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Endocrine Review. Eric L. Johnson, MD Assistant Professor Department of Family and Community Medicine UNDSMHS Assistant Medical Director Altru Diabetes Center Grand Forks, ND. Objectives. Understand basic principles of endocrine function

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Endocrine review

Endocrine Review

Eric L. Johnson, MD

Assistant Professor

Department of Family and Community Medicine

UNDSMHS

Assistant Medical Director

Altru Diabetes Center

Grand Forks, ND


Objectives
Objectives

  • Understand basic principles of endocrine function

  • Understand basic principles of endocrine dysfunction

  • Understand management and referral of common endocrine diseases


Endocrine pathology
Endocrine Pathology

  • Disease state results from excess or insufficiency of hormone

  • Clinical challenge is determination of the origin of excess or insufficiency, i.e., Hypothalamus (tertiary), Pituitary (secondary) or target gland (primary)


Endocrine disorders other than diabetes
Endocrine Disorders (other than diabetes)

  • Thyroid

  • Adrenal

  • Parathyroid

  • Pituitary gland

  • Gonadal

  • Gout (uric acid)


The endocrine system
The Endocrine System

Brain

Hypothalamus

Pituitary

Hypothyroid

Thyroid

Pancreas

Adrenal

Gonads



Hypothalamus1
Hypothalamus

AVP = arginine vasopressin

CRH = corticotropin-releasing hormone

GHRH = growth hormone-releasing hormone

GnRH = gonadotropin-releasing hormone

SRIF = somatotropin release–inhibiting factor

(somatostatin)

TRH = thyrotropin-releasing hormone;

VIP = vasoactive intestinal polypeptide.DA = dopamine

ACTH = adrenocorticotropic hormone

LH = lutenizing hormone

FSH = follicle-stimulating hormone

GH = growth hormone

TSH = thyroid-stimulating hormone

PRL = prolactin

Goldman: Cecil Medicine, 23rd ed. 2007



Anterior pituitary hormones
Anterior Pituitary Hormones

  • TSH, ACTH, FSH, and LH hormones are tropic hormones that simulate other endocrine glands

  • TSH-Thyroid

  • ACTH- Adrenal Cortex

  • FSH, LH- Gonads


Posterior pituitary hormones
Posterior Pituitary Hormones

  • Vasopressin(ADH)- kidney, baroreceptors (plasma osmolality, water retention, thirst)

  • Oxytocin- breast, uterus (no known function in males)

  • Both are synthesized in specialized neurons in the hypothalamus (neurohypophysial neurons)


Prolactinomas
Prolactinomas

  • Pituitary adenomas may present with visual impairment, headache, or hormonal abnormalities

  • Prolactinomas most common. Manifest with galactorrhea and gonadal dysfunction

  • Laboratory testing: serum prolactin, creatinine levels and thyroid function tests

  • MRI is the imaging modality of choice for the anatomic evaluation of the hypothalamus and pituitary gland


Panhypopituiarism
Panhypopituiarism

  • Neoplasm

  • Radiation

  • Infiltrative/Infection

  • Empty sella syndrome (herniation of subarachnoid tissue)

  • Apoplexy (hemorrage)

  • Sheehan’s syndrome (pregnancy)


Growth hormone excess acromegaly
Growth Hormone Excess (Acromegaly)

  • Acromegaly cause: growth hormone–secreting adenoma of the anterior pituitary

  • Elevated serum levels of IGF-1 are found in acromegaly (best single test)

  • The diagnosis of acromegaly is confirmed by a glucose tolerance test

  • Transsphenoidal surgery to remove the pituitary adenoma is the initial treatment of choice in individuals with acromegaly


Growth hormone excess acromegaly1
Growth Hormone Excess (Acromegaly)

Acromegaly manifestations

  • Increased hand/foot size

  • Prognathism/teeth space widening

  • Frontal bossing/coarsening of facial features

  • Weakness/fatigue


Growth hormone excess acromegaly2
Growth Hormone Excess (Acromegaly)

