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Panhypopituitarism

- caused by any condition that compression or damage to pituitary gland
- look for tumors (e.g. metastatic cancer, adenomas, Ranthke cleft cysts)
- look for conditions (e.g. hemachromatosis, sarcoidois)

1

Panhypotpituitarism: presentation

symptoms dependent of deficiency of a specific hormone

2

Prolactin deficiency

- in women, prolactin deficiency inhibits lactation after childbirth

3

Deficiency of LH and FSH

- women are unable to menstruate (become anovulatory)
- men unable to produce sperm and have erectile dysfunction
- both men and women have decreased libido and decreased axillary, pubic, and body hair

4

Kellman syndrome

- decreased FSH and LH from decreased GnRH
- anosmia
- renal agenesis

5

Growth hormone deficiency

- children present with short stature and dwarfism
- adults have few symptoms b/c catecholamines, glucagon, and corticol act as stress hormones

6

Adult presentation of GH deficiency

- Central obesiry
- increased LDL and cholesterol levels
- reduced lean muscle mass

7

Growth hormone diagnostic tests

- Hyponatremia (2/2 hypothyroidism and isolated glucocorticoid underpoduction)
- potassium remains levels b/c aldosterone is not affected
- MRI detects compressing mass lesions

8

Low TSH and low thyroxine

confirm w/ decreased TSH response to TRH

9

decreased ACTH and decreased cortisol level

normal response to cosyntropin stimulation of adrenal, cortisol will rise in recent disease and cortisol is abnormal b/c of adrenal atrophy

10

Metyrapone

inhibits 11- B hydroxlase
- decreases output of adrenal gland
- should cause ACTH to rise b/c cortisol goes down

11

Insulin stimulation

- insulin decreases glucose levels so GH should rise
- failure to rise in response to insulin indicates pituitary insufficiency

12

Posterior pituitary

- produces ADH and oxytocin
- no deficiency disease for oxytocin

13

Oxytocin deficeiency

- aids with uterine contraction
- delivery still occurs even if active

14

Diabetes Inspidus

- decrease in amt of ADH from pituitary (central DI) or decease in response to ADH on collecting tubules (nephrogenic DI)

15

Central DI

any destruction of brain from stroke, tumor, trauma, hypoxia, or infiltration of gland from sarcoidosis or infection

16

Nephrogenic DI

Kidney diseases (e.g chronic pyelonephritis, amyloidosis, myeloma, and sickle cell disease) damaged kidney enough to inhibit effect of ADH

17

Electrolyte abnormalities that can cause nephrogenic DI

- Hypercalcemia
- Hypokalemia

18

DI: presentation

- presents with high volume urine and excessive thirst resulting in volume depletion and hypernatremia
- hypernatremia sx (condusion, disorientation, lethargy then later seizures, coma)

19

classic cause of nephrogenic DI

Lithium
- look for bipolar patients

20

Diabetes inspidus

- serum sodium is elevated
- decreased urine osmolality and urine sodium is decreased

21

Difference btwn central DI and nephrogenic DI

Response to vasopressin (desmopression(

22

Central DI: Treatment

- treated with long term vasopression

23

Nephrogenic DI: treatment

- correct underlying cuase (e.g. hypokalemia or hypercalcemia)
- treat with thiazides, amiloride, or prostiglandin inhibitors (NSAIDS)

24

Acromegaly

overproduction of growth hormone leading to soft tissue overgrowth

25

Acromegaly: Etiology

- often cuased by pituitary adenoma
- can be associated with MEN (e.g. parathyroid or pancreatic disorders)
- rarely caused by ectopic GH or GHrH production from lymphoma or bronchial carcinoid

26

Acromegaly: presentation

- increased hat, ring, and shoe size
- carpal tunnel syndrome and sleep apnea from enlarged soft tissues
- body odor from sweat gland hypertrophy
- coarsening facial features
- colonic polyps and skin tags
- arthralgias
- hypertension
- cardiomegaly and CHF

27

Best initial test for suspected acromegaly?

