Endocrinology Flashcards
1
Q
Regular Insulin
A
- onset: 30-60 minutes
- peak effect: 2-4 hrs
- duration: 5-8 hrs
2
Q
Short acting insulin
A
Lispro
Aspart
Glulisine
3
Q
Short acting insulin
A
- onset: 5 - 20 minutes
- peak effect: 0.5 - 5 hrs
- duration: 3-8 hrs
4
Q
NPH
A
- onset: 2-4 hrs
- peak effect: 6-10 hrs
- duration: 18 - 28 hrs
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
6
Q
DM II: Hx
A
- presents with hyperglycemia (polyuria, polydipsia, polyphagia, blurred vision, fatigue)
- nonketotic hyperosmolar hyperglycemia
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%
8
Q
Are anti-islet cell and anti GAD antibodies negative or positive in DM II
A
NEGATIVE
- only positive in DM type 1
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
10
Q
DM1
A
autoimmune pancreatic B-cell destruction, leading to insulin deficiency and abnormal glucose metabolism
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
12
Q
DM Type 1: Dx
A
anti-islet cell and anti-glutamic acid decarboxylase antibodiies
+ glucose levels under the required diagnoses
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%
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
15
Q
Treatment Complications of DM
A
- Dawn phenomenon (caused by too little pm insuliN)
- Somogyi effect (caused by too much pm insulin)
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
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
18
Q
Acute Complications of DM
A
DKA (diabetic ketoacidois)
Hyperosmoler hyperglycemic state
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
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
21
Q
DKA: Treatment
A
- Fluids, potassium, insulin, bicarb (if pH < 7), and treatment of initiating disease process
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
23
Q
Hypersomolar hyperglycemic state: Treatment
A
Aggressive fluid
Electrolyte replacement
Insulin
Treat initiating event
24
Q
Chronic Complications
A
Retinopathy (nonproliferative, preliferative)
Diabetic nephropathy
Neuropathy
MAcrovascular complications
25
DM retinopathy
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
26
Diabetic nephropathy
characterized by glomerular hyperfiltration followed by microalbuminuria
- preventative measures include ACEis/ARBs and BP/glucose control
27
DM Neuropathy
peripheral, symmetric sensorimotor neuropathy leading to burning pain, foot trauma, infections, and diabetic ulcers
- treat w/ preventative foot care and analgesics
28
Late complications of neuropathy
autonomic dysfunction include delayed gastric emptying, esophageal dysmotility, impotence and orthostatic hypotension
29
Macrovascular complications 2/2 DM
cardiovascular, cerebrovascular disease and PVD
- Goal is SBP < 130 and SDP < 80
- LDL < 100
- Triglycerides < 120
- patients should be on lose ASA
30
MC cause of death in diabetic patients
CV disease
31
Type 2 DM
dysfunction in glucose metabolism due to degrees of insulin resistance in peripheral tissues that ultimately lead to B-cell failure and complete insulin dependence
32
Type 2 DM: History and PE
- 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
33
Diagnosis of Type DM 2
- same as DM 1
| - negative anti-islet cell and anti-GAD antibodies
34
Screening recs for DM 2
Patient w/ no risk factors: HbA1C at 45 y/o retest every 3 years
35
Treatment of DM2
Tight glucose control (80 - 120 mg/dl) and H1Ac < 7%
36
Metabolic Syndrome
- AKA insulin resistance syndrome or syndrome X
| - associated w/ increased risk of CAD and CV mortality from CV event
37
Metabolic Syndrome: PE and HX
presents w/ abdominal obesity, high BP, impaired glycemic control and dyslipidemia
38
Metabolic Syndrome: Diagnosis
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
39
Metabolic Syndrome: Treatment
Intensive weight loss
Aggressive cholesterol management
BP control
- metformin shown to slow onset of diabetes in high risk populations
