity
  • bone loss
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50
Q

Thiazolidinediones contraindicated in which patients

A

Contraindicated in patients w. heart failure

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51
Q

Alpha-glucosidase inhibitors (e.g. acarbose)

A
  • decreases GI absorption of starch and disaccharides

- used in pts with good dietar control of DM

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52
Q

Alpha-glucosidase inhibitors (e.g. acarbose): Side Effects

A

Flatulence
Diarrhea
Hypoglycemia

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53
Q

DPP-4 inhibitors (e.g. sitagliptin)

A

inhibit degradation of glucagon-like peptide 1 (GLP -1)

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54
Q

Incretins (e.g. exenatide)

A

GLP-1 agonists

  • injected subcutaneousl
  • delay absorption of food
  • increases insulin secretion and glucagon secretion
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55
Q

Incretins (e.g. exenatide)

A

Nausea

Pancreatitis (rarely)

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56
Q

Diabetes and CV risk modifications

A

Presence of diabetes is equivalent to highest risk for CV disease regardless of other factors

  • ASA for pts > 40 y/o
  • statins for HLD ( goal LDL < 100 or < 70 w/ cardiac dz)
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57
Q

Primary hyperthyroidism

A
  • decreased TSH

- increased T4 and T3

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58
Q

Causes of primary hyperthyroidism

A
  • Graves disease
  • Toxic multinodular goiter
  • Toxic adenoma
  • Amiodoarone
  • Postpartum thyrotoxicosis
  • Postviral thyroiditis
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59
Q

Primary hypothyroidism

A
  • increased TSH

- decreased T4 and T3

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60
Q

Single best test for screening thyroid disease and assessment for thyroid fxn

A

TSH measurement

  • high TSH associated w/ primary hypothyroidism
  • low TSH associated w/ primary hyperthyroidism
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61
Q

Radioactive iodine uptake (RAI) and scan

A
  • determines level and distribution of iodine by thyroid

- useful for differentiation of hyperthyroid state but limited in determining malignancy

62
Q

Total T4 measurement

A

not adequate sceening test

99% of T4 is bound to thyroglobulin

63
Q

Free T4 measured

A
  • preferred screening test for thyroid hormne levels
64
Q

In primary endocrine disturbances

A

Gland itself is abnormal

65
Q

In secondary endocrine disturbances

A

The pituitary gland is the source

66
Q

In tertirary endocrine disturbances

A

Hypothalamus malfunctions

67
Q

Causes of primary hypothyroidism

A

Hashimoto’s thyroiditis
Iatrogenic (radioactive ablation, excision)
Drugs (lithium, amiodarone)

68
Q

Most common cause of hyperthyroidism

A

Graves disease

69
Q

Exophthalmos, pretibial myxedema, and thyroid bruits are specific for which disorder?

A

Graves disease

70
Q

Graves disease

A
  • autoimmune form of hyperthyroidism
  • thyroid stimulating antibodies
  • increased T4 and T3
  • RAI percent uptake will be high
  • RAI will show diffuse iodine uptake
71
Q

Toxic adenoma/toxic multinodular goiter

A
  • result in hyperthyroidism due to autonomous hyperactive thyroid nodules
  • RAI percent uptake will be normal to high
  • RAI scan will show nodules/region of increased uptake
72
Q

Thyroiditis (postpartum, postviral, subacute)

A
  • due to transient inflammation of thyroid gland w/ release of previously synthesized thyroid hormone
  • causes temp increase in T4 and T3
  • RAI uptake will be low
  • RAI scan will show low iodine uotake
  • hypothyroid phase may follow hyperthyroid phase
73
Q

Hyperthyroidism

A
  • weight loss, heat intolerance, anxiety, palpitations, increased bowel frequency, insomnia
  • sinus tachycardia, A-fib, fine tremor, lid lag
74
Q

10 yr old M presents to ER with 2 weeks of polyuria and polydipsia together w/ new onset of lethargy. PE show signs of dehydration and labs reveal sugars > 800. DKA diagnosis is made and pt is started on insulin and IV fluids. Next step in management?