Insulin growth factor (IGF -1) levels

28

Acromegaly: lab testing

- Glucose interolerance and hyperlipidemia, which contribute to cardiac dysfunction

29

Most accurate test for acromegaly

Glucose suppression test
- normally glucose suppreses GH levels

30

When is the MRI done in diagnosis of acromegaly?

Only after lab identification of acromegaly

31

Acromegaly: Treatment

1. Surgery: transphenoidal resection of pituitary
2. Medications
- cabergoline
- octreotide or lanreotide
- pegvisomant
3. Radiotherapy

32

Cabergoline

dopamine will inhibit GH release

33

Octreotide or lanreotide

somatostatin inhibits GH release

34

Pegvisomant

Gh receptor antagonist, inhibits IGF release from the liver

35

Hyperprolactinoma

- prolactin can be cosecreted with GH and increase simply b/c of acromegaly

36

Physiologic cause of hyperprolactinoma

- Pregnancy
- Intense exercise
- Renal insufficiency
- Increased chest wall stimulation

37

Drug induced hyperprolactinoma

- Antipsychotic meds
- Methyldopa
- Metoclopromide
- Opioids
- TCAs
- Verapramil

38

Which the only CCB that raises prolactin levels?

Verapramil

39

Hyperprolactinoma: presentation

- women present with galactorrhea, amenorrhea, and infertility
- men experience erectile dysfunction and decreased libido

40

Hyperprolactinoma: Diagnostic tests

1. Thyroid fxn tests
2. Pregnancy tests
3. BUN/Cr (kidney disease elevates prolactin)
4. Liver fxn test (cirrhosis elevates prolactin)

41

When is the MRI done in diagnosis of hyperprolactinemia

1. High prolactin level is confirmed
2. Secondary causes such as meds are exclused
3. Patient is not pregnant

42

Hyperprolactinemia: Treatment

1. Dopamine agonitsts: cabergoline
2. Transphenoidal surgery: when refractory to meds
3. Radiation is rarely indicated

43

Hypothyroidism

- often of failure of thyroid gland from burn out (e.g Hashimoto thyroiditis)

44

Less common causes of hypothyroidism

- Dietary deficiency of iodine
- Amiodarone

45

Hypothyroidism: common sifns

- all bodily processes being slowed
- high TSH (2x upper limit) with T4

46

If patient has hypothyroidism and TSH is less than double normal, what's next step?

- Get antithyroid peroxidase/antithyroidglobulin antibodies
- if antibodies are positive, replace thyroid hormone

47

Hypothyroid: presentaiton

- Bradycardia
- Constipation
- Weight gain
- Fatigue, lethargy, coma
- Cold intolerance'
- Hypothermia (hair loss, edema)

48

Hyperthyroidism

- Tachycardia, palpitations, arrhythmia
- Diarrhea
- Weight loss
- Anxiety, nervousness, restlessness
- Hyperreflexia
- Heat intolerance
- Fever

49

Best diagnostic test for suspected thyroid disorders

TSH levels
- if TSH is suppressed then meausre T4 levels
- if TSH is markedly elevated then gland has likely failed

50

Hypothyroidism: treatment

Thyroid hormone replacement

51

Pt has hyperthyroidism and presents with proptosis (eye drooping) and skin findings. Likely diagnosis?

Graves disease

52

Pt has hyperthyroidism and presents with a tender thyroid. What's the most likely diagnosis?

Subacute thyroiditis

53

Patient has low TSH and high T4 but presents with nontender thyroid and normal exam results. Likely diagnosis?

Painless "silent" thyroiditis

54

Pt has high T4 levels and low TSH with an involuted gland that is not palpable. Likely diagnosis?

Exogenous thyroid hormone use

55

Patient has has T4 and high TSH. Likely diagnosis?