Acromegaly manifestations cont’d

  • Sweating

  • HTN>>>cardiomyopathy

  • Obstructive sleep apnea

  • Insulin resistance


Growth hormone excess acromegaly3
Growth Hormone Excess (Acromegaly)

Treatment

  • Surgical resection

    Best if tumor small, 10-20% result in pan hypo pit

  • Radiation

    Slow to diminish GH, 50% pan hypo pit

  • Bromocriptine

    Blocks GH effect

  • Octreotide

    Lowers GH secretion, SC route w/frequent dosing


Growth hormone deficiency
Growth Hormone Deficiency

  • Fatigue or hypoglycemia in the adult

  • Dwarfism in child

    Born normal length at birth but growth “falls off curve”

  • Diagnosis: IGF1 level (GH varies too much)

  • Treatment: formerly used human pit gland extract, synthetic GH since late 80’s


Diabetes insipidus adh
Diabetes Insipidus (ADH)

  • Deficiency of posterior pituitary hormone ADH

    (aka vasopressin)

  • ADH acts on kidney collecting duct to

    retain free water deficiency causes free water loss

  • ADH maintains blood volume via: - -Osmoreceptors in brain

    -Stretch receptors in heart

    -Baroreceptors in carotids and aorta


Diabetes insipidus adh1
Diabetes Insipidus (ADH)

  • Decreased urinary specific gravity (≤1.005)

  • Decreased urinary osmolarity

    (<200 mOsm/kg) even in the presence of high serum osmolality   

  • Hypernatremia, increased plasma osmolarity, hypercalcemia, hypokalemia

  • Normal Serum osmolarity: 282 - 295 mOsm/kg

  • Normal Urine osmolarity: 500 - 800 mOsm


Diabetes insipidus adh2
Diabetes Insipidus (ADH)

Etiology

-CNS insult -head trauma, surgery, tumor, infection

-Genetic

-MS, Metastatic Disease

-Drugs (lithium is classic)

-Nephrogenic vs. Neurogenic vs. Psychogenic

Sx

–Thirst, polyuria, polydipsia (with a normal glucose)


Diabetes insipidus adh3
Diabetes Insipidus (ADH)

  • Diagnostic workup: decreased ADH or insensitivity to ADH?

  • Water Deprivation Test:

    -Baseline measurement of weight, ADH, plasma sodium, urine and plasma osmolarity -Patient is deprived of fluids under strict medical supervision.   

    -Frequent (q2h) monitoring of plasma and urine osmolarity       

  • Test terminated when plasma osmolarity

    >295 mOsm/kg or the patient loses ≥3.5% of initial body weight.   

  • Diabetes insipidus is confirmed if the plasma osmolarity is >295 mOsm/kg and the urine osmolarity is <500 mOsm/kg (typical referral point)


Diabetes insipidus adh4
Diabetes Insipidus (ADH)

  • Nephrogenic vs. neurogenic

  • Patient given 5 U of vasopressin (ADH),

    change in urine osmolarity is measured

  • Significant increase (>50%) in urine osmolarity after administration of ADH is indicative of neurogenic diabetes insipidus.


Diabetes insipidus adh5
Diabetes Insipidus (ADH)

Treatment

  • Desmopressin

  • Thiazides in mild neurogenic


Syndrome of inappropriate adh siadh
Syndrome of Inappropriate ADH(SIADH)

  • Hyponatremia

  • Urinary osmolarity > serum osmolarity

  • Normal BUN, creatinine,TSH,glucose


Siadh
SIADH

  • Neoplasm

  • Pulmonary disorders: pneumonia, emphysema, cystic fibrosis, status asthmaticus, respiratory failure

  • Intracranial pathology: trauma, neoplasms, infections (meningitis, encephalitis, brain abscess)  

  • Postoperative period: surgical stress, ventilators with positive pressure, anesthetic agents     