A

Add 5% dextrose to IV fluids

  • in DKA important to start insulin and gluids
  • initially goal is to rehydrate patient and lower blood glucose, but as glucose reaches 250-300, must add dextrose to avoid hypoglycemia
75
Q

Hyperthyroidism: Dx

A
  • initial test is TSH level followed by T4 test
76
Q

Symptomatic tx for hyperthyroidism

A
  • Propranolol or atenolol to manage adrenegic symptoms
77
Q

Pharmacologic tx for hyperthyroidism

A

Antithyroid drugs (methimazole or propylthiouracil)

78
Q

Definitive tx for hyperthyroidism

A
  • Radioactive ablation or total thyroidectioy
  • administer levothyroxine (oral T4 replacement) to prevent hypothyroidism in pts who have undergone ablation or surgery
79
Q

Hypothyroidism

A
  • state involved decreased levels of T4/T2

- most commonly due to Hashimoto’s thyroiditis

80
Q

Complications of hyperthyroidism

A

Thyroid storm

81
Q

Thyroid storm

A
  • acute life-threatening form of thyrotoxicosis
  • treat w/ IV propranolol, PTU, and corticosteroids
  • high dose potassium iodide is effective
82
Q

Hashimoto’s thyroiditis

A
  • autoimmune hypothyroidism
  • associated with positive anti-thryoglobulin and anti-microsomal (anti-TPO) antibodies that precipitate thyroid destruction
83
Q

Thyroiditis (post-partum, postviral, subacute)

A

can have hypothyroid phase that follows hyperthyroid phase

- hypothyroidism can be permanent

84
Q

Hypothyoridism: Hx and PE

A

presents with weakness, fatigue, COLD INTOLERNCE, CONSTIPATION, weight gain, hair loss, menstrual abnormalities, and HOARSENESS
- exam shows DRY, COLD, PUFFY SKIN accompanied by edema, bradycardia, and delayed relxation of DTRs

85
Q

Hypothyroidism: Diagnosis

A
  • best initial test is TSH level, followed by free T4
86
Q

Tx for uncomplicated hypothyroidism

A

Administer levothyroixine

87
Q

Complications of hypothyroidism

A

Myxedema coma

88
Q

Myxedema coma

A
  • severe hypothyroidism with decreased mental status, hypothermia, and other parasympathetic symptoms
  • mortality is 30 - 60%
89
Q

Tx of myxedema coma

A
  • Treat urgently with IV levothyroxine and IV hydrocortisone (if adrenal insufficiency has not been excluded)
90
Q

Thyroiditis

A 
inflammation of thyroid gland 
subtypes include: 
subacute granulomatous
radiation-induced
autoimmune
postpartum
drug (e.g. amiodarone) thyroiditis
91
Q

Subacute thyroiditis: Hx and PE

A
  • tender thyroid
  • malaise
  • URI symptoms
92
Q

Thyroiditis: Diagnosis

A

Thyroid dysfunction (thyrotoxiciosis followed by hypothyroidismz) with decreaed uptake on TAI and scan during hyperthyroid phase

93
Q

Thyroiditis: Treatment

A

B-blockers for hyperthyroidism:

Levothyroxine for hypothyroidism

94
Q

Subacute thyroiditis

A
  • usually self-limited

- for severe cases treat with NSAIDS or oral corticosteroids

95
Q

Thyroid Neoplasm

A
  • very common and have increased incidence with age

- most (95%) are benign

96
Q

Most popular thyroid neoplasm

A
  • Papillary thyrid cancer
97
Q

Papillary thyroid cancer

A
  • papillae (branching)
  • palpable lymph nodes
  • “pupil” nuclei (Orphan Annie nuclei)
  • psamomma bodies within lesion
  • Positive prognois
98
Q

Thyroid Neoplasm: Hx and PE

A
  • usually asymptomatic, discovered incidentally

- large nodules adjacent to trachea/esophagus may cause dysphagia, dyspnea, cough, choking and have + family history