Pituitary adenoma

56

Graves disease: lab findings

- low TSH
- high RAIU
- positive antibody testing

57

Subacute thyroiditis: lab findings

- low TSH
- low RA iodine uptake
- confirm with tender thyroid

58

Painless "silent" thyroiditis: lab findings

- low TSH
- low radioactive iodine uptake
- no confirmatory testing

59

Exogenous thyroid hormone: lab findings

- low TSH
- low radioiodine uptake
- confirm with hx and involuted thyroid nonpalpable gland

60

Pituitary adenoma

- high TSh
- radioactive iodine uptake not dones
- confirm with MRI of head

61

Graves disease: treatment

Radioactive iodine

62

Subacute thyroiditis: treatment

Aspirin

63

Painless "silent" thyroiditis: treatment

None

64

Exogenous thyroid hormone: tx

Stop use

65

Pituitary adenoma: tx

Surgery

66

Thyroid Storm / Acute hyperthyroidism: Treatment

1. Propranolol
2. Thiourea drugs (methimazole and PTU)
3. Iodinated contract material
4. Steroids
5. Radioactive iodine

67

Propranolol in thyroid storm

- blocks target organ effect, inhibits peripheral conversion of T4 to T3

68

Thiourea drugs: Methimazole and Propylthiouracil) in management of thyroid storm

- Blocks hormone production

69

Use of iodinated contrast material (iopanoic acid and ipodate) in thyroid storm mgmt

Blocks peripheral conversion of T4 to T3 (more active)
- blocks release of existing hormone

70

Graves Ophthalmopathy: Treatment

Steroids are best initial therapy
- radiation used when pt is unresponsive to steroids

71

Which is preferred in management of thyroid storm? Methimazole or PTU

Methimazole

72

Thyroid nodules

- extremely common
- 95 % benign (adenoma, colloid nodule, cyst)
- rarely associated with hyperfunctioning and hypofunction

73

46 y.o woman comes to the office b/c of small mass she found on palpation of her own thyroid. A small nodule is found in thyroid. No tenderness. Otherwise symptomatic and uses medications. Next step for management of this patient?

Check T4 and TSH levels

74

If patient has thyroid nodule > 1 cm and has normal thyroid fxn (T4/TSH). What's the next step?

FNA
- no need for U/S or radionucleotide because they cannot exclude cancer

75

When patient has a nodule... next steps?

1. Perform thyroid function tests (TSH and T4)
2. If tests are normal, biopsy the gland

76

46 y.o woman with thyroid nodule is found to have normal thyroid function testing. The FNA comes back as "indeterminant for follicular adenoma. What is the most appropriate next step?

Surgical removal (excisional biopsy)

77

Hypercalcemia

- most common cause in hyperparathyroidism
- most patients are asymptomatic
- symptomatic patients have high prevalence of cancer and hypermalignancy of malignancy

78

Other causes of hypercalcemia

- Vitamin D intoxication
- Sarcoidosis and other granulomatous disease
- Thiazide diuretics
- Hyperthyroidism
- Metastases to bone and multiple myeloma

79

Hypercalcemia: Presentation

- acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy, and constipation

80

CV presentation: hypercalcemia

- short QT syndrome and hypertension

81

Hypercalcemia: Treatment

1. Saline hydration at high volume
2. Bisphosphonate: pamidronate, zoledronic acid

82

75 y/o man with a hx of malignancy is admitted with lethargy, confusion, and abdominal pain. He is found to have a a markedly elevated calcium level. After 3 liters of normal saline and pamidronate, his calcium level is still markedly elevated the following day. What is the most appropriate next step in management?

