Download CM Endocrine Exam II

CM Endocrine Exam II
13-14 Congenital and Genetic Endocrine Disorders in Kids
Adrenal Disorders
Congenital Adrenal Hyperplasia
 Autosomal Recessive, usually 21-hydroxylase deficiency (CYP21A2 gene), but can be 11
b-hydroxylase, 3 b-hydroxysteroid dehydrogenase, or 17-hydroxylase deficiency
o 21-hydroxylase deficiency = block progesterone   aldosterone
 blocks 17-hydroxyprogesterone cortisol
 Presentation = salt-wasting type (most common), non-salt-wasting (simple-virilizing)
o Males-salt-wasting = hypoNa, hyperK, metabolic acidosis, hypotension (can lead
to shock), first week of life
o Male-non-salt-wasting = early virilization (2-4 yo)
o Female = hirsutism, menstrual irregularity, ambiguous genitalia (clitoromegaly)
 DX = high 17-hydroxyprogesterone, measure DHEA, ACTH, pelvic U/S, karyotype
 Treatment = dexamethasone prenatally (crosses placenta)
o For neonates = hydrocortisone, fludrocortisone, NaCl surgical management of
ambiguous genitalia
 11 b-hydroxylase deficiency = no salt wasting, HTN, dx w/ high deoxycorticosterone
 3 b-hydroxysteroid dehydrogenase deficiency = check ratio of delta-5 steroids to delta-4
steroids in plasma and urine
Primary Adrenal Insufficiency = from adrenal cortex problem (secondary/tertiary =
pituitary/hypothalamus)
 Congenital = inborn defects of steroid synthesis, adrenal hypoplasia, disorder of cholesterol
metabolism, steroid-binding-globulin def.
 Acquired (Addison Disease) = autoimmune (most common), infection (TB), drugs, hemorrhage
of adrenals
 Presentation = hyponatremia and hyperkalemia
o Glucocorticoid def. = hypoglycemia, ketosis, muscle weakness, HA, hyperpigmentation
o Mineralocorticoid def. = low BP, dizzy, salt-craving, wt loss, dehydration, abnormal
electrolytes
o Adrenal androgen def. = lack of axillary/pubic hair and libido in females
o Adrenal Crisis = hypotension, electrolyte abnormalities, shock
 Treatment = mineralocorticoids + glucocorticoids
Cushing Syndrome = hypercortisolism
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Etiology
o Exogenous steroids (most common) e.g., prednisone
o ACTH independent carcinoma (primary adrenal)
o ACTH dependent carcinoma (pituitary) = Cushing’s Disease (high ACTH + high)
o ectopic ACTH (paraneoplastic syndrome)
o Primary pigmented nodular adrenocortical disease (Carney complex, McCune
Albright syndrome)
o Adrenocortical lesions = diffuse hyperplasia, nodular
hyperplasia/adenoma/carcinoma
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Clinical = central obesity, thin skin, easy bruising, low bone density, blood clot risk, moon facies,
buffalo hump, purple striae, short stature in children, HTN, hyperglycemia (DM), increased
susceptibility to infxn
Labs = circadian rhythm lost (AM and PM cortisol equal), dexamethasone suppression test,
abnormal GTT, increased urinary cortisol, PM salivary and serum cortisol increase
DX = ACTH (Cushing’s dz), CT (adrenal tumors), MRI (functional pituitary adenoma), bilateral
petrosal blood sampling (ACTH before/after CRH admin.)