99
Q

Thyroid neoplasm: risk factors

A
  • Hx of childhood radiation
  • Cold nodules (minimal uptake on RAI scan)
  • Female < 20 or > 70
  • Firm and fixed solitary nodules
  • Family History (esp medullary thyroid cancer)
  • Rapidly growing nodules with hoarseness
100
Q

Management of thyroid nodule

A
  1. Perform thyroid function tests (TSH and T4)

2. If tests are normal, biopsy the gland (esp if > 1 cm)

101
Q

Treatment of acute hyperthyroidism

A
  1. Propranolol: blocks target organ effect, inhibits converiosion of T4 to T3
  2. Thiourea drugs (methimazole and PTU): blocks hormone production
  3. Iopanoic acid and ipodate: blocks peripheral concersion of T4 to T2
  4. Steroids (hydrocortisone)
  5. Radioactive iodine: ablates gland for permanent cure
102
Q

Gastroparesis

A

complication of DM

  • DM decreases the ability of gut to sense stretch of bowel walls
  • stretch stimulates gastric motility
103
Q

Gastroparesis

A
  • immobility of bowels that leads to bloating, constipation, early satiety, vomiting, and abdominal comfort
104
Q

Tx of gastroparessis

A

Metoclopromide and Erythromycin which increase gastric motility

105
Q

Thyroid neoplasm: diagnosis

A
  • TFTSs to detect hyperfunctioning nodules, followed by RA scan
  • U/S to determine if nodule is solid or cystic
  • FNA to assess for malignancy
106
Q

Papillary thyroid carcinoma

A

represents 75 - 80% of thyroid cancers

  • female to male ratio is 3:1
  • found in thyroid hormone producing follicular cells
  • 90% pts survive in 10 years
107
Q

Follicular thyroid carcinoma

A
  • accounts for 17% of thyroid cancers
  • found in thyroid hormone producing follicular cells
  • 90% surivive 10 years after diagnosis
108
Q

Medullary thyroid cancer

A
  • responsible for 6-8% of thyroid cancers
  • found in calcitonin-producing C cells
  • prognosis related to degree of vascular invasion
  • 80% survive 10 years after surgery
  • consider MEN2A or MEN2B if family hx
109
Q

Anaplastic

A
  • accounts for < 2% of thyroid cancers
  • rapidly enlarges and metastasizes
  • ten percent of patients survive for > 3 years
110
Q

If FNA of thyroid is benign, Next step?

A

Follow with Physical Exam and U/S to assess for continued nodule growth or for development of suspicious characteristics

111
Q

Malignant FNA of thyroid nodule. Now what?

A

First line tx: surgical resection w/ hemi or total thyroidectomt
- adjunctive radioiodine ablation folliwng excision

112
Q

Indeterminate FNA of thyroid lesion

A

Watchful waiting vs hemithyroidectomy (10 - 30% change of malignancy)
- if resected, await final patholog to guide further treatment

113
Q

Osteoporosis

A

common metabolic bone disease characterized low bone mass and microarchitectural disruption

  • bone mineral density (BMD) < 2.5 SDs from normal peak bone mass
  • affects mostly thin postmenopausal women (esp. Whites and Asians)
114
Q

Osteoporosis: Hx and PE

A
  • commonly assymptomatic even with vertebral fracture
  • exam may show HIP FRACTURES, VERTEBRAL COMPRESSION FRACTURES (loss of height and progressive thoracic kyphosis) and/or distal radius fractures (Colles’ fracture) following minimum trauma
115
Q

Risk factors: osteoporosis

A
  • SMOKING and AGE (biggest risk factors)
  • Excessive alcohol or caffeine
  • Hx of estrogen depleting conditons)
  • Excess corticosteroids
116
Q

Osteoporosis: Diagnosis

A

DEXA (dual energy x-ray absorptiometry): standard technique for diagnosing osteoporosis
- reveals BMD > 2.5 SDs from normal peak level