Calcitonin
- inhibits osteoclasts
- onset of action of calcitonin is very rapidly

83

Hyperparathyroidism

- Solitary adenoma (** most common cause**)
- Hyperplasia of all 4 glands
- Parathyroid malignancy

84

Hyperparathyroid: presentation

- Asymptomatic elevation in calcium levels found on routine testing
Slower manifestations
- osteoporosis
- nephrolithiasis and renal insufficiency
- muscle weakness, anoreia, nausea
- peptic ulcer disease

85

Hyperparathyroidism: diagnostic tests

- high calcium and high PTH
- low phosphate levels
- EKG shows short QT
- alkaline phosphotase may be elevated due to PTH effect on bone

86

Best test to determine PTH effect on bone

DEXA scan

87

Hyperparathyroidism: Treatment

Surgical removal of gland
- if surgeon is poor surgical candidate

88

Primary hypoparathyroidism

- often a complication of prior neck surgery (e.g. thyroidectomy)

89

Common causes of hypoparathyroidism

- prior neck surgery (*most common*)
- hypomagnesemia
- renal failure

90

Hypocalcemia 2/2 hypomagnesemia

Mg is necesssary for PTH to be released from gland
- low Mg levels also leads to increased urinary loss of calcium

91

Hypoparathyroidism 2/2 renal failure

Leads to hypocalcemia
- kidney converts 25 hydroxy vitamin D to 1,25 dihydroxy Vitamin D

92

Calcium correct with albumin levels

For every 1 point decrease in albumin, decrease calcium by 0.8

93

Discuss low albumin and low total calcium

Lab testing measures calcium bound to albumin thus less albumin means less calcium

94

Hypocalcemia: presentation

Signs of neural hyperexcitability in hypocalcemia:
- Chvostek sign (facial nerve hyprexcitability)
- Carpopedal spasm
- perioral numbess
- mental instability
- seizures
- tetany (Trousseau)

95

Hypocalcemia: treatment

Replace with vitamin D and calcium
- only done orally if symptoms are severe

96

Hypocalcemia: diagnostic testing

- Low Ca levels
- EKG shows prolonged QT that can cause arrhythmia
- slit lamp may show early cataracts

97

Low calcium: presentation

Twitchy and hyperexcitable

98

High calcium: presentation

Lethargic and slow

99

Diabetes Mellitus

- persistently high fasting glucose levels greater than 125 on at least 2 separate occasions

100

Type 1 DM

- onset in childhood
- insulin dependent from early age
- not related to obesity
- defined as insulin deficiency

101

Type 2 DM

- onset in adulthood
- directly related to obesity
- defined as insulin resistance

102

Diabetes Mellitus: presentation

- polyuria, polyphagia, and polydipsia
- type 1 diabetics usually thinner than type 2
- type 2 diabetics less likely to present with polyphagia

103

Diabetes Mellitus: Diagnostic Tests

- Two fasting blood glucose measurements > 125 mg/dL
- Single glucose level > 200 mg/dL with above symptoms
- Increased glcose level on oral glucose tolerance test
- Hemoglobin A1c > 6.5% is a diagnostic criterion and best to follow response to therapy for the past few months

104

Diabetes Mellitus: Treatment

- weight loss since less adipose tissue decreases insulin resistance

105

Best initial medical treatment for diabetes mellitus

Oral metformin
- blocks glucogenesis

106

Contraindications of metformin

In DM pts with renal dysfunction because it can accumulate and cause metabolic acidosis

107

Why aren't sulfonyureas first line drugs for DM?

- Sulfonyureas increase insulin release from pancreas, thereby driving glucose intracellularly and increasing obesity
- goal of therapy < 7%

108

Thiazoledinediones (glitazones)

- provide no clear benefit over the other hypoglycemic conditions
- contraindicated in CHF because they increase fluid overload

109

Nateglinide and repaglinide

- stimulators of insulin release from pancrease
- don't contain sufa

110

Alpha glucosidase inhibitors (e.g. acarbose, miglitol)

- block glucose absorption in the bowel
- add about 1/2 point decrease in HgA1c
- can cause flatus, diarrhea, and abdominal pain
- can be used with renal insuffiency