  • Drugs: chlorpropamide, thiazide diuretics, chemotherapeutic agents carbamazepine, phenothiazines, MAO inhibitors, tricyclic antidepressants, narcotics, nicotine, clofibrate, haloperidol, SSRIs, NSAIDs

  • Other: acute intermittent porphyria, myxedema, psychosis, delirium tremens, ACTH deficiency (hypopituitarism), general anesthesia, endurance exercise


Siadh1
SIADH

  • Treatment

    Fluid Restriction

    Careful use of hypertonic saline IV

    Resolution/Treatment of underlying problem


Cushing s disease
Cushing’s Disease

  • Pituitary adenoma>>excess production of ACTH>>excess cortisol production

  • Distinguished from Cushing’s syndrome, which includes other causes of cortisol excess (ectopic production of ACTH and CRH)

  • Cushing’s disease causes 60-70% of excess cortisol disease states

  • Occurs 8 times more often in women than men


Cushing s
Cushing’s

  • Classic Cushing's features: Centripetal obesity, moon facies, and ‘buffalo’ hump

  • Striae are common

  • Fine (lanugo) hair growth

  • Muscle wasting

  • Bone demineralization

  • Hypertension

  • IGT

  • Psych


Cushing s diagnosis
Cushing’s Diagnosis

  • Distinguish between:

  • Cushings Disease

    -Pituitary Causes

  • Cushing’s Syndrome

    -Adrenal causes of cortisol excess;

    -Ectopic sources of ACTH or Ectopic CRH (Cortisol Releasing Hormone)


Cushing s diagnosis1
Cushing’s Diagnosis

  • Serum Cortisol is elevated

  • Abnormal tests can be seen in up to 30% of hospitalized and/or depressed patients

  • 24 hour free urinary cortisol can be a useful adjunct

  • Overnight Dexamethasone suppression test……


Cushing s diagnosis2
Cushing’s Diagnosis

  • Overnight Dexamethasone Suppression Test:

    1 gram at 11pm, measure plasma cortisol at 8 am the next morning

  • The normal response is suppression to less than 3mcg/dl

  • If no suppression, they have ectopic or adrenal production

  • If supression, they may have pituitary cause


Cushing s diagnosis3
Cushing’s Diagnosis

  • Can Measure ACTH

    -ACTH low in Adrenal gland tumor

    -ACTH high in ectopic or pituitary adenoma


Cushing s diagnosis summary
Cushing’s DiagnosisSummary

  • High serum or 24 hour urine cortisol

  • Dexamethasone suppression

    -No supression: Ectopic or adrenal

    -Supression: Pituitary

  • ACTH

    -Low: Adrenal

    -High: Likely pituitary or ectopic


Addison s disease adrenocortical hypofunction
Addison’s Disease(Adrenocortical Hypofunction)

  • Can result in all loss of corticosteroid production if the adrenal cortex suffers destruction (primary)

  • Can result from diminished ACTH production (secondary)


Addison s disease
Addison’s Disease

  • Loss of cortisol:

    -Loss of vascular tone and CV output

    -Hypoglycemia-Cortisol important for Gluconeogenesis

    -Hypercalcemia (Loss of inhibition of intestinal absorption and renal reabsorption)

    -Serum ACTH levels are usually used for initial screening (Low)


Addison s disease1
Addison’s Disease

  • Skin changes-Hyperpigmentation in Palmar creases, scars, oral mucosa

  • Longitudinal pigmented bands under nails

  • Vitiligo in up to 15% of patients

  • Decreased pubic and axillary hair in females

  • Weakness, fatigue, nausea and vomiting, and a craving for salt


Addison s disease2
Addison’s Disease

  • Associated with other endocrine insufficiencies (thyroid, parathyroid, type 1 DM, etc)

  • Treatment is to replace adrenal hormones

  • Case I’ve seen: Pt. also had Type 1 DM and hypothyroidism; died at age 27 from profound hypoglycemia


Aldosterone disorders
Aldosterone Disorders

  • Aldosterone-a mineralocorticoid secreted by the adrenal glands

  • Primary secretion affected by

    Angiotensin II>renin (part of fluid and electrolyte balance)

