Endocrine MDT Flashcards
Blood glucose <70mg/dl
Clinical signs of hypoglycemia (confusion, irritability, fatigue, anxiety, sweating, irregular heart rhythm, perioral paresthesia)
Clinical signs resolve with glucose
Whipple’s Triad
Hypoglycemia symptoms begin at plasma glucose levels at ___mg/dl or less
60
Hypoglycemia symptoms that impair brain function start at ___mg/dl
50
Two types of spontaneous hypoglycemia
Fasting
Postprandial
Fasting hypoglycemia is often subacute or chronic and usually presents with ________ as its principal manifestation
Neuroglycopenia
Postprandial hypoglycemia is relatively acute and is often heralded by symptoms of:
Neurogenic autonomic discharge (sweating, palpitations, anxiety, and temulousness)
Postprandial hypoglycemia may be seen after _______ surgery
Gastrointestinal surgery
The clinical manifestations of hypoglycemia are divided into what two broad categories?
Neuroglycopenic
Sympathomimetic
Most episodes of symptomatic hypoglycemia include ______ dysfunction
Neurological
Hypoglycemia
Sx: Alterations in consciousness, lethargy, confusion, combativeness, agitation, and unresponsiveness, seizures, and focal neurologic deficit
Neuroglycopenic
A rapid fall in blood glucose levels or the hypothalamic sensing of neuroglycopenia causes the release of the counter-regulatory hormones, primarily:
Catecholamines
- Epinephrine
- Norepinephrine
Hypoglycemia
Sx: Anxiety, nervousness, irritability, nausea, vomiting, palpitations, and tremors
Sympathomimetic
Labs if considering hypoglycemia is auto immune in nature
Serum antibody testing (GAD-65, anti-islet cell, anti-insulin antibodies)
Labs if considering hypoglycemia is a surreptitious cause
C-Peptide
Serial glucose/insulin levels in supervised setting
Serum Sulfonylurea levels
Treatment for hypoglycemia
Glucose
Hypoglycemia
Do not give PO glucose to:
Patients with altered mental status
Treatment for hypoglycemic patients unable to eat or drink
Glucagon 0.5 or 1mg SC/IM
Dextrose 50-100 mL IV Bolus
Hypoglycemia
Once patients are alert and safe to do so they should do what in order to prevent immediate hypoglycemia recurrence?
Eat a meal
Complications of Hypoglycemia
Coma
Brain Damage
Traumatic Injuries
Death
Essentials of the diagnosis
- Impaired fasting glucose (100-125mg/dl)
- Borderline Hgb-A1C elevation (5.7-6.4%)
- 2 Hour post-prandial glucose (140-199mg/dl)
Prediabetes
Risk factors for Prediabetes
Family history
Obesity
Diet
Physical inactivity
Race
Women who deliver a baby >9 lbs or had gestational diabetes
Symptoms of Prediabetes
Usually, no physical exam findings
Early sensory nerve toxicity
Treatment for Prediabetes
Weight loss
Metformin may lower risk by 30%
Increase physical activity
Complications of prediabetes
Progression to Type 2 Diabetes
Increased cardiovascular / ischemic stroke risk
Peripheral neuropathy
Metabolic disorder or disease that is brought about by either the insufficient production of insulin or inadequate activity of insulin receptors
Diabetes mellitus
Three categories of Diabetes
Type 1
Type 2
Gestational Diabetes
Symptoms:
- Polyuria / Polydipsia
- Weight loss
- Glucose >126 mg/dl after a fast on more than one occasion
- Ketonemia / Ketonuria
Diabetes
Auto immune antibodies
May develop in adults up to age 30
Partial or absolute deficiency of endogenous insulin production and require exogenous insulin for survival
Type 1 Diabetes
The presence of polyuria, polydipsia, fatigue, polyphagia, unexplained weight loss, poor wound healing, blurry vision and a high prevalence of infections should lead the IDC to do what test?
Blood glucose level
Lab findings in a Type 1 diabetic
Glucosuria
Ketonemia, ketonuria, or both
The average renal threshold for glucose is approximately
150-180 mg/dl
Testing used if the fasting plasma glucose level is <126 mg/dL in suspected cases, most commonly used to screen for gestational diabetes
Oral Glucose Tolerance Test (GTT)
Form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over time
Provides an estimate of glucose control for the preceding 2-3 months
Glycosylated Hemoglobin (HbA1c)
What lab tests are diagnostic for diabetes if confirmed by repeat testing?