Disorders Affecting Growth
Normal Growth
 GHRH (from hypothalamus)  GH (from anterior pituitary)  IGF-1 (from liver) 
linear growth at growth plate of long bones and growth at other tissues
o Somatostatin (hypothalamus)= inhibition of GH, IGF-1 (liver) = inhibition of GH
o GH peaks at midnight, puberty, increased by stress, AA, hypoglycemia
 Growth chart = worry if height >2 SD below for mean age, growth fallen across 2 %iles
on chart in 6 mo, height is inconsistent w/ siblings, growth velocity is unlikely to lead to
predicted adult height
 Normal growth velocity after 2 yo = 2”/year
Genetic Short Stature
 Presentation = child is short, normal growth velocity, normal onset of puberty, look at
midparental height for adult height potential, bone age = chronological age on wrist
xray, other family members short
 DDX = constitutional delay, genetic short stature, GH def., hypoT3/4, Cushing’s, chronic
dz, nutrition def., intrauterine growth retardation, Turner, Down (trisomy 21),
achondroplasia
 DX = weight v. height (endocrine disorders = low height but normal weight)
 Other problems = weight v. height are proportionally low
o Midparental height (5” = 13 cm)
 Boys = [father height + (mother height + 5’’)] / 2
 Girls = [(father height – 5”) + mother height] / 2
o Growth Velocity = change in growth overtime (normal = 2” per y)
Constitutional Growth Delay
 Presentation = short stature, delayed puberty, normal adult height eventually,
parenteral delay hx, growth velocity normal, bone age delayed, no tx necessary
 DX = delayed bone age on wrist X ray (best way to differentiate from genetic short
stature)
Growth Hormone Deficiency
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Presentation = child is short, hasn’t grown much for a few years, decreased linear
growth velocity, normal weight gain, puberty delayed, bone age delayed, slender long
bones
 Labs = low IGF1, low IGFBP3 (binding protein)  Thus, GH is low (but direct GH not
useful for dx)
 DX = high IGF1 and failure to release GH after exposure to 2 stimuli that usually release
GH (e.g., hypoglycemia, stress), MRI before tx
 Congenital GH def. = mutation in GH1 gene or GHRH receptor, size is normal at birth
(drop to 4 SD below by 1yo), frontal bone prominent, saddle-shaped nose, bulging eyes,
small mandible, small hands/feet, fontanel stays open past 2 yo
 Acquired GH def. = any age, growth initially normal but growth velocity slows and
eventual growth failure, sexual maturity delayed, sx from tumor (N/V, HA, neuro def.)
o Etiology = idiopathic (most common), infection, radiation, trauma, surgical
damage, tumors (craniopharyngioma)
 Treatment = SQ GH shots each night until growth plates close
o AE = pseudotumor cerebri, edema, glucose intolerance, slipped capital femoral
epiphysis (SCFE), rapid growth of nevi, increased scoliosis
Pituitary Gigantism
 Background = rare, during puberty, longitudinal growth acceleration secondary to GH
excess, pituitary adenoma is most common cause, can also be from GHRH increase,
tumor may cause HA/bitemporal hemionopsia
 Presentation = coarse facial features, broad nose, wide tongue, large mandible, large
head/hands/feet, delayed puberty, behavioral problems, visual problems
 DDX for tall pt = familial, cerebral gigantism, exogenous obesity, excess GH (pituitary
gigantism), McCune-Albright syndrome or MEN w/ excess GH
o Precocious puberty = Marfan, Klinefelter (XXY), fragile X syndrome,
homocystinuria, XYY, hyperthyroidism
 Labs = GH, IGF-1, IGFBP-3 elevated. Gold Standard = failure to suppress GH during
glucose tolerance test
 Treatment = tumor removal, somatostatin analogs (octreotide) to inhibit GH secretion,
dopamine agonists, GH receptor competitive agonist (blocks endogenous GH binding)
15 Obesity and Metabolic Syndrome Management
Define and classify levels of obesity
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Obesity
o BMI > 30 kg/m2 (“extreme obesity” is BMI > 40)
 Grade 1:BMI 30-34.9 kg/m2
 Grade 2: BMI 35-39.9 kg/m2
 Grade 3: BMI 40 kg/m2
 Grade 4: BMI 50 kg/m2
 Grade 5: BMI 60 kg/m2
o Waist Circumference
 Men > 40” (102 cm) or 35” for Asian American
 Women > 35” (90 cm) or 32” for Asian American
Why does increased fat mass increase disease risk?