  • Increased aldosterone-increased sodium retention and increased potassium secretion by the kidney


Hyperaldosteronism
Hyperaldosteronism

  • Primary-more common in women 3rd to 5th decade of life

  • Presents with hypertension, weakness, fatigue, hypokalemia, polyuria, polydipsia

  • Most cases are from benign adenomas (Conn’s Syndrome)

  • Screening: aldosterone:renin ratio of greater than 30

    (off of anti-hypertensives, except Ca++ channel blockers)

  • CT scanning for adrenal adenomas


Secondary hyperaldosteronism
Secondary Hyperaldosteronism

  • Usually occurs in edematous states-i.e. CHF, cirrhosis or renal artery stenosis

  • Causes intravascular volume depletion, stimulating renin production

  • Elevated renin and aldosterone levels

  • Can occur in Bartter’s syndrome (impaired chloride re-absorption)


Hypoaldosteronism
Hypoaldosteronism

  • Sodium wasting and hyperkalemia

  • May be up to 10% of hyperkalemia

  • Hyper-reninemic hypoaldosteronism (more common)

    Defect is in aldosterone synthesis or angiotensin II action

    Genetic, ACEI, ARB, heparin, Lead poisoning, Severe Illness

  • Hyporeninemic

    DM, HTN, renal insufficiency


Hypoaldosteronism1
Hypoaldosteronism

  • Lab:

    Plasma renin

    K+

    Glucose

    Kidney functions

    Hyperchloremic metabolic acidosis


Parathyroid
Parathyroid

  • Purpose

    –Maintain serum calcium levels

  • Target tissues

    –Bone, kidney, intestine

  • Feedback loop

    –As Calcium rises, PTH lowers

    –As calcium lowers, PTH rises


Hyperparathyroidism
Hyperparathyroidism

  • Etiology

    –Tumor (adenoma)

    –Hyperplasia

    –Drugs (lithium is classic)

    –Ectopic PTH

  • Secondary Hyperparathryroidism can occur in chronic renal disease


Hyperparathyroidism1
Hyperparathyroidism

  • Elevated PTH, Serum Ca++, urine Ca++

  • Polyruia, Polydipsia

  • Kidney stones

  • Peptic ulcer disease

  • Pancreatitis

  • Nausea, vomiting or loss of appetite

  • Osteopenia/porosis, leading to an increased risk of fractures

  • Confusion or poor memory

  • Muscle weakness or fatigue


Hyperparathyroidism2
Hyperparathyroidism

  • Treatment (loop diuretics, hydration)

  • Observation

  • Surgery


Hypoparathyroidism
Hypoparathyroidism

  • Low PTH (idiopathic, iatrogenic-thyroid surgery)

  • Low Serum Ca++ (low Vit D?)

  • Elevated Phosphorous

  • Parasthesthias

  • Alopecia/ vitiligo/ candidiasis

  • Long Q-T on EKG

  • Muscle cramps or tetany

    -Chvostek’s sign: facial twitch after a gentle tapping over the facial nerve

    -Trousseau's sign: carpopedal spasm after inflation of blood pressure cuff above the patient's systolic blood pressure for 2 to 3 minutes


Hypoparathyroidism1
Hypoparathyroidism

  • Ca++ plus Vitamin D

  • Low Phosphorous diet


Hypothyroidism
Hypothyroidism

  • Incidence in the U.S. is about 1%

  • Primary hypothyroidism accounts for 90-95% of all cases

  • Autoimmune most common (Hashimoto’s)

  • May or may not have enlarged (goitrous) thyroid

  • End Stage Grave’s/treatment/can result in hypothyroidism

  • Iatrogenic-surgical

  • Iodine deficiency


Hypothyroidism1
Hypothyroidism

  • Decreased secretion of thyroid hormone from the thyroid gland. Most frequently reflects a disease of the gland itself (primaryhypothyroidism) 95%

  • Pituitary disease (secondaryhypothyroidism)