Plasma glucose >126 mg/dL or HbA1c of >6.5%
Only medication that is effective in lowering blood glucose levels in type 1 diabetics
Insulin
Insulin supplied in AMMAL
10 mL bottles containing 100 un/ml, short-acting
Immediate short-term goal of Type 1 Diabetes
Control hyperglycemia
Maintain serum electrolytes and hydration
Therapeutic goal for long term therapy treatment of Type 1 Diabetes
Maintain normal glucose levels WITHOUT causing hypoglycemia
Type 1 Diabetes
Physician monitor blood glucose and HbA1c every __ months until at goal, then every __ months indefinitely
3 months
6 months
Helps control blood sugar and weight
Regular exercise
Drug of choice for diabetes with hypertension because of their renal protection action
ACE inhibitors
Goal for HTN in diabetic patients
<130/80
Dramatically reduces the risk of developing both the microvascular and macrovascular complications of diabetes
Keeping glucose levels at or near normal (Normal A1c = 4.0-6.0)
Type 1 diabetes requires _______ for continued military service
Medical Board
Patients determined to have new onset diabetes should be referred to:
Internal Medicine or Endocrinology
Insulin overdose treatment
Check blood glucose level
- Drink 1/2 cup of regular soda or fruit juice
- Eat a hard candy
- Glucose paste, tablets, or gel
Recheck blood sugar after 15-20 minutes
Insulin overdose
Patient is still symptomatic after first treatment
Provide 15-20 grams of sugar
Once safe to do so patient should eat a meal
Uncontrolled glucose often leads to damage of:
Small arteries and nerves
Most common diabetic complication, affecting 50% of older patients with Type 2
Neuropathies
Diabetic nephropathy is initially manifested by:
Proteinuria
Diabetic nephropathy
As kidney function declines, what will accumulate in blood?
Metabolic acids and waste products
- Creatinine
- Urea
Hypertension from diabetes is most likely from?
Progressive kidney involvement
MI is ____ times more common in DM patients
3-5x
Leading cause of death in Type 2 DM patients
Heart disease (coronary atherosclerosis)
Correlate with both the duration of diabetes and the severity of chronic hyperglycemia
Diabetic cataracts
Diabetic retinopathy after 10-15 years
25-50%
Diabetic Retinopathy after 15 years
75-95%
Diabetic Retinopathy after 30 years
100%
Glaucoma occurs in __% of diabetics
6%
Insulin resistance due to inadequate activity of insulin receptors
Most patients are over 40 y/o and obese
Type 2 Diabetes
Random glucose 200 mg/dL or higher
Hemoglobin A1c >6.5%
HTN, Dyslipidemia, and Atherosclerosis associated
Polyuria / Polydipsia
Candida vaginitis in women
Glucose >126 on more than one occasion
Type 2 Diabetes
DM 2
Resistance to the action of insulin at the ______ level
Receptor
Accounts for 90% of patients with DM
Type 2
Cause of death in over 70% of Type 2 diabetics
Vascular Disease
Symptoms:
- Polyuria / Polydipsia
- Fatigue
- Weight loss
- Poor wound healing
- Blurred vision
- Infections
- NO KETONES IN BLOOD
DM 2
Urine dipstick is sensitive to as little as __% glucose
0.1%
Normal Glucose Tolerance
Fasting plasma glucose ______
Two hours after glucose load _____
HbA1c _____
<100
<140
<5.7
Impaired Glucose Tolerance
Fasting plasma glucose ______
Two hours after glucose load _____
HbA1c _____
100-125
> 140-199
5.7-6.4 (Prediabetes)
Diabetes Mellitus
Fasting plasma glucose ______
Two hours after glucose load _____
HbA1c _____
> 126
> 200
> 6.5 (diabetes)
Stage 1 Glycemic Control in Type 2 patients
Diet (record food eaten)
Exercise
Stage 2 Glycemic Control in Type 2 patients
Oral Antidiabetic medications
-FIRST LINE: Biguanides (Metformin/Glucophage)
Stage 3 Glycemic Control in Type 2 patients
Insulin
Most important modifiable risk factor
Obesity
Leading cause of diabetic-related deaths
Heart Disease (40% in men; 32% in women)
Leading cause of new cases of blindness in patients aged 25-74 in the United States