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Adipocytes are for fat storage and endocrine function
Adipocytes ‘sense’ energy state of body and sends signals to organs to coordinate their function
Adipocytes expand when they fill w/ fat (hyperplasia) or they shrink in size (not #) with wt loss
List the criteria for metabolic syndrome
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Dx can be made when 3 of the 5 are present
1. Abdominal obesity, given as waist circumference
a. Men  40 in
b. Women  35 in
2. Triglycerides  150 mg/dL
3. HDL cholesterol
a. Men <40 mg/dL
b. Women <50 mg/dL
4. Blood pressure  130/ >85 mmHg
5. Fasting glucose  100 mg/dL
Pathophysiology = INSULIN RESISTANCE (genetics, nutrient deficiencies, metabolic defects,
lifestyle, environment  inflammatory state
Risk factors = smoking, obesity, hispanic, aging, genes, hormone changes, lack of exercise, insulin
resistance
Discuss the treatment options for obesity and metabolic syndrome
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Goal = prevent/delay onset of DB, HTN, and CVD
Primary therapy = diet + exercise (weight loss improves all aspects of metabolic syndrome)
o Exercise = reduce skeletal muscle lipid levels and insulin resistance regardless of BMI
 Must be done regularly as the insulin sensitivity impact of exercise is only for
24-48 hours and disappears in 3-5 d
 Combination of resistance + aerobic exercise = best
 Sedentary pts  start walking and gradually increase duration/intensity
o Diet = low Na+, low fat, DASH diet (low fat, high carb to stop HTN)
 DASH = more fruits, veggies, low-fat dairy, whole grains, poultry, fish, nuts
 less saturated fats, red meat, sweets, sugary beverages
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Mediterranean diet = improves vascular inflammation, endothelial dysfunction,
insulin resistance, cognitive function, lowers DM2 risk
Pharmacology = for pts whose risk factors are not reduced by lifestyle changes
o Aspirin = reduce inflammation (CRP)
o Statins = reduce inflammation (CRP), reduce LDL (goal = lower LDL-C < 100)
o Metformin = increase insulin sensitivity in tissues, reduce resistance and blood sugar
 life-threatening AE = lactic acidosis
o Thiazolidinediones = reduce insulin sensitivity in tissues and decrease glucose from liver
Surgery = wt loss surgery is only method w/ long-term effects that improve complications
Explain the complications and different body systems involved in patients with metabolic
syndrome
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Coronary heart dz, DB, gout, low testosterone and hypogonadism (males), polycystic ovarian
syndrome (females)
Poor glycemic control, HTN, hyperlipidemia, insulin resistance
Even 5-10% wt loss improves these complications
Describe different techniques used for counseling patients with metabolic syndrome
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Education = start where you patient is at! Make short and long term goals and help ID barriers to
change.
Sedentary pts  start walking and gradually increase duration/intensity
Practice Questions
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Larry comes to your clinic for weight management. His BMI is 28, and his waist circumference is
41 inches. The results of his fasting labs revealed the following: HDL cholesterol 45mg/dl,
Triglycerides 170 mg/dl, and fasting glucose 120 mg/dl. His Blood pressure is 125/80. Are Larry’s
risk profile data consistent with metabolic syndrome?
o YES (3 of 5 criteria are met)
Don is a 55-year-old African American male who is 5’7”, weighs 198 lbs., and has a BMI of 31. He
reports a family history positive for diabetes type 2. He suffers from sleep apnea and reflux. His
review of systems is unremarkable.
o His blood pressure is 120/96. His baseline labs are: total cholesterol 239 mg/dl, LDL
cholesterol 182 mg/dl, HDL cholesterol 34 mg/dl, and triglycerides 116 mg/dl. His fasting
blood glucose is 93.
o How should Don’s weight be classified? Grade 1 Obesity
o What level of weight loss will help improve his lipids? 5-10%
What are some complications noted with metabolic syndrome?
o inflammation - coronary heart dz, DB, gout, low testosterone and hypogonadism
(males), polycystic ovarian syndrome (females)
o Poor glycemic control, HTN, hyperlipidemia, insulin resistance
What lab tests would best indicate a metabolic syndrome patient’s risk for heart disease?
o Highly sensitive C-reactive protein (hs-CRP)  for risk stratification
What are some ways to improve insulin sensitivity in patients with metabolic syndrome?
o Regular resistance/aerobic exercise, Mediterranean diet, metformin, thiazolidinediones
16 DBM Medical Nutrition
Distinguish diabetes mellitus (DM) as a manageable disease from other chronic conditions.