117
Q

Osteoporosis: Tx

A

Prevention and treatment with calcium and Vit D supplements

  • weightbearing and smoking cessation
  • antiresorptive meds
118
Q

Osteoporosis Anti-Resorptive Meds

A
  • Bisphosphonates (“-dronates”)
  • Selective estrogen receptor modulator (e.g. raloxifene)
  • Intranasaal calcitonin
  • Denosumab (a monoclonal antibody to RANK-L)
119
Q

Osteoporosis: Complications

A
  • Fracture is severe consequence of low BMD/osteoporosis

- 50% chance of mortality

120
Q

Paget’s disease

A
  • characterized by increased rate of bone turnover w/ excess resportion and formation of bone
  • “MOSAIC” lamellar bone pattern on X-ray
  • suspected to be caused by latent viral infection
121
Q

Paget’s Disease: Hx and PE

A
  • usually asymptomatic but may present w/ aching bone or joint pain or headaches (if skull is involved)
  • fx at paget’s site
  • nerve entrapment (leads to loss of hearing in 30% of cases)
  • skull, vertebral bodies, pelvis, long bones most commonly affected
122
Q

Paget’s Disease: Diagnosis

A

Labs:
- INCREASED alk phos w/ normal calcium and phosphate levels
Imaging:
radionuclide bone scans is most sensitive for Paget’s

123
Q

Paget’s Disease: Treatment

A

MOST ARE ASYMPTOMATIC and REQUIRE NO TREATMENT

  • no cure for Parget’s disease
  • if severe pain or involvement of vulnerable site (femoral neck):
  • bisphonates and calcitonin can slow osteoclastic bone resorption
124
Q

Complications of Paget’s Disease

A
  • Pathological fractures
  • High output cardiac failure
  • Osteosarcoma
125
Q

Hyperparathyroidism

A

elevated serum PTH level with variable effects on calcium and phosphate

126
Q

Primary hyperparathyroidism

A

Most cases (80%) are due to single hyperfunctioning adenoma with rest resulting from parathyroid hyperplasia and rarely parathyroid carcinoma

127
Q

Secondary hyperparathyroidism

A

physiologic increase of PTH in response to renal insufficiency, calcium insufficiency or Vitamin D deficiency

128
Q

Tertiary hyperparathyroidism

A
  • seen in dialysis patient w/ long-standing secondary hyperparathyrodism leads to hyperplasia of parathyroid glands
  • when 1 or more PT glands become autonomous tertiary parathyroidism results
129
Q

Classic radiologic signs of Paget’s disease

A
  • thickened cortex
  • thickened trabeculae
  • expasion of femoral head
130
Q

Hyperparathyroidism: Hx and PE

A

asymptomatic but often sx of hypercalcemia (stones, bones, groans, and psych overtones)

131
Q

Hypercalcemia: Sx

A

Stones, Bones, Groans, and Psych Overtones

  • Stones (nephrolithiasis)
  • Bones (bone pain, myalgia, arthralgia)
  • Groans (GI sx, n/v. PUD, pancreatitis)
  • Psych Overtones (fatigue, depression, anxiety
132
Q

Hyperparathyroidism: Diagnosis

A
  • Hypercalcemia, Hypophosphotemia, Hypercalciuria
  • High PTH levels
  • EKG wit short WT
133
Q

Hyperparathyroidism: Treatment

A
  • Parathyroidectomy: if patient is symptomatic or if certain criteria is met
  • solitary adenoma: 1 gland must be removed
  • PT hyperplasia: 3.5 glands must be reomoved
134
Q

Tx for acute hypercalcemia

A

Give IV fluids, loop diuretics, and IV bisphosphonates

135
Q

Patient has hyperparathyroidism and renal insufficiency. Next step?