Diabetic retinopathy
Patients with diabetic retinopathy are __ times more likely to become blind than those without retinopathy
29 times
__% of new cases of renal failure each year are due to diabetic nephropathy
43%
Diabetes
Typical entry on feet is from:
Broken skin secondary to tinea pedis
Diabetes related foot and lower extremity ulcers
Account for __% of diabetes related admissions
___% if all lower extremity amputations
20%
60%
Diabetes
A comprehensive foot examination should be conducted by a clinical provider ______
Annually
Mothers who have untreated gestational diabetes may give birth to babies with:
Macrosomia (high birth weight)
Congenital heart & nervous system anomalies
Respiratory distress syndrome
Malformations of skeletal muscles
Hyperglycemia >250 mg/dL
Acidosis with blood pH <7.3
Serum bicarbonate < 15 mEq/L
Serum positive for ketones
Diabetic Ketoacidosis
May be the initial manifestation of both type 1 or type 2 diabetes
Diabetic Ketoacidosis
Commonly occurs with poor compliance in Type 1 diabetes
During Infection, trauma, myocardial infarction, or surgery
May develop in type 2 diabetics under severe stress
DKA
Common serious complication of insulin pump therapy
DKA
Symptoms:
- Dehydration
- Rapid deep breathing with “fruity” bread odor
- Hypotension with tachycardia
- Mild Hypothermia
- Abdominal pain and tenderness in the absence of abdominal disease
DKA
Treatment for DKA
Fluids & Insulin
Initial management priority for DKA
Fluids (LR fluid of choice)
DKA fluid treatment
When blood glucose falls to 250 mg/dL or less, use 5% glucose solutions to maintain blood glucose _____ mg/dL while continuing insulin to clear serum ketones
200-300 mg/dL
DKA
Intravenous fluids may be reduced to maintenance levels when:
Vital signs improve
Hyperglycemia is 250 mg/dL or less
Adequate urine output of 30-50 mL/h
The cornerstone therapy for acute hyperglycemia is restoration of ________ and reperfusion of vital organs, especially the kidneys
Intravascular volume
DKA Fluid Treatment
Excessive fluid replacement may contribute to acute respiratory distress syndrome or cerebral edema
> 5L in 8h
Mainstay therapy for DKA
Insulin plus fluid and electrolyte replacement
DKA insulin treatment dosage
0.15 unit/kg as IV Bolus
Follow by:
0.1 unit/kg/h
DKA Insulin treatment
If plasma glucose level fails to fall at least __% in the first hour, give repeat loading dose
10%
DKA complications
Cerebral edema occurs rarely and is prevented by avoiding sudden reversal of marked hyperglycemia
Maintain glycemic levels of _______ mg/dL for the initial 24 h after correction of severe hyperglycemia reduces this risk
200-300 mg/dL
Abnormal growth of the thyroid gland.
Can be normal, decreased, or increased thyroid production depending on the cause.
Goiter
Iodine deficiency disorder
Common in regions with low-iodine diets
Most adults with endemic goiter are found to be euthyroid
Endemic Goiter
Most common cause of endemic goiter is:
Iodine deficiency
Mild-to-moderate and sometimes severe iodine deficiency exists in ___ countries
30
Usually, asymptomatic
Can cause tracheal compression, respiratory distress and failure, and dysphagia if large enough
Goiter
Lab findings for Goiter
T4 and TSH are normal
Thyroid Radioactive Iodine Uptake is ELEVATED
Treatment for endemic goiter
Addition of Potassium iodine to table salt
Surgery for cosmetic reasons or compressive symptoms
Weakness, cold intolerance, constipation, depression, menorrhagia, hoarseness, dry skin, bradycardia
Delayed return of deep tendon reflexes
Serum free tetraiodothyronine aka Thyroxin (T4) LOW
TSH hormone elevated in primary disease
Hypothyroidism
Primary hypothyroidism is due to:
Thyroid gland disease
Secondary hypothyroidism is due to:
Lack of pituitary TSH
Maternal hypothyroidism during pregnancy results in cognitive impairment in child.