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DM = can be controlled with appropriate treatment, nutrition, and exercise
Recognize the demographic trends in diabetes mellitus prevalence and incidence and
describe the clinical significance of this.
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DB = most common cause of new renal failure in US, 2.3x the medical cost vs. non-DB pts
50% of expenditures are related to DB-related complications (MI, CVA, ESRD, retinopathy, foot
ulcers)~9% of US has DB
State the screening and diagnostic criteria for diabetes mellitus.
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Screening
o Age > 45
o BMI > 25 regardless of age (Repeat every 3 years)
o Asymptomatic adults with sustained BP (either treated or untreated) > 135/80mmgHg
(Grade B recommendation)
o Consider screening in individuals who are overweight (BMI > 85th percentile) and have 1
of the following:
 1st or 2nd degree relative with type 2 DM
 Belongs to High – Risk population (African American, Native American, Latino,
Asian American)
 Begin at age 10 or onset of puberty. (Normal  repeat every 2 years)
Diagnosis
o fasting plasma glucose > 126 mg/dL x 2
o Random > 200 mg/dL
o 2 hour Oral Glucose Tolerance Test (OGTT) > 200 mg/dL with SX
o A1C > 6.5%
Describe the nutritional complications and nutritional recommendations for patients with
diabetes mellitus.
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Goals = keep BG < 120, LDL < 100, HDL > 50, TG < 150, BP < 130/80
o For adolescents = maintain normal growth and development
Carbs
o DB1 = % CHO based on individual assessment
 intensive insulin therapy  adjust pre-meal insulin dose to meal CHO
 fixed daily insulin  be consistent w/ daily CHO intake
o DB2 = CHO and monosaturated fat should be 60-70% of energy (individualized)
 Fiber > 25 g/d (up to 50 g/d is beneficial)
Protein
o controlled DB2  protein doesn’t increase plasma glucose
o uncontrolled DM  requirements may be higher than normal (> 0.8g/kg BW)
 Do not increase protein intake >20% of daily energy
o diet high in protein and low in CHO = short-term weight loss, but long-term LDL effects
Fat
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o if LDL<100  saturated fat should be <10% of total calories
o if LDL > 100  saturated fat should be <7% of total calories
o avoid trans fats (increases cholesterol)
o if LDL<100  cholesterol should be <300 mg/d
o if LDL > 100  cholesterol should be <200 mg/d
o monounsaturated fat + CHO  60-70% of total energy (lowers LDL)
o PUFAs and omega-3s are beneficial too
o Plant stanol or sterol food lower LDL and total chol (spreads, milk, yogurt, veggies)
Micronutrients (Vit/minerals) = no clear evidence, may need Vit D supplements
etOH = 1 drink/d (female), 2 drink/d (male) and drink w/ food to reduce hypoglycemia risk
Exercise
o Monitor BG before + after exercise or periodically during prolonged/intensive exercise
o Insulin/secretagogues = 30-50% reduction of dose during time of exercise
o Moderate exercise < 30 min does NOT require insulin or CHO adjustment
o Pre-exercise BG <100 = increase CHO intake to compensate (snack 1-3 h before)
 Consume 15g of CHO / 30-60 min of prolonged/intense exercise
o Post-exercise = intake 1.5 g CHO / kg BW w/in 30 min of exercise > 90 min
 Intake 1.5 g CHO / kg BW 2 hr later will support glycogen repletion and decrease
risk for post-exercise hypoglycemia
Characterize the special populations at risk for diabetes complications.