40
Nonproliferative DM retinopathy
- presents w/ exudates, dot-blot hemorrhages, and microaneurysms
41
Proliferative DM retinopathy
- presents w/ macular edema, vitreous traction and neovascularizaion of retinal vasculature
42
Lifestyle mods with DM2 treatment
- low fat, low carb, low cal diet
- 5 - 10% body weight loss w/ combo of diet and exercize
- moderate intensity exercise for 30 mini
43
Sulfonylureas (e.g. glipizide, glyburide, glimepriride)
- increased endogenous insulin secretion from B-cells
Reduce serum glucagon
- increase binding of insulin to tisse receptors
44
Sulfoylyureas: side effects
hypoglycemia
| weight gain
45
Metformin (giguanides)
inhibits hepatic gluconeogenesis and increased peripheral sensitivity to insulin
46
Metformin: side effects
Weight loss
GI upset
Lactic acidosis (rarely)
47
Metformin contraindicated in which patients
Elderly (> 80 y/o)
Renal insufficiency
Hepatic failure
Heart Failure
48
Thiazolidinediones (e.g. rosiglitazone, pioglitazone)
- decreases hepatic gluconeogenesis,
| - increases tissue uptake of glucose
49
Thiazolidinediones (e.g. rosiglitazone, pioglitazone)
- weight gain
- edema
- hepatotoxicity
- bone loss
50
Thiazolidinediones contraindicated in which patients
Contraindicated in patients w. heart failure
51
Alpha-glucosidase inhibitors (e.g. acarbose)
- decreases GI absorption of starch and disaccharides
| - used in pts with good dietar control of DM
52
Alpha-glucosidase inhibitors (e.g. acarbose): Side Effects
Flatulence
Diarrhea
Hypoglycemia
53
DPP-4 inhibitors (e.g. sitagliptin)
inhibit degradation of glucagon-like peptide 1 (GLP -1)
54
Incretins (e.g. exenatide)
GLP-1 agonists
- injected subcutaneousl
- delay absorption of food
- increases insulin secretion and glucagon secretion
55
Incretins (e.g. exenatide)
Nausea
| Pancreatitis (rarely)
56
Diabetes and CV risk modifications
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)
57
Primary hyperthyroidism
- decreased TSH
| - increased T4 and T3
58
Causes of primary hyperthyroidism
- Graves disease
- Toxic multinodular goiter
- Toxic adenoma
- Amiodoarone
- Postpartum thyrotoxicosis
- Postviral thyroiditis
59
Primary hypothyroidism
- increased TSH
| - decreased T4 and T3
60
Single best test for screening thyroid disease and assessment for thyroid fxn
TSH measurement
- high TSH associated w/ primary hypothyroidism
- low TSH associated w/ primary hyperthyroidism
61
Radioactive iodine uptake (RAI) and scan
- determines level and distribution of iodine by thyroid
| - useful for differentiation of hyperthyroid state but limited in determining malignancy
62
Total T4 measurement
not adequate sceening test
| 99% of T4 is bound to thyroglobulin
63
Free T4 measured
- preferred screening test for thyroid hormne levels
64
In primary endocrine disturbances
Gland itself is abnormal
65
In secondary endocrine disturbances
The pituitary gland is the source
66
In tertirary endocrine disturbances
Hypothalamus malfunctions
67
Causes of primary hypothyroidism
Hashimoto's thyroiditis
Iatrogenic (radioactive ablation, excision)
Drugs (lithium, amiodarone)
68
Most common cause of hyperthyroidism
Graves disease
69
Exophthalmos, pretibial myxedema, and thyroid bruits are specific for which disorder?
Graves disease
70
Graves disease
- autoimmune form of hyperthyroidism
- thyroid stimulating antibodies
- increased T4 and T3
- RAI percent uptake will be high
- RAI will show diffuse iodine uptake
71
Toxic adenoma/toxic multinodular goiter
- 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
Thyroiditis (postpartum, postviral, subacute)
- 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
Hyperthyroidism
- weight loss, heat intolerance, anxiety, palpitations, increased bowel frequency, insomnia
- sinus tachycardia, A-fib, fine tremor, lid lag
74
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?