Generally, increase dose of thyroid replacement hormone by ___%
30%
Drugs that can cause hypothyroidism
Lithium Amiodarone Propylthiouracil Methimazole Phenylbutazone Sulfonamides Interferon
Causes of hypothyroidism with goiter
Autoimmune (Hashimoto’s, Thyroiditis)
Subacute
Iodine deficiency
Genetic thyroid enzyme defects
Hep C
Drugs
Infiltrating diseases
Causes of hypothyroidism without goiter
Thyroid Surgery, Irradiation, or Radioiodine treatment
Deficient pituitary TSH
Severe illness
Drugs
Sub-clinical hypothyroidism (High TSH and Normal T4 occurs commonly in elderly women ___%
10%
Early Symptoms:
Fatigue, lethargy, weakness Arthralgias, myalgias, muscle cramps Cold Intolerance Difficulty concentrating Constipation Dry Skin Headache Weight Gain Menorrhagia
Hypothyroidism
Late Symptoms
Slow speech Peripheral edema Pallor Hoarseness Decreased senses of taste, smell, and hearing Dyspnea Absent sweating Amenorrhea or menorrhagia Galactorrhea
Hypothyroidism
Early signs
Thin, brittle nails Thinning of hair Pallor Poor turgor of mucosa Delayed return of deep tendon reflexes
Hypothyroidism
Late signs
Goiter Puffiness of face and eyelids Thinning of outer eyebrows Tongue thickening Hard pitting edema Pleural, peritoneal, pericardial, and joint effusions
Hypothyroidism
Hypothyroidism
Serum TSH is Increased in:
PRIMARY Hypothyroidism
Hypothyroidism
TSH is low or normal in _______ hypothyroidism
Secondary
Hypothyroidism
Free T4 may be:
Low or Low Normal
Hypothyroidism
Serum cholesterol, triglycerides, liver enzymes, creatine kinase, prolactin ________
INCREASED
Lab findings:
- Hyponatremia
- Hypoglycemia
- Anemia (MCV normal or increased)
Hypothyroidism
Treatment for hypothyroidism
Levothyroxine (T4)
25-75 mcg/day
Hypothyroidism treatment
Thyroid function tests should be repeated every ___ weeks for medication titration until TSH is at goal
4-6 weeks
Complications of hypothyroidism
Myxedema coma (long term untreated, ‘Hypo’ everything)
Increased susceptibility to infection
Megacolon
Organic psychoses with paranoid delusions
Angina Pectoris, CHF, dysrhythmias
Adrenal crisis
Sweating, weight loss, heat intolerance, menstrual irregularity, tachycardia, tremors, eye stare
Hyperthyroidism
Goiter, often with bruit
Ophthalmopathy
Thyroid stimulating immunoglobulins (active TSH receptor in thyroid
gland)
Grave’s disease
In primary hyperthyroidism the thyroid is acting:
Autonomously (independent from pituitary gland)
In primary hyperthyroidism, what would the lab values for T4, T3 and TSH be?
Increased Free Thyroxine (T4) and Triiodothyronine (T3)
Low TSH
Most common cause of hyperthyroidism
Grave’s disease
Signs:
- Fever
- Tachycardia
- Diaphoresis
- Tremors
- Disorientation/psychosis
- Goiter
- Exophthalmos
- Hyperreflexia
- Pretibial myxedema
Hyperthyroidism
Symptoms:
- Weight loss despite INCREASED appetite
- Dysphagia or dyspnea due to goiter
- Rash/pruritis/hyperhidrosis
- Palpations/Chest pain
- Diarrhea
- Myalgias and weakness
- Nervousness/anxiety
- Menstrual irregularities
- Heat Intolerance
- Insomnia and fatigue
Hyperthyroidism
Eye signs in hyperthyroidism
Stare and lid lag
Ophthalmopathy
Diplopia
Skin symptoms in hyperthyroidism
Moist warm skin
Fine hair
Onycholysis
Dermopathy
Heart symptoms in hyperthyroidism
Palpitations or angina pectoris
Arrythmias
Thyrotoxic cardiomyopathy due to thyrotoxicosis
Heart failure (Rarely)
Extreme form of thyrotoxicosis that may be triggered by stressful illness, thyroid surgery, or radioactive iodine (RAI) administration
Sx: Delirium, severe tachycardia, vomiting, diarrhea, dehydration, very high fever
Thyroid Storm
Treatment for Graves’ diseease
Radioactive Iodine
Treatment for hyperthyroid symptoms like tachycardia, tremors, diaphoresis, and anxiety until hyperthyroidism is resolved
Propranolol (Beta Blocker)
Most widely recommended permanent treatment of hyperthyroidism
Radioactive Iodine
Longterm treatment options for hyperthyroidism result in the patient developing hypothyroidism and lifelong need for:
Levothyroxine (Thyroid hormone replacement)
Commonly found during careful thyroid examinations
Small nodule on the thyroid
Usually, asymptomatic/benign
Thyroid nodule
What tests are mandatory for a thyroid nodule?
