Endocrinology - MTB Flashcards
(181 cards)
0
Q
Panhypotpituitarism: presentation
A
symptoms dependent of deficiency of a specific hormone
1
Q
Panhypopituitarism
A
- 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)
2
Q
Prolactin deficiency
A
- in women, prolactin deficiency inhibits lactation after childbirth
3
Q
Deficiency of LH and FSH
A
- 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
Q
Kellman syndrome
A
- decreased FSH and LH from decreased GnRH
- anosmia
- renal agenesis
5
Q
Growth hormone deficiency
A
- children present with short stature and dwarfism
- adults have few symptoms b/c catecholamines, glucagon, and corticol act as stress hormones
6
Q
Adult presentation of GH deficiency
A
- Central obesiry
- increased LDL and cholesterol levels
- reduced lean muscle mass
7
Q
Growth hormone diagnostic tests
A
- Hyponatremia (2/2 hypothyroidism and isolated glucocorticoid underpoduction)
- potassium remains levels b/c aldosterone is not affected
- MRI detects compressing mass lesions
8
Q
Low TSH and low thyroxine
A
confirm w/ decreased TSH response to TRH
9
Q
decreased ACTH and decreased cortisol level
A
normal response to cosyntropin stimulation of adrenal, cortisol will rise in recent disease and cortisol is abnormal b/c of adrenal atrophy
10
Q
Metyrapone
A
inhibits 11- B hydroxlase
- decreases output of adrenal gland
- should cause ACTH to rise b/c cortisol goes down
11
Q
Insulin stimulation
A
- insulin decreases glucose levels so GH should rise
- failure to rise in response to insulin indicates pituitary insufficiency
12
Q
Posterior pituitary
A
- produces ADH and oxytocin
- no deficiency disease for oxytocin
13
Q
Oxytocin deficeiency
A
- aids with uterine contraction
- delivery still occurs even if active
14
Q
Diabetes Inspidus
A
- decrease in amt of ADH from pituitary (central DI) or decease in response to ADH on collecting tubules (nephrogenic DI)
15
Q
Central DI
A
any destruction of brain from stroke, tumor, trauma, hypoxia, or infiltration of gland from sarcoidosis or infection
16
Q
Nephrogenic DI
A
Kidney diseases (e.g chronic pyelonephritis, amyloidosis, myeloma, and sickle cell disease) damaged kidney enough to inhibit effect of ADH
17
Q
Electrolyte abnormalities that can cause nephrogenic DI
A
- Hypercalcemia
- Hypokalemia
18
Q
DI: presentation
A
- presents with high volume urine and excessive thirst resulting in volume depletion and hypernatremia
- hypernatremia sx (condusion, disorientation, lethargy then later seizures, coma)
19
Q
classic cause of nephrogenic DI
A
Lithium
- look for bipolar patients
20
Q
Diabetes inspidus
A
- serum sodium is elevated
- decreased urine osmolality and urine sodium is decreased
21
Q
Difference btwn central DI and nephrogenic DI
A
Response to vasopressin (desmopression(
22
Q
Central DI: Treatment
A
- treated with long term vasopression
23
Q
Nephrogenic DI: treatment
A
- correct underlying cuase (e.g. hypokalemia or hypercalcemia)
- treat with thiazides, amiloride, or prostiglandin inhibitors (NSAIDS)
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Acromegaly
overproduction of growth hormone leading to soft tissue overgrowth
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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
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Best initial test for suspected acromegaly?
Insulin growth factor (IGF -1) levels
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Acromegaly: lab testing
- Glucose interolerance and hyperlipidemia, which contribute to cardiac dysfunction
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Most accurate test for acromegaly
Glucose suppression test
| - normally glucose suppreses GH levels
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When is the MRI done in diagnosis of acromegaly?