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
Hyperthyroidism: Dx
- initial test is TSH level followed by T4 test
76
Symptomatic tx for hyperthyroidism
- Propranolol or atenolol to manage adrenegic symptoms
77
Pharmacologic tx for hyperthyroidism
Antithyroid drugs (methimazole or propylthiouracil)
78
Definitive tx for hyperthyroidism
- Radioactive ablation or total thyroidectioy
- administer levothyroxine (oral T4 replacement) to prevent hypothyroidism in pts who have undergone ablation or surgery
79
Hypothyroidism
- state involved decreased levels of T4/T2
| - most commonly due to Hashimoto's thyroiditis
80
Complications of hyperthyroidism
Thyroid storm
81
Thyroid storm
- acute life-threatening form of thyrotoxicosis
- treat w/ IV propranolol, PTU, and corticosteroids
- high dose potassium iodide is effective
82
Hashimoto's thyroiditis
- autoimmune hypothyroidism
- associated with positive anti-thryoglobulin and anti-microsomal (anti-TPO) antibodies that precipitate thyroid destruction
83
Thyroiditis (post-partum, postviral, subacute)
can have hypothyroid phase that follows hyperthyroid phase
| - hypothyroidism can be permanent
84
Hypothyoridism: Hx and PE
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
Hypothyroidism: Diagnosis
- best initial test is TSH level, followed by free T4
86
Tx for uncomplicated hypothyroidism
Administer levothyroixine
87
Complications of hypothyroidism
Myxedema coma
88
Myxedema coma
- severe hypothyroidism with decreased mental status, hypothermia, and other parasympathetic symptoms
- mortality is 30 - 60%
89
Tx of myxedema coma
- Treat urgently with IV levothyroxine and IV hydrocortisone (if adrenal insufficiency has not been excluded)
90
Thyroiditis
```
inflammation of thyroid gland
subtypes include:
subacute granulomatous
radiation-induced
autoimmune
postpartum
drug (e.g. amiodarone) thyroiditis
```
91
Subacute thyroiditis: Hx and PE
- tender thyroid
- malaise
- URI symptoms
92
Thyroiditis: Diagnosis
Thyroid dysfunction (thyrotoxiciosis followed by hypothyroidismz) with decreaed uptake on TAI and scan during hyperthyroid phase
93
Thyroiditis: Treatment
B-blockers for hyperthyroidism:
| Levothyroxine for hypothyroidism
94
Subacute thyroiditis
- usually self-limited
| - for severe cases treat with NSAIDS or oral corticosteroids
95
Thyroid Neoplasm
- very common and have increased incidence with age
| - most (95%) are benign
96
Most popular thyroid neoplasm
- Papillary thyrid cancer
97
Papillary thyroid cancer
- papillae (branching)
- palpable lymph nodes
- "pupil" nuclei (Orphan Annie nuclei)
- psamomma bodies within lesion
- Positive prognois
98
Thyroid Neoplasm: Hx and PE
- usually asymptomatic, discovered incidentally
| - large nodules adjacent to trachea/esophagus may cause dysphagia, dyspnea, cough, choking and have + family history
99
Thyroid neoplasm: risk factors
- 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
Management of thyroid nodule
1. Perform thyroid function tests (TSH and T4)
| 2. If tests are normal, biopsy the gland (esp if > 1 cm)
101
Treatment of acute hyperthyroidism
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
Gastroparesis
complication of DM
- DM decreases the ability of gut to sense stretch of bowel walls
- stretch stimulates gastric motility
103
Gastroparesis
- immobility of bowels that leads to bloating, constipation, early satiety, vomiting, and abdominal comfort
104
Tx of gastroparessis
Metoclopromide and Erythromycin which increase gastric motility
105
Thyroid neoplasm: diagnosis
- 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
Papillary thyroid carcinoma
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
Follicular thyroid carcinoma
- accounts for 17% of thyroid cancers
- found in thyroid hormone producing follicular cells
- 90% surivive 10 years after diagnosis
108
Medullary thyroid cancer
- 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
Anaplastic
- accounts for < 2% of thyroid cancers
- rapidly enlarges and metastasizes
- ten percent of patients survive for > 3 years
110
If FNA of thyroid is benign, Next step?
Follow with Physical Exam and U/S to assess for continued nodule growth or for development of suspicious characteristics
111
Malignant FNA of thyroid nodule. Now what?