111

Incretins (exenatide, sitagliptin, saxagliptin, linagliptin)

- part of mechanism by which oral glucose normally produces rise in insulin and decreases glucagnon levels
- decreases gastrin motlity and help in weight loss, decreasing Type 2 diabetes

112

Exenatide: side effects

Pancreatitis

113

Pramlinitide

- analog of protein called amylin that is secreted normally with insulin
- amylin decrease gastric emptying
- decreases glucagon levels and decreases appetitie

114

Insulin use in Type 2 DM

used when oral hypoglycemics cannot control

115

Short acting insulin
- lispro
- aspart
- glulisine

- onset in 5 - 15 minutes
- peak action in 1 hr
- lasts for 3-4 hrsw

116

Regular insulin

- onset in 30 to 60 minutes
- peak action in 2 hrs
- duration of 6 - 8 hrs

117

NPH

- onset in 2 to 4 hrs
- peak action in 6 to 7 hrs
- lasts for 10 - 20 hrs

118

Glargine

- onset in 1 to 2 hrs
- peak action in 1 to 2 hrs
- lasts for 24 hrs

119

Diabetic ketoacidosis

- more common in type 1 diabetics
- Patients present w/
- hyperventilation
- possibly AMS
- metabolic acidosis w/ increased anion gap
- acetone odor on breath
- polydipsia and polyuria
- hyperkalemia in blood but decreased total body K
- increased anion gap on blood testing
- serum positive for ketones
- nonspecific abdominal pain

120

DKA: Treatment

Large volume saline and insulin replacement
- replace K when potassium level comes down to a level approaching normal
- correct underlying cause: meds, infection, pregnancy

121

57 y.o man is admitted to ICU with AMS, hyperventilation and markedly elevated glucose level. Which is the following is the most accurate measure of the severity of the condition?

Serum bicarbonate
- measure of anion gap acidosis
- the lower the bicarb, the more severe the acidosis

122

DM patients should receive the following for health maintenance:

- Pneumococcal vaccine
- Yearly eye exam for proliferative neuropathy
- statin meds if LDL > 100
- ACEis or ARBS if BP is > 130/80 mm Hg
- ACEis or ARBS if microalbuminuria is present
- Aspirin if diabetic patients > 50
- foot exam for neuropathy

123

Complications of DM

- CV risk
- Diabetic nephropathy
- Gastroparesis
- Retinopathy
- Neuropathy

124

CV complications of DM

- DM patients are at increased risk of MI
- CHF from premature atherosclerotic disease
- why BP goal is < 130/80
- target LDL goal < 100 mg/DL when initiating stain treatments

125

Diabetic Nephropathy

- DM can lead to microalbuminuria (30 - 300 mg per 24 hrs)
- should be screened annually for microalbuminuria
- if detected, DM pt should be started on ACEis and ARBs by decreasing intraglomerylar HRn and decreasing kidney damage

126

Gastroparesis

- immobility of bowels that leads to bloating, constupation and early satiety
- DM decreases ability of gut to sense the stretch of walls of bowel, important as stretch stimulates gastric motility

127

Gastroparesis: Treatment

Metoclopromide
Erythromycin
-- increases gastric motility

128

Diabetic nonproliferative retinopathy

- DM affects nonproliferative retinopathy for tighter control of glucose

129

Diabetic proliferative retinopathy

- neovascularization and vitreous hemorrhages are present
- treat with laser photocoagulation, which markedly retards progression to blindness

130

Diabetic neuropathy

- damage to microvasculature damages vasonervorum that surrounds large peripheral nerves
- decreased sensation in the feet - main cause of skin ulcers

131

Diabetic neuropathy: treatment

- Preglabin
- Gabapentin
- Tricyclic antidepressants

132

Cushing syndrome

- aka hypercortisolism
- can be cased by prednisone or other glucocorticoid

133

Cushing disease

- pituitary overproduction of ACTH from carcinoid or cancer or from overproduction autonomously in the the adrenal gland
- can be caused by prednisone or other glucorticoids