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1st or 2nd degree relative with type 2 DM
Belongs to High – Risk population (African American, Native American, Latino, Asian American)
Practice Questions
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What are some ways to diagnose DM?
o fasting plasma glucose > 126 mg/dL x 2
o Random > 200 mg/dL
o 2 hour Oral Glucose Tolerance Test (OGTT) > 200 mg/dL with SX
o A1C > 6.5% (pediatric > 7.5%)
Are there any clear benefits to vitamin or mineral supplementation in DM?
o NO clear evidence of benefit
Are there any general dietary supplements that will help lower blood sugar?
o Cinnamon  reduce blood glucose
What adjustments are needed to medications or carbohydrate intake in regards to less than 30
minutes of moderate exercise?
o 30%-50% reduction in dosage of insulin acting during the time of exercise is generally
accepted safe guideline.
o May need greater reduction for prolonged, vigorous activity ( long distance running)
o Moderate exercise less than 30 minutes usually do NOT require any additional
carbohydrate or insulin adjustment
What is the overall goal of nutrition when treating children with diabetes?
o Maintenance of normal growth and development
17 DBM Adults
Define Type 1 Diabetes Mellitus (DM)
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Definition = Type 1 diabetes mellitus (DM) is a chronic disorder characterized by hyperglycemia
resulting from an absolute insulin deficiency
Diagnosis
o Symptoms + random glucose of > 200 mg/dL
o A fasting (≥8-hour) glucose concentration ≥ 126 mg/dL
o A 2-hour post-load glucose concentration ≥ 200 mg/dL during a 75-g oral glucose
tolerance test
o A hemoglobin A1c ≥ 6.5% (non-fasting)
o C-peptide levels help distinguish endogenous insulin production
 DB1 = no insulin (no c-peptide); DB2 = has endogenous insulin (c-peptide)
Recognize the differences between Type 1 and Type 2 DM
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DB 1 clinical = wt loss, younger, abrupt onset
DB 2 clinical = obesity, older, hypertriglyceridemia, acanthosis nigricans, hirsuitism, candida, eye
sx (hemorrhage, exudates, neovascularizations, macular edema), sensory sx (touch, DTRs,
proprioception)
o Cause of vision changes = hyperglycemia  blood sugar is hyperosmotic  sugar flows
into hyposmotic vitreous humor of the eyes
Both = potential DKA, polyuria, polydipsia, polyphagia, blurred vision, fatigue, neuropathies, foot
ulcers
Chronic Complications
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Microvascular changes (DB1 = DB2)
 Nephropathy (tx depends on keeping glucose intensively controlled)
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Neuropathy (tx depends on keeping glucose intensively controlled)
 Focal = oculomotor n, median n, radial n, lateral popliteal n
 pain, self-limited, lasts 6-8 wk
 Distal symmetric polyneuropathies (“stocking glove” distribution of
pain/tingling)  Charcot’s joint (feet/hand), sensory ataxia, muscle-wasting
 Proximal motor = DB amyotrophy (men, DB2, pain/weakness of proximal pelvic
muscles)
 Autonomic neuropathies (from insulin resistance  high sugar  nerve
problems)
 CV – resting tachy, diminished variability, prolonged QT interval
 Vascular – postural hypotension
 GI – motility problems, gastroparesis [VERY COMMON]
 Tx = metoclopramide (pro-motility), smaller meals
GU – bladder dysfunction, erectile dysfunction
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Retinopathy
 non-proliferative DM retinopathy – microaneurysyms  hemorrhages
 proliferative DM retinopathy – above plus neovascularizations + vitreous or
preretinal hemorrhages.