First line tx: surgical resection w/ hemi or total thyroidectomt
- adjunctive radioiodine ablation folliwng excision
112
Indeterminate FNA of thyroid lesion
Watchful waiting vs hemithyroidectomy (10 - 30% change of malignancy)
- if resected, await final patholog to guide further treatment
113
Osteoporosis
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
Osteoporosis: Hx and PE
- 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
Risk factors: osteoporosis
- SMOKING and AGE (biggest risk factors)
- Excessive alcohol or caffeine
- Hx of estrogen depleting conditons)
- Excess corticosteroids
116
Osteoporosis: Diagnosis
DEXA (dual energy x-ray absorptiometry): standard technique for diagnosing osteoporosis
- reveals BMD > 2.5 SDs from normal peak level
117
Osteoporosis: Tx
Prevention and treatment with calcium and Vit D supplements
- weightbearing and smoking cessation
- antiresorptive meds
118
Osteoporosis Anti-Resorptive Meds
- Bisphosphonates ("-dronates")
- Selective estrogen receptor modulator (e.g. raloxifene)
- Intranasaal calcitonin
- Denosumab (a monoclonal antibody to RANK-L)
119
Osteoporosis: Complications
- Fracture is severe consequence of low BMD/osteoporosis
| - 50% chance of mortality
120
Paget's disease
- 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
Paget's Disease: Hx and PE
- 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
Paget's Disease: Diagnosis
Labs:
- INCREASED alk phos w/ normal calcium and phosphate levels
Imaging:
radionuclide bone scans is most sensitive for Paget's
123
Paget's Disease: Treatment
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
Complications of Paget's Disease
- Pathological fractures
- High output cardiac failure
- Osteosarcoma
125
Hyperparathyroidism
elevated serum PTH level with variable effects on calcium and phosphate
126
Primary hyperparathyroidism
Most cases (80%) are due to single hyperfunctioning adenoma with rest resulting from parathyroid hyperplasia and rarely parathyroid carcinoma
127
Secondary hyperparathyroidism
physiologic increase of PTH in response to renal insufficiency, calcium insufficiency or Vitamin D deficiency
128
Tertiary hyperparathyroidism
- 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
Classic radiologic signs of Paget's disease
- thickened cortex
- thickened trabeculae
- expasion of femoral head
130
Hyperparathyroidism: Hx and PE
asymptomatic but often sx of hypercalcemia (stones, bones, groans, and psych overtones)
131
Hypercalcemia: Sx
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
Hyperparathyroidism: Diagnosis
- Hypercalcemia, Hypophosphotemia, Hypercalciuria
- High PTH levels
- EKG wit short WT
133
Hyperparathyroidism: Treatment
- 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
Tx for acute hypercalcemia
Give IV fluids, loop diuretics, and IV bisphosphonates
135
Patient has hyperparathyroidism and renal insufficiency. Next step?
- Administer phosphate binders (Ca salts, sevelamer, and lanthanum carbonate) and restrict dietary phosphate
- Calcicanet - calcimetic that lowers serum PTH
136
Complications of hyperparathyroidism
Hypercalcemia
- can present acutely with coma or altered mental status
- bone disease
- nephrolithiasis
- Abdominal pain with nausea and vomiting
137
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?
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
Cushing's syndrome
too much cortisol
| - usually caused by too much excess steroids
139
Cushing's disease
too much cortisol from an ACTH producing pituitary adenoma
140
Other causes of Cushing's disease
- excess adrenal secretion of cortisol
- bilateral adrenal hyperplasia
- ectopic ACTH production from occult neoplasm
141
Cushing's disease: History and PE
- 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
Cushing's disease: Diagnosis
- 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
How to distinguish ACTH-dependent (pituitary/ectopic) from ACTH-independent causes (adrenal) causes of Cushing's disease
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
Treatment: Cushing's disease
- Surgical resection of source (pituitary, adrenal, neoplasm)
- Inhibitors of adrenal steroidogenesis (e.g. spironolactone, epelerone) are helpful for bilateral
- permanent hormone replacement therapy
145
Acromegaly
elevated growth hormone (GH) in adults, most commonly due to benign pituitary GH secreting adneoma
- children with excess GH production present with gigantism
146
Acromegaly: Hx and PE
- 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
Acromegaly: Dx
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
Acromegaly: Tx
Transsphenoidal surgical resection or external beam radiation
- Octeotride (somatostatin analog) can suppress GH secretion
- Pegvisomant (GH antagonist) can block peripheral actions of GH
149
Hyperprolactinoma
elevated prolactin levels, most commonly due to pituitary adenoma
- most common functionaing pituitary tumor
150
Other causes of prolactinoma
- Masses (e.g. craniopharyngioma,
- Drugs (e.g. dopamine blockers)
- Renal Failure
- Cirrhosis
151
Hyperprolactinoma: Hx and PE
- elevaed GnRH secretion and consequently lowers LH and FSH secretion
- INFERTILITY, GALACTORRHEA, ANEMORRHEA