  • Hypothalamic disease (tertiaryhypothyroidism)


Hypothyroidism2
Hypothyroidism

  • Generally leads to a slowing of metabolic processes

  • Myxedema-occurs in severe disease-accumulation of of mucopolysaccharides in the skin (non-pitting edema)

  • Congenital hypothyroidism is rare. Leads to developmental delay if not recognized and treated

  • Can have bradycardia, CHF, coma in advanced cases


Hypothyroidism3
Hypothyroidism

Symptomatology

  • Patients may have no symptoms

  • Common (Seen in >50% of Patients)

    • Weakness, Fatigue, Lethargy, Decreased energy

    • Cold intolerance

    • Dry skin, Decreased sweating, Hair loss

    • Inability to concentrate, Memory loss

    • Constipation

    • Weight gain

    • Dyspnea

    • Peripheral paresthesias


Hypothryroidism
Hypothryroidism

Symptomalotogy

Less common (Seen in <50% of Patients)

-Depression

-Anorexia

-Muscle cramps, Musculoskeletal pain, Arthralgias,

-Infertility, Menorrhagia, anovulation

-Decreased hearing

-Carpal Tunnel Syndrome

-Impaired Glucose Tolerance


Hypothyroidism laboratory evaluation
HypothyroidismLaboratory Evaluation

  • Serum TSH sufficient for Screening for most Patients (elevated)

  • Total T4 if clinically suspicious and TSH normal

  • If TSH elevated, Primary Hypothyroidism

  • If TSH, T4, T3 all low, suspect pituitary/brain


Hypothyroidism treatment
HypothyroidismTreatment

  • Synthetic thyroxine

  • Start dose often 25 to 50 mcg daily

  • Recheck TSH in about 4 to 6 weeks

  • Titrate thyroxine based on symptoms, TSH


Hypothyroidism special circumstances
HypothyroidismSpecial Circumstances

  • Hypothyroid in Pregnancy-Require more frequent monitoring. Check TSH at beginning of pregnancy, end of first trimester, optional again at end of second trimester

  • Down Syndrome -high incidence-check annually

  • Type 1 Diabetes -higher incidence than general population. Check regularly


Hyperthyroidsim thyrotoxicosis
Hyperthyroidsim(Thyrotoxicosis)

  • Graves' Disease 60-90% of all cases

  • Toxic multinodular goiter

  • Solitary ‘hot’ nodule

  • TSH secreting pituitary tumor

  • Molar pregnancy

  • Choriocarcinoma


Hyperthyroidism signs and symptoms
HyperthyroidismSigns and Symptoms

  • Common (Seen in >50% of Patients)

    -Nervousness, Irritability, Hyperactivity, Hand tremor

    -Insomnia

    -Hand tremor

    -Excessive sweating

    -Palpitations, tachycardia, arhythmias

    -Weight loss


Hyperthyroidism signs and symptoms1
HyperthyroidismSigns and Symptoms

  • Common (Seen in >50% of Patients)

    -Increased appetite-Heat intolerance-Pruritus-Hyperdefecation-Oligomenorrhea or amenorrhea


Hyperthyroidism signs and symptoms2
HyperthyroidismSigns and Symptoms

  • Less Common (Seen in <50% of Patients)

    -Nausea and vomiting, Dysphagia-Decreased libido-Impotence-Dyspnea on exertion-Periodic paralysis-Exacerbation of angina

    -Loose nails (Plummer’s nails)


Hyperthyroidism diagnosis
HyperthyroidismDiagnosis

  • Diffuse nodular Goiter is classic finding, along with opthalmopathy

  • TSH is suppressed,elevated T4

  • If T4 is normal,

    check serum T3-patient may have a T3 thyrotoxicosis


Hyperthyroidism
Hyperthyroidism

  • Toxic multinodular goiter

  • Functional autonomy of thyroid independent of TSH stimulation

  • Disease of the elderly (usually)