 macular edema (DB2)
Macrovascular complications (DB2 > DB1)
 Atherosclerosis
 Coronary heart disease
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Recall underlying pathophysiology of Type 1 DM
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T-cell mediated beta-cell injury  insulin deficiency
Genetics = HLA-DR3/4 (Chr 6), IDDM2 (Chr 11), CTLA4 (Chr 2)
Environment = viruses (mumps, congenital rubella, coxsackievirus), diet, toxins
Autoimmune = Ig against secretory granule islet cell Ag (ICA512), insulin and glutamic acid
decarboxylase dysfunction (GAD 65, 67) from beta-cells
Correctly identify Type 1 DM using the appropriate clinical manifestations
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Associated with other autoimmune diseases (Hashimoto’s, SLE, Grave’s)
List the most appropriate treatment options for patients with both Type 1 and Type 2 DM
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DB 1 = Insulin
DB 2 = Lifestyle and exercise + Metformin (if A1C is > 7%, add insulin)
o Lisinopril (if HTN)
o Asprin (if CVD risk > 10% for 10 y), Clopidogrel if allergic to aspirin and CVD risk > 10%
o Statin therapy (reduce LDL<100)
o ACE-I/ARB (if pt has DB nephropathy)  control BP in DM pts
o Gabapentin, Duloxetine (FDA approved for polyneuropathy treatment)
Correctly identify and list the components of a comprehensive management plan for a
patients with DM
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DB 1 = Insulin, education, diet, screening (same as DM2 below)
DB 2 = lifestyle/exercise (lecture 15)  pharm treatments for DB and risk factors  screening
o Regular screening =
 HbA1C every 3-6 mo <6.5-7%)
 lipid panel (LDL < 100 or < 70 for CAD; HDL > 40; TG < 150)
 dilated eye exam
 foot exam (check DB neuropathy) at EVERY VISIT
 microalbumin urine checks (best for detecting DB nephropathy early)
 BP (<130/80)
 dental check-ups
 immunizations (DB pts are at higher risk for infections)
o Revisit newly dx DB2 pt in 3 months
18 DB Emergency Management
Know the first diagnostic test in the approach to any potential diabetic emergency
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First test  Finger stick blood sugar
o if low = tx with glucose (and glucagon to increase gluconeogenesis)
o if high = tx with fluids first  insulin  acid/base monitoring  electrolyte
monitoring/replacement
Hypoglycemia (DB1 > DB2; insulin-dependent > non-insulin dependent)
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The criteria for diagnosing hypoglycemia (Whipple’s Triad)
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Blood glucose < 50 – 70 mg/dL
Symptoms consistent with diagnosis
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o
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confused, somnolent, appear intoxicated, acute/permanent brain dysfunction
hx of contributing causes (incorrect med dose, missed meals, uncompensated exercise,
stress, infection, etOH)
Symptoms resolve following glucose
Specific findings
o Neuroglycopenic – “brain not working”
 Catecholamine release  anxiety, nervous, irritable, high HR, palpitations,
tremors, shaking, sweating, vomiting (sx masked w/ pts on beta-blockers)
o Sympathomimetic – “ANS not working”
 Lack of glucose for CNS  altered mental status, focal neuro deficits, Seizures,
confusion, lethargy, combative, unresponsive
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The 2 medications most likely to cause hypoglycemia
o Insulin = direct tissue effect  hypoglycemia
o sulfonylureas = increase pancreatic insulin secretion  hypoglycemia
The 3 most common treatments for hypoglycemia
o PO glucose replacement (commercial glucose, avoid orange juice [K+])
o IV Dextrose (D50W 1g/kg, 1 amp [50mL])
o Glucagon = 1mg IM/SC, glycogenolysis (delayed, don’t use this alone)  stimulates
gluconeogenesis
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Additional treatments in management of hypoglycemia
o Octreotide = somatostatin analogue, inhibits insulin release, IV
 Use if the cause is slow-acting drug overdose (adjunct to IV glucose)
o Thiamine = coenzyme in several metabolic reactions
 Use if hypoglycemic alcoholics/malnourished
The indications for admission for patients with hypoglycemia
o Continued/recurrent AMS, recurrent hypoglycemia, large dose of dextrose, concurrent
malnutrition/sepsis, no adult supervision, hypoglycemia secondary to long-acting insulin
or OHA (hypoglycemia will continue > 24 h)