Thyroid U/S
Thyroid Function Tests
___% of thyroid nodules are benign
90%
Disposition for a thyroid nodule
Referral to endocrinology
Causes of solitary thyroid nodule:
Benign adenoma
Colloid nodule
Cyst
Primary thyroid malignancy or metastatic neoplasm
Thyroid nodule
Higher risk of malignancy if:
History of head-neck radiation in childhood
Family history of thyroid cancer
Personal history of another malignancy
Toxic multinodular goiter and hyperfunctioning nodules can cause:
Hyperthyroidism
Thyroid nodules or multinodular goiter can grow and cause:
Cosmetic embarrassment, discomfort, hoarseness, or dysphagia
Large retrosternal multinodular goiters can cause:
Dyspnea due to tracheal compression
Thyroid nodules with:
- Hoarseness or vocal cord paralysis
- Nodules in men or young women
- Nodule that is solitary, firm, large, or adherent to trachea or trap muscles
- Vocal cord paralysis
- Enlarged lymph nodes
- Distant metastatic lesions
Malignancy
History for distant metastatic lesions in regards to thyroid nodules
Family History of Goiter
Residence in area of endemic goiter
Physical characteristics of distant metastatic lesions of thyroid nodules
Older women
Soft Nodule
Multinodular goiter
Preferred imaging for thyroid nodules for its accuracy
U/S
Thyroid
Solid nodules are often:
Malignant
Thyroid
Cystic nodules are usually:
Benign
Treatment for thyroid nodules
Refer to endocrinology
U/S guided fine-needle aspiration
MEDEVAC
Weakness, abdominal pain, fever, confusion, vomiting
Low blood pressure, dehydration
Skin pigmentation may be increased
Insufficient aldosterone will result in elevated serum potassium and low sodium
Insufficient cortisol may result in hypoglycemia
Dehydration and hypotension may result in poor kidney perfusion
Adrenal Crisis
Primary renal crisis results from:
Destruction of dysfunction of the adrenal cortex
Secondary renal crisis results from:
ACTH hyposecretion
May occur during stress in a patient with latent insufficiency or treated adrenal insufficiency with sudden withdrawal of adrenocortical hormones
Adrenal Crisis
Drugs that if stopped or decreased too quickly will result in the adrenal gland not making cortisol again fast enough to meet the body needs
Resulting in adrenal insufficiency
Steroids (glucocorticoids & mineral corticoids)
Symptoms:
- Headaches
- Lethargy
- Nausea/Vomiting
- Abdominal pain and diarrhea
- Confusion or coma
- Cyanosis
- Dehydration
- Sparse Axillary hair
Adrenal Crisis
Signs:
- Skin hyperpigmentation
- Fever
- Hyperkalemia
- Hyponatremia
- Hypotension
- Eosinophilia
Adrenal Crisis
Lab findings in Adrenal Crisis
Eosinophilia
Hyponatremia or hyperkalemia (or both)
Hypoglycemia
Hypercalcemia (due to renal injury)
Blood, sputum, and urine may be positive for bacteria
Diagnostic tests for Adrenal Crisis
Cosyntropin stimulation test with serum ACTH level
Early morning (0600-0800) serum cortisol
What tests helps to determine adrenal insufficiency is primary or secondary?