Only after lab identification of acromegaly
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Acromegaly: Treatment
1. Surgery: transphenoidal resection of pituitary
2. Medications
- cabergoline
- octreotide or lanreotide
- pegvisomant
3. Radiotherapy
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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
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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)
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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
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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)
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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
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Hypothyroid: presentaiton
- Bradycardia
- Constipation
- Weight gain
- Fatigue, lethargy, coma
- Cold intolerance'
- Hypothermia (hair loss, edema)
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Hyperthyroidism
- Tachycardia, palpitations, arrhythmia
- Diarrhea
- Weight loss
- Anxiety, nervousness, restlessness
- Hyperreflexia
- Heat intolerance
- Fever
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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
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Hypothyroidism: treatment
Thyroid hormone replacement
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Pt has hyperthyroidism and presents with proptosis (eye drooping) and skin findings. Likely diagnosis?
Graves disease
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Pt has hyperthyroidism and presents with a tender thyroid. What's the most likely diagnosis?
Subacute thyroiditis
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Patient has low TSH and high T4 but presents with nontender thyroid and normal exam results. Likely diagnosis?
Painless "silent" thyroiditis
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Pt has high T4 levels and low TSH with an involuted gland that is not palpable. Likely diagnosis?
Exogenous thyroid hormone use
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Patient has has T4 and high TSH. Likely diagnosis?
Pituitary adenoma
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Graves disease: lab findings
- low TSH
- high RAIU
- positive antibody testing
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Subacute thyroiditis: lab findings
- low TSH
- low RA iodine uptake
- confirm with tender thyroid
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Painless "silent" thyroiditis: lab findings
- low TSH
- low radioactive iodine uptake
- no confirmatory testing
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Exogenous thyroid hormone: lab findings
- low TSH
- low radioiodine uptake
- confirm with hx and involuted thyroid nonpalpable gland
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Pituitary adenoma
- high TSh
- radioactive iodine uptake not dones
- confirm with MRI of head
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Graves disease: treatment
Radioactive iodine
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Subacute thyroiditis: treatment
Aspirin
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Painless "silent" thyroiditis: treatment
None
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Exogenous thyroid hormone: tx
Stop use
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Pituitary adenoma: tx
Surgery
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Thyroid Storm / Acute hyperthyroidism: Treatment
1. Propranolol
2. Thiourea drugs (methimazole and PTU)
3. Iodinated contract material
4. Steroids
5. Radioactive iodine
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Propranolol in thyroid storm
- blocks target organ effect, inhibits peripheral conversion of T4 to T3
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Thiourea drugs: Methimazole and Propylthiouracil) in management of thyroid storm
- Blocks hormone production
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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
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Graves Ophthalmopathy: Treatment
Steroids are best initial therapy
| - radiation used when pt is unresponsive to steroids
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Which is preferred in management of thyroid storm? Methimazole or PTU
Methimazole
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Thyroid nodules
- extremely common
- 95 % benign (adenoma, colloid nodule, cyst)
- rarely associated with hyperfunctioning and hypofunction
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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
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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
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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
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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
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High calcium: presentation
Lethargic and slow
99
Diabetes Mellitus
- persistently high fasting glucose levels greater than 125 on at least 2 separate occasions
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Type 1 DM
- onset in childhood
- insulin dependent from early age
- not related to obesity
- defined as insulin deficiency
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Type 2 DM
- onset in adulthood
- directly related to obesity
- defined as insulin resistance
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Diabetes Mellitus: presentation
- polyuria, polyphagia, and polydipsia
- type 1 diabetics usually thinner than type 2
- type 2 diabetics less likely to present with polyphagia
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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
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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%
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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
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Insulin use in Type 2 DM
used when oral hypoglycemics cannot control
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Short acting insulin
- lispro
- aspart
- glulisine
- onset in 5 - 15 minutes
- peak action in 1 hr
- lasts for 3-4 hrsw
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Regular insulin
- onset in 30 to 60 minutes
- peak action in 2 hrs
- duration of 6 - 8 hrs
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NPH
- onset in 2 to 4 hrs
- peak action in 6 to 7 hrs
- lasts for 10 - 20 hrs
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Glargine
- onset in 1 to 2 hrs
- peak action in 1 to 2 hrs
- lasts for 24 hrs
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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