Hyperglycemic Emergencies – DKA & HHS
 Compare/contrast the pathophysiology of these 2 disorders (a disease continuum)
o DB ketoacidosis (DKA)
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insulin deficiency, ketoacidosis, lack of significant hyperosmolarity, usually DB1
 Insulin def. = cells less able to use CHO  more lipolysis
 lipolysis  increase FFA to liver  increase ketogeneisis and decrease
alkali reserve  increase metabolic anion gap metabolic keto acidosis
 Ketone bodies from FFA to liver (betahydroybutyric acid, acetoacetic acid)
o Hyperosomalar Hyperglycemic nonketonic Syndrome (HHS)
 insulin resistance, lack ketoacidosis, usually DB2
 Hyperosmolality (>320)  dehydration (altered mental status)
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Differentiate these two disorders using important historical features
o DKA = onset < 24 h, usually younger, usually DB1, N/V/abdominal pain, fruity odor
o HHS = onset > 24 h, usually older or physiologically impaired, usually DB2, mental status
change
o Both = inadequate/inappropriate insulin therapy or infection (UTI, pneumonia)
 less common = stress, MI, trauma, corticosteroids, new-onset DB, no clear cause
 polyuria, polydipsia, dehydration, weakness, wt loss, tachycardia, hypotension,
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increase RR (DKA>HHS), fever, decrease skin turgor, dry mucous membranes
Name the diagnostic criteria for both DKA and HHS (measure glucose, ABG, urine ketones)
o DKA = high glucose accucheck (>250), anion gap acidosis, serum bicarb <15, pH< 7.35,
(+) urine ketones
o HHS = high glucose accucheck (>600), usually no acidosis (pH > 7.3), serum bicarb > 15,
(-) urine ketones
Utilize common laboratory and/or imaging studies for diagnosis, and predict the
abnormalities expected in regards to sodium, potassium, osmolality & acid-base status
o K + = total is depleted, measured is normal/elevated
 Recall low insulin  less K+ in cells  H+ will leave cell so K+ enter cell
 Measured K+ only measures in ECF  which may be high at 1st
 Caution if measured K+ is low (severe total-body K+ def.)
o Na+ = total is depleted, measured is artificially low (must calculate corrected Na+)
o CBC = Hct and Hb elevated (dehydration), WBC 10-15K in DKA (>25K  infection)
o BMP = high Cr (secondary azotemia), high BUN/Cr (secondary dehydration)
o Osmolality = >300 (significant), >320 (alters conginition)
o Urine ketones = (+) in DKA, less false negatives than serum
Calculate a corrected sodium and anion gap
o Corrected Sodium = for each 100 mg/dL glucose above 100  multiply 1.6 and add to
the measured Na+
o Anion Gap = [Na+] – ([HCO3-] + [Cl-])
 reflects unmeasured anions, normal = 8 mEq/L
 AG > 10-12 mEq/L = anion gap metabolic acidosis
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Name the treatment of these disorders in regards to IV fluids, insulin and potassium
replacement
o Volume repletion = FLUID first priority (IV access, 0.9% NS fluid bolus)
 Actions = rapid accucheck (glucose check), EKG, pulse ox
 Give 1-1.5 L NS w/in 1st hour, then 250-500 mL/h
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o HOLD INSULIN until K+ is replenished (must close anion gap)
 Replenish K+ if < 3.3
o Add D51/2NS once blood gas goal is reached
o Insulin = if K+>3.3 mEq/L, do NOT bolus in kids (bolus in adults controversial)
 Do not pull off of insulin until anion gap remains closed (<12)
o Bicarb = controversial, not used routinely, maybe in adults w/ pH<6.9
Predict the common complications of treatment, including the recognition, diagnosis,
treatment and prevention of these complications
o Complications =
 Most common = hypoglycemia, hypokalemia
 Hypokalemia EKG = ST depression, T-wave flattening, U-wave, QT

prolongation
 Hyperkalemia EKG = tall peaked T-waves, QRS weakening, P-wave
disappears, progress to sine wave appearance
Others = ARDS, cerebral edema (kids)
 Cerebral edema = rare, fatal, osmotically driven movement of free H2O
into CNS
 SX = severe HA, change in behavior, pupil changes, papilledema, high
BP, low HR, seizures, incontinence
 TX = mannitol, order CT, +/- intubation w/ controlled ventilation
19 DBM Complications
Screening for DB
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Symptoms suggesting diabetes: weight loss, hunger, urinary frequency, blurred vision
Age >45 (>30 if patient has other risk factors)
Prior Impaired Glucose Tolerance or Impaired Fasting Glucose or family history of diabetes