134

Most common cause of hypercorticolism

Pituitary ACTH (Cushing disease)

135

Cushing syndrome: presentation

- Fat redistribution: "moon facies" , truncal obesity
- Skin: striae
- Osteoporosis
- Hypertension
- Menstrual disorders in women
- Erectile dysfunction in men
- Cognitive disturbance
- Polyuria

136

Best initial test for presence of hypercorticolism

24 hr urine cortisol

137

Test for hypercorticolism other than 24 hr urine cortisol

- 1mg overnight dexamethasone suppression test

** if suppression doesn't occur, hypercorticolism can be excluded

138

More specific test of hypercorticolism

24 hr urine cortisol

139

Causes of false positive 1 mg dexamethasone suppression testing

- Depression
- Alcoholism
- Obesity

140

Best initial test to determine the cause (source) or location of hypercortisolism

ACTH testing

141

If ACTH level is high in someone with suspected hypercortisolism, the source could be from:

- Pituitary (suppresses w/ high dose dexamethsone)
- Ectopic production: lung cancer, carcinoid (dexamethasone doesn't suppress)

142

If the ACTH level is elevated and doesn't suppress with high dose dexamethasone

- Scan the brain MRI

143

If patient has suspected hypercortisolism and the MRI does not show pituitary lesion. What's the next step?

Sample the inferior pretrosal sinus for ACTH, possible after the stimulating the patient with CRH

144

Why should the petrosal venous sinus must be sampled in cases of suspected hypercortisolism when head MRI is negative?

Some pituitary lesions are too small detected on RI

145

If patient has suspected hypercortisolism and the ACTH is levated and cannot find defect in pituitary either by MRI or petrosal sinus sampling, what's the next step?

Scan chest for ectopic source of ACTH production

146

Patient has suspected hypercortisolism but low ACTH. Source of cortisol?

Adrenal srouce

147

Patient has suspected hypercortisolism but has high ACTH and has been given high dose dexamethasone. Source?

If dexamethasone test suppresses: pituitary source
If dexamethasone test does not suppress: ectopic + cancer

148

Effects of hypercortisolism

- Hyperglycemia
- Hyperlipidemia
- Hypokalemia
- Metabolic alkalosis
- Leukocytosis (from demargination of WBC cells)

149

Why does hypercortisolism cause hypokalemia and metabolic alkalosis?

Cortisol has an aldosterone-like effect on distal tubules in which potassium and hydrogen ions are excreted

150

Hypercortisolism: Treatment

Surgically remove the source of hypercortisolism
- transsphenoidal surgery is done for pituitary sources
- laparoscopic removal is adrenal sources

151

Evaluation of adrenal incidentaloma (unexpected, asymptomatic adrenal lesion found on CT)

- metanephrines of blood or urine to exclude pheochromocytoma
- renin and aldosterone levels to exclude hyperaldosternism
- 1 mg overnight dexamethasone suppression test

152

Adrenal source hypercortisolism: findings

- low ACTH
- petrosal sinus not does
- no suppression of high dose dexamethasone

153

Pituitary source hypercortisolism: findings

- high ACTH
- high ACTH found on petrosal sinus
- high dose dexamethasone suppresses ACTH

154

Ectopic source hypercortisolism findings

- high ACTH level
- low ACTH in petrosal sinus
- no suppression on high dose dexamethasone

155

Addison disease

- chronic hypoadrenalism
- caused by autoimmune destruction of the gland in more than 80% of causes

156

Most common cause of hypoadrenalism

Addison disease

157

Less common causes of hypoaldrenalism

- Infection (tuberculosis)
- Adrenoleukodystrophy
- Metastatic cancer to the adrenal gland