Corsyntopin stimulation with serum ACTH
Acute abdomen is neutrophilia
Adrenal Insufficiency is ________ and ________
Lymphocytosis & Eosinophilia
If symptomatic adrenal insufficiency is suspected, immediately treat with:
Hydrocortisone 100-300 mg IV and saline
-Continue 50-100mg IV Q 6h on first day, then Q 8h on second day; taper off
Labs for adrenal crisis
Electrolytes
Cortisol
ACTH
Screen for infection (PNA, UTI)
Patients treated for acute adrenal insufficiency and diagnosed with Addison’s disease require lifelong replacement therapy with both:
Glucocorticoids
Mineralocorticoids
Weakness, fatigability, anorexia, weight loss; nausea/vomiting, diarrhea; abdominal pain, muscle and joint pains; amenorrhea
Sparse axillary hair; increased skin pigmentation especially of creases, pressure areas, and nipples
Hypotension, small heart
Potassium high, sodium low, blood urea nitrogen high
Plasma cortisol levels are low or fail to rise after administration of corticotropic
Elevated ACTH level
Chronic Adrenal Insufficiency
Uncommon disorder caused by destruction or dysfunction of the adrenal cortices
Addison Disease
Chronic deficiency of cortisol, aldosterone, and adrenal androgens and causes skin pigmentation that can be subtle or strikingly dark
Chronic Adrenal Insufficiency
Chronic Adrenal Insufficiency
Skin pigmentary changes are not encountered when:
ACTH is not elevated
Most common cause of Addison disease in the US
Autoimmune destruction of the adrenals
Leading cause of Addison disease
Tuberculosis
Symptoms:
- Weakness and Fatigability
- Weight loss
- Myalgias
- Arthralgia’s
- Anorexia
- Nausea/Vomiting
- Anxiety
- Mental irritability
Chronic Adrenal Insufficiency
Signs:
- Hyperpigmentation skin changes
- Hypopigmented skin (Vitiligo 10%)
- Hypoglycemia
- Hypotensive blood pressure
- Nail beds (longitudinal pigmented bands)
- Small Heart
- Scant axillary and pubic hair
Chronic Adrenal Insufficiency
Lab Findings:
- Moderate neutropenia, lymphocytosis, eosinophilia
- Low Na+, High K+
Hypoglycemic
Low Cortisol
High ACTH
Chronic Adrenal Insufficiency
Chronic Adrenal Insufficiency
Chest X-ray, look for:
TB
Fungal infection
Cancer
Edema
Chronic Adrenal Insufficiency
Abdominal CT, Look for:
Small noncalcified adrenal in autoimmune Addison disease
Adrenals are enlarged (85%)
Calcification is noted in 50% of TB cases
Drug of choice for Chronic Adrenal Insufficiency
Hydrocortisone
Most Addison patients are well maintained on:
15-30mg of hydrocortisone orally daily in two divided doses
Common endocrine disorder of unknown pathophysiology affecting up to 10% of women of reproductive age
Polycystic Ovarian Syndrome
Menstrual disorders
Infertility
Hirsutism
Obesity
Acne
Insulin resistance, DM2, metabolic syndrome
Dyslipidemia
Perinatal complications if able to become pregnant
Polycystic Ovarian Syndrome
Labs for Polycystic Ovarian Syndrome
LH / FSH (Ratio is 2:1 or 3:1; normal is 1:1)
TSH
Hgb A1c and Fasting Glucose
Prolactin
Free testosterone
Lab test for Polycystic Ovarian Syndrome if clinical evidence of Cushing Syndrome
Midnight salivary cortisol or dexamethasone suppression test
Treatment for Polycystic Ovarian Syndrome
Weight loss and exercise
Metformin
Contraceptives
Polycystic Ovarian Syndrome drug of choice that will increase FSH and will increase chances of ovulation
Clomiphene
Deficient testosterone secretion by the testes or sperm production
Hypogonadism
Hypogonadism
Insufficient gonadotropin by the pituitary
Hypogonadotropic
Hypogonadism
Pathology in the testes themselves
Hypergonadotropic
Fatigue
Decreased strength
Poor libido
Hot flushes
Erectile dysfunction
Gynecomastia
Infertility
Small testes
Hypogonadism
Total testosterone
General rule is low
<200ng/dl
Total testosterone that is normal
> 350ng/dl
For values of free testosterone between 200-350ng/dl measures it with:
Albumin to calculate Bioavailable testosterone
Hypogonadism
If testosterone is low, obtain what labs?