Hyperthyroidism treatment
HyperthyroidismTreatment

  • Radioactive Iodine (RAI131) is ablative, and is definiitive (not used in children or pregnancy)

  • Hypothyroidism develops in 80% of patients


Hyperthyroidism1
Hyperthyroidism

  • Propylthiouracil –blocks thyroid hormone synthesis

  • Propanalol –blocks hormone effects, inhibits conversion T3 to T4

  • Surgery can be done for large goiters-many are then hypothyroid


Hyperthryoidism
Hyperthryoidism

  • Thyroid Storm

  • Preciptated by ‘medical crisis/stress’

  • Extreme irritability, delirium, coma, fever, tachycardia, hypotension, vomiting

  • Treatment: Antithyroid agents, beta blocker, steroids, supportive measures


Thyroiditis
Thyroiditis

  • Usually from a viral infection

  • Can be suppurative

  • Presentation is a tender thyroid with fever and malaise

  • Can have transient thyroid test abnormalities

  • If transiently hyperthyroid (mild), sometimes managed with beta-blockers

  • Usually managed symptomatically


Ovaries
Ovaries

  • Premature Ovarian failure

    -Occurs before age 40

    -Genetic

    -Autoimmune

    -Infectious

    -Iatrogenic

    -Idiopathic


Ovaries1
Ovaries

  • Polycystic Ovarian Syndrome

    -Prediabetes Syndrome

    -Hirsuitism

    -Amenorrhea/infertility (may start with dyfunctional uterine bleeding)

    -Obesity

    -6 to 7% of reproductive age women


Ovaries2
Ovaries

  • PCOS

    -Clinical diagnosis: progesterone withdrawal test (5 days- bleeding)

    -Lab: Elevated LS/FSH ratio >2.5

    Elevated PRL in 25%


Ovaries3
Ovaries

  • PCOS

    -Lab: Glucose every 6mos-2 yrs

    Lipids/LFT’s every 6mos-2yrs

    Serum testosterone

    (may be tumor)


Ovaries4
Ovaries

  • PCOS:

    Lab

    TSH

    17-hydroxyprogesterone

    (rule out congenital adrenal hyperplasia)

    Cushing’s testing

    Ovarian Imaging


Ovaries5
Ovaries

  • PCOS

    Treatment

    -Surgical (Ovarian wedge resection)

    -TZD’s, Metformin

    -Oral contraceptives

    -Spironolactone

    -Weight loss


Testosterone deficiency
Testosterone Deficiency

  • Many causes

  • Many settings

  • In adult men, reduction of spermatogenesis, erectile dysfunction, fatigue, weight gain

  • Treated easily with testosterone replacement (should monitor PSA)


Gout

Etiology

  • Purines (from proteins) metabolized to uric acid

  • Serum level > 7.0 urate exceeds solubility and precipitates


Gout

  • Increased production of uric acid

    –Lympho/myeloproliferative dz

    –Hemolysis

    –High level exercise/rhabdomyolysis

    –Alcohol

  • Decreased elimination

    -EtOH,NSAIDS, Down Syndrome, renal


Gout

  • Signs/symptoms

    –Monoarticular, acute, inflammatory arthritis

    Great toe classic, can be any joint

    –Tophi (finger joints, achilles tendon, ears)

    –Urolithiasis

    -Renal damage

    (deposition in renal parenchyma)


Gout

Exacerbation ‘Attack’

  • Red, swollen, inflamed, painful joint(s)

  • 90% monoarticular

  • Acute onset, worst at 24 –48 h

  • Resolves in 7 –10 days


Gout

  • Diagnosis

    -Exam

    -Joint aspiration- crystals visible in polarizing microscopy (don’t always need aspirate for clinical decision)

    -Serum uric acid level


Gout

  • Treatment

    -NSAIDS (Indomethacin-classic) 1st line

    -Corticosteroids may be considered

    -Colchicine

  • Preventive

    -Colchicine

    -Allopurinol

    -Probenicid


Endocrine review1
Endocrine Review

  • QUESTIONS?

  • Diabetes is next……


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