Prior gestational diabetes or baby weighing >9 lb
Women with polycystic ovarian syndrome (PCOS)
Obesity (BMI >25 kg/m2), especially adolescents
African, Latino, Asian, or Native American ancestry (also increase rate of complications)
History of vascular disease or hypertension
Neuropathy (complications decrease w/ glycemic control)
 Peripheral neuropathy = axonal neuropathic degeneration from damage to myelin sheath, mostly
sensory, motor defects are mild/late
o
o
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Mononeuropathy = self-limiting radiculopathy in one peripheral nerve (CN III, IV, VI)
Polyneuropathy = most common, “stocking-glove” distribution
 numbness, tingling, burning, paresthesia
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**KNOW THESE DISTRIBUTIONS**
 A. Symmetric diabetic sensorimotor polyneuropathy (most common, bilateral)
 B. Proximal diabetic neuropathy (amyopathy) proximal motor
 C. Asymmetric diabetic mononeuropathy (CN and truncal radiculopathy)
 D. Limb mononeuropathy (entrapment syndromes)
o Treatments for peripheral neuropathy
 Tricyclic antidepressants (Amitriptyline, desipramine and nortriptyline)
 SSRI (Duloxetine) – frequently additive in the management
 Gabapentin (pregabalin) – Has made the biggest difference in morbidity
 Carbamazepine
 Topical agents (Capsaicin cream and lidocaine gels)
Autonomic neuropathies
o Postural hypotension due to the inability to maintain vascular tone;
o Gastroparesis and reflux due to imbalance in PS tone (tx = metoclopramide)
o Encopresis imbalance b/w the sympathetic and parasympathetic innervation of the
rectum and anus;
o Incontinence and urinary retention due to imbalance in the control of the specters and
damage to the sensory nerves in the bladder wall.
o
Impotency due to damage in sensory and motor nerves as well as vascular compromise
is a common complication.
o Cardiac Arrhythmias due to alteration at the SA and AV node as well as autonomic
abnormalities are common.
o Cardiac muscle dysfunction, from ischemia to decreased cardiac output. This may be
due to the combined effects of direct toxicity of hyper-insulinemia and hyperglycemia
on the cardiac muscle and defects produced in endothelial lining of vessels with
advanced arteriosclerosis from altered lipoproteins.
Nephropathy (complications decrease w/ glycemic control)
 Half of all ESRD and new dialysis pts, DB1 > DB2 w/in 20 y
 Microalbuminemia = loss of 30-300 mg in 24 h (proteinuria >300mg/24h)
 Treatment = ACE-I for all pts w/ microalbuminemia unless contraindicated (can do ARBS instead)
Retinopathy
 Annual eye exam to look for: macular degeneration, neovascularization, exudate, hemorrhage
 Common complications = DB cataracts, DB retinopathy, glaucoma, neuropathy of optic nerve
 Non-proliferative DB retinopathy = aneurysm, hard exudate (proteins/lipds), “flame”
hemorrhage
Proliferative DB retinopathy = growth of abnormal blood vessel, neovascularization
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Gastroparesis
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Sx = bloating, early satiety, post prandial N/V
Dx = gastric emptying study (barium swallow  tests motility)
Treatments = metoclopramide (alpha-agonist, best one), erythromycin, gastric pacemaker
Infectious Complications

Keep vaccinations up to date in DB pts because they have impaired cell mediated immunity,
diminished vascular supply, hyperglycemia  Candida and other pathogens
 Others (unusual)
o Rhinocerebral mucormycosis
o Emphysematous cholecystitis
o S. aureus
o Candida (oral thrush or skin rash)
o Malignant otis externa- P. Aerugenosa  treat with fluroquinolone
Foot Care [do a foot exam at EVERY VISIT]
 Test for neuropathic sensory loss in every DB pt at least 2x/y
 Early education and aggressive tx of any lesion or nail abnormality to avoid ulcerative changes,
osteomyelitis, and amputation
o
Nail abnormality = onychomycosis (really yellow toenail)
Skin Changes
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Scarring on lower extremity, axilla, groin (recurrent pyogenic
infections + abscesses)
Xanthomas over eyelids/orbit (elevated cholesterol)
Necrobiosis Lipoidica Diabetorium = shiny yellow irregular shaped
lesion on lower extremity of DB, more common in women
Atrophic lesions = wasting of skin, fat, and muscles (brown)
Fungal infections and onychomycosis of nails are common and hard to
tx