LH, FSH, and Prolactin
Hypogonadism
High FSH/LH indicates _______ failure
Primary testicular
Hypogonadism
High prolactin indicates possible:
Prolactinoma
Hypogonadism
Low FSH/LH indciates:
Secondary hypogonadism
Hypogonadism
Low FSH/LH should prompt additional screening for:
Hemochromatosis w/ Transferrin, Ferritin, and genotypic for HFE Gene
Pituitary mass with MRI of the Sella
Anabolic steroid or supplement use
Treatment for Hypogonadism should only be initiated:
With guidance from a medical officer
Testosterone replacement is contraindicated in ______ cancer
Prostate cancer
Testosterone
HCT of ___% or greater is of high risk of developing erythrocytosis
55%
Treatment for Hypogonadism
Transdermal testosterone 25-100mg (PREFERRED)
IM Testosterone 100mg (LONG ACTING)
Higher doses >100mg of IM testosterone sometimes spread-out injection intervals to ___ weeks
2-4 weeks
Normal hypothalamus-pituitary-gonadal (HPG) axis is down regulated by estrogen sensing in the hypothalamus.
This negative feedback mechanism can be blocked by inhibiting the hypothalamic estrogen receptors with:
Clomiphene (Clomid)
Hypogonadism
Preferable therapy if patient desires fertility
Clomiphene (Clomid)
Hypogonadism
This modality is used to attempt to restore normal physiology before committing life-long testosterone replacement therapy
Clomiphene (Clomid)
Regimen of Clomiphene that may be attempted 3 times
Daily 25mg for 3 months, followed by 6 weeks off
Therapeutic target for testosterone levels
800ng/dl
Do not titrate testone dose to:
Patient-reported symptoms
Sub-areolar glandular hyper density which may be unilateral or bilateral, and may be painful or non-painful
Common transient finding in pubertal males which general self-resolves
Gynecomastia
Any condition resulting in excess estrogen, or testosterone which is metabolically linked to the estrogen via:
Aromatase
Gynecomastia
Excess estrogen may be from:
Normal Physiology (Aging, obesity, puberty)
Endocrine Disease
Systemic Disease
Neoplasms
Drugs
Gynecomastia
Physical exam, use what fingers as pincers to examine subareolar tissue as compared to nearby adipose tissue
Thumb and index finger
Tissue that is diffuse and non-tender
Adipose
Tissue that is dense and may be tender
Breast tissue
True Gynecomastia will be localized to ________ region only
Subareolar
Red flags of Gynecomastia
Asymmetry
Density located away from subareolar region
Nipple retraction
Nipple bleeding or discharge
Unusual firmness
Gynecomastia
What else should you examine for size and masses?
Testicles
All masses or presence of HCG warrant:
Testicular U/S
Labs for Gynecomastia
Free testosterone
LH / FSH
Liver function panel
Renal panel (BUN and Creatinine)
Beta HCG (not pregnancy test; specific Tumor Marker)
Estradiol
Thyroid function panel
Prolactin
Treatment for Gynecomastia
Selective estrogen receptor modulator (SERM)
- Raloxifine
- Tamoxifine
Aromatase inhibitor
-Anastrozole
Testosterone therapy for males with hypogonadism
Treatment for Gynecomastia Refractory cses
Radiation therapy
Surgery
Referral for Gynecomastia
Family Practice or Internal Medicine
Constellation of 3 or more of the following:
- Abdominal Obesity
- Triglycerides 150mg/dl or higher
- HDL <40mg/dl for men or 50mg/dl for women
- Fasting glucose of 110mg/dl or higher
- HTN
Metabolic Syndrome
Metabolic Syndrome
Waist measurement if BMI is ____
> 25
Metabolic Syndrome
Lipid screening every __ years
5 years
Metabolic Syndrome
Check fasting glucose or A1c every __ years in patients BMI >25 with one or more additional risk factor
3 years
Metabolic Syndrome
Most important modifiable risk factor
Obesity
Management for Metabolic Syndrome
Weight management and physical activity
Diet modification
Nutrition referral
Metformin
Blood pressure medications