A
  • Administer phosphate binders (Ca salts, sevelamer, and lanthanum carbonate) and restrict dietary phosphate
  • Calcicanet - calcimetic that lowers serum PTH
136
Q

Complications of hyperparathyroidism

A

Hypercalcemia

  • can present acutely with coma or altered mental status
  • bone disease
  • nephrolithiasis
  • Abdominal pain with nausea and vomiting
137
Q

Asymptomatic 36 y/o M presents for annual physical. Patient has no sign PMH and takes no meds. PE is unremarkable. PE reveal serum Ca level of 11.3. Returns in 2 weeks and his serum Ca level is elevated. Further w/u is initiated and add’l studies show normal PTH level and low 24 urinary calcium level. Likely diagnosis?

A

FAMILIAL HYPOCALCIURIC HYPERCALCEMIA

  • inherited disorder due to mutations in Ca sensing receptor present in parathyroid and kidney present in elevated Ca levels
  • unlike patient w/ primary hyperparathyroidism, patients are asmptomatic and have low urinary Ca levels
  • no treatment required
138
Q

Cushing’s syndrome

A

too much cortisol

- usually caused by too much excess steroids

139
Q

Cushing’s disease

A

too much cortisol from an ACTH producing pituitary adenoma

140
Q

Other causes of Cushing’s disease

A
  • excess adrenal secretion of cortisol
  • bilateral adrenal hyperplasia
  • ectopic ACTH production from occult neoplasm
141
Q

Cushing’s disease: History and PE

A
  • presents with HYPERTENSION, DM2, depression, and weight gain and muscle weakness, increased risk of infection, HIRSUITISM
  • exam shows CENTRAL OBESITY, EXCESSIVE HAIR GROWTH, PURPLE STRIAE, MOON FACIES, BUFFALO HUMP
  • Headache
142
Q

Cushing’s disease: Diagnosis

A
  • 2 of 3 following tests:
    1. elevated 24 hr urine cortisol
    2. 1mg dexamethsone suppression test if AM cortisol is persistently elevated
    3. elevated midnight salivary test on 2 separate nights
143
Q

How to distinguish ACTH-dependent (pituitary/ectopic) from ACTH-independent causes (adrenal) causes of Cushing’s disease

A

Measure AM cortisol and ACTH levels
- if ACTH is elevated then Cushing’s disease or ectopic ACTH likely
- Pituitary MRI should be orderd if lab testing suggests Cushing’s disease
-

144
Q

Treatment: Cushing’s disease

A
  • Surgical resection of source (pituitary, adrenal, neoplasm)
  • Inhibitors of adrenal steroidogenesis (e.g. spironolactone, epelerone) are helpful for bilateral
  • permanent hormone replacement therapy
145
Q

Acromegaly

A

elevated growth hormone (GH) in adults, most commonly due to benign pituitary GH secreting adneoma
- children with excess GH production present with gigantism

146
Q

Acromegaly: Hx and PE

A
  • presents with ENLARGEMENT OF SKULLS, HANDS, FEET, and COARSE FACIAL FX
  • associated with increased risk of carpal tunnel synrome, OSA, type 2 DM, diastolic dysfuncton
  • BITEMPORAL HEMIANOPSIA ma result from compression of optic chiasm
  • Excess GH may lead to GLUCOSE INTOLERANCE or DIABETES
147
Q

Acromegaly: Dx

A

Labs: MEASURE IGF-1 levels (increased with acromegaly)

  • confirm with oral glucose suppression test (GH levels remain high despite glucose)
  • MRI shows sellar lesion
148
Q

Acromegaly: Tx

A

Transsphenoidal surgical resection or external beam radiation

  • Octeotride (somatostatin analog) can suppress GH secretion
  • Pegvisomant (GH antagonist) can block peripheral actions of GH
149
Q

Hyperprolactinoma

A

elevated prolactin levels, most commonly due to pituitary adenoma
- most common functionaing pituitary tumor

150
Q

Other causes of prolactinoma

A
  • Masses (e.g. craniopharyngioma,
  • Drugs (e.g. dopamine blockers)
  • Renal Failure
  • Cirrhosis
151
Q

Hyperprolactinoma: Hx and PE

A
  • elevaed GnRH secretion and consequently lowers LH and FSH secretion
  • INFERTILITY, GALACTORRHEA, ANEMORRHEA

First AId 2CK (22 decks)

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