158

Acute adrenal crisis

- caused by hemorrhage, surgery, hypotension, or trauma that rapidly destroys the gland
- sudden remove of high dose prednisone (steroid) can precipitate episode

159

Hypoadrenalism: presentation

- weakness, fatigue, AMS
- hypotension
- hyponatremia
- hyperkalemia
- hyperpigmentation from chronic adrenal insufficiency

160

Acute adrenal crisis

- presents with profound hypotension, fever, confusion, and coma

161

Hypoadrenalism: diagnostic test

- Hypoglycemia
- Hyperkalemia
- Metabolic acidosis
- Hyponatremia
- High BUN
- Eosinophilia

162

Most specific test of adrenal function

Cosyntropin test
- cosyntropin is synthetic ACTCH
- measure the cortisol level before and after the administration of cosyn

163

Hypoadrenalism (acute adrenal crisis): treatment

1. Replace steroids with hydrocortisone
2. Fludrocortisone is steorid hormone that is particularly high in mineralicorticoid or aldosteroine-like effect
- fludrocortisone most useful in cases of postural instability
- mineralocorticoid supplements shoud be used in primary adrenal insufficiency

164

Patient is brought to the ED after a MVA in which he sustains severe abdominal trauma. On the 2nd hospital day, the patient necomes markedly hypotensive w/o evidence of bleeding. There is a fever, high eosinophil count, hyperkalemia, hyponatremia, and hypoglycemia. What is the most appropriate next step in management?

Draw cortisol level and administer hydrocortisone
- in suspected acute adrenal insufficiency, treatment is more important than diagnosis

165

Primary hyperaldosteronism

- autonomous overproduction of aldosterone despite high pressure with low renin activity
- 80% are from solitary adenoma
- other causes are from bilateral hyperplasia

166

Most common cause of primary hyperaldosteronism

Solitary adenoma

167

Risk factors for secondary hypertension

- under age 30 or after age 60
- not controlled by 2 anti-BP meds
- has characteristic finding on hx, physical, or labs

168

Primary hyperaldosteronism findings

- high blood pressure in association with low potassium level
- low K found on routine lab testing or b/c of symptoms of muscular weakness or diabetes insipidus from hypokalemia

169

Best test to measure primary hyperaldosteronism

Ratio of plasma aldosterone to plasma renin
- elevated plasma renin excludes primary aldosteronism

170

Most accurate test to confirm unilateral adenoma in primary hyperaldosteronism

- Sample of venous blood draining the adnreal
- it will show high aldosterone levels

171

Diagnostic order in suspected hyperaldosteronism

1. ratio of plasma aldosterone to plasma renin
2. CT scan of adrenals (only AFTER biochemical confirmation of low K, high aldosteronism, low plasma renin)

172

High BP + hypokalemia =

Primary hyperaldosteronism

173

Hyperaldosteronism: Treatment

- Unilateral adenoma is resected by laparascopy
- Bilateral hyperpaslia is treated with eplerenone or spironolactone

174

Phemochromocytoma

- nonmalignant lesion of adrenal medulla autonomously overproducing catecholamines despite high BP

175

Pheochromocytoma: presentation

- Hypertension that is episodic in nature
- Headache
- Sweating
- Palpitations and tremor

176

Best initial test for pheochromocytoma

Plasma level of free metanephernes

177

Pheochromocytoma: diagnostic testing

1. plasma level of free metanepherines
- confirmed with 24 hr urine collection for metanepherines
2. imaging of adrenal glands w/ CT or MRI done after bio chemical testing

178

MIBG scanning

nuclear isotope scan that detects location of pheochromocytoma that originates outside of gland

179

Pheochromocytoma: treatment

1. Phenoxybenzamine (alpha blocker) is best initial therapy
2. CCBs and B-blockers are used afterwards
3. Pheochromocytoma is removed surgically or by laparscopy

180

Spironolactone: side effects

- causes gynecomastia and decreased libido b/c it is antiadrenogenic