Endocrine Disorders

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Diabetes Mellitus

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•Chronic metabolic disorder characterized by high blood sugar (hyperglycemia = > 126 mg/dl)
•Affects CHO, Fat & Protein Metabolism
• Damages:
 Blood Vessels (Heart Disease, Stroke, HTN, PAD);
 Nerves (neuropathy);
 Kidney (nephropathy);
 Eyes (retinopathy)

•Caused by Insulin Deficiency, Insulin Resistance Or both

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Incidence of DM

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•Affects all age groups
•Affects 18.2 million people in US

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Glycogenesis

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•Liver converts glucose to glycogen
•Glycogen stored in liver and muscle cells

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Glycogenolysis

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•Liver converts glycogen to glucose

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Gluconeogenesis

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•Liver Synthesizes glucose from non-carbohydrate sources:
•Amino acids, lactic acid, glycerol

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Glucose

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Primary energy source, provides 4kcal/gram

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fat metabolism
9kcal/gram

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CHO to triglycerides (via liver) -> fatty acids (via lipase) -> Ketones (via liver) this occurs when large amounts of fatty acids are used for energy source, causes ketoacidosis/ metabolic acidosis

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Protein Metabolism
4kcal/gram

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excess AA converted to FA ketones, or glucose. •Body breaks down proteins and uses the amino acids as a major substrate for GLUCONEOGENESIS

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Kidney Regulation of Glucose

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•Glucose almost totally reabsorbed by renal tubules
•However, when plasma glucose is > 180 mg/dl, glucose spills in urine (glycosuria)

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Brain & NS and Glucose

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•Can only use glucose as energy source
•Only stores enough glucose to last few minutes
•Prolonged & severe hypoglycemia can result in brain death

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Muscle tissue and glucose

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•Uses either glucose or fatty acids
•At rest -> fatty acids
•Exercise -> glucose
•Muscle fibers more permeable to glucose during exercise due to contraction process even in absence of insulin.

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Alpha Cells of Pancreas

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•Secretes Glucagon: ↑ BS
•Glucagon: Regulated by blood sugar level
•↓ BS= ↑ Glucagon = ↑ BS
•Maintains BS between meals & fasting/starvation states
•↑ BS by ↑ hepatic glucose production

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Beta Cells of Pancreas

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•Secretes Insulin= ↓ BS
•Insulin: Regulated by blood sugar level
•↑ BS = ↑ Insulin = ↓ BS
•Insulin receptors on cells of the body recognize insulin and allow glucose to be transported into the cell where glucose is converted to energy

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Action of Insulin

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Promotes glucose uptake by target cells,
Promotes storage of excess glucose in fat cells,
•Increases protein synthesis by increasing transport of amino acids into body cells
•Inhibits protein breakdown

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Glucagon

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↑ BS •Maintains BS between meals & fasting-starvation states
•↑ Hepatic glucose production

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Catecholamines

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•Epinephrine & Norepinephrine (adrenal medulla)
•↑ BS during stress
•Promotes conversion of glycogen to glucose (Glycogenolysis)

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Glucocorticoid

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•Cortisol (adrenal cortex)
•↑ BS during stress
•↑ Hepatic glucose production

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Growth Hormone

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•Secreted by anterior pituitary
•Promotes protein synthesis in all cells, increases fat mobilization and use of fatty acids for energy and decrease use of CHO

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Diabetes Mellitus Type I
(juvenile onset, insulin dependent)

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accounts for 10% of cases, occurs at any age, Genetics and autoimmune responses plays a role,

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S/S DM Type 1

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Sudden onset,Body type  thin, Peak age = 12 (although may occur any age)
,Fatigue / Listlessness, Polyuria, Polydipsia, Polyphagia, Weight Loss, Glucosuria, Ketoacidosis

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Diabetes Mellitus Type II
(adult onset, non-insulin dependent)

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•Accounts for 90% of all cases of diabetes characterized by
•Insulin Resistance
↓ Insulin Secretion
↑ Hepatic Glucose Production

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DM I etiology

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Genetics: associated w/ Human Leukocyte antigen
Hypothetical Environmental Antigen: triggers autoimmune response, autoimmune response: destroys Beta cells

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Etiology of DM II

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Insulin Resistance:
Fewer insulin receptor sites on cell membrane
Insulin receptor abnormality
Abnormality in glucose transporter
-Function only after insulin binds to receptor site

↓ Insulin Secretion: •Hyprinsulinemia leads to beta cell exhaustion
•Beta cells “poop out”

↑ Hepatic Glucoseroduction:• Insulin Deficiency  Cells unable to use glucose as energy source
•Cells starving
•Liver converts glycogen to glucose
•Worsens hyperglycemia

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DM II Risk Factors

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Age >20, obesity (85% obese), Genetics (20-50%.. greater than type 1), Race (Black, Native Americans, Hispanics) Impaired Fasting Glucose (pre diabetes 110-125mg/dl), Gestational Diabetes (hyperglycemia in pregnancy 5-10yrs later), Insulin Resistance Syndrome (Metabolic Syndrome,Syndrome X,Presence of Four atherosclerotic risk factors:
Insulin resistance, Hypertension, Hyperlipidemia, Central obesity)

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MODY (maturity onset diabetes of the young)

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DM II onset age <25yo,
•Often Obese
•Genetic Defect ==> Autosomal Dominant

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S/S DM II

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Asymptomatic,
> 40, Obese, 3 P's: (Polyuria, Polydipsia, Polyphagia), Skin infections, Vaginal Yeast Infections, Cystitis
NO WEIGHT LOSS
NO KETOACIDOSIS

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FPG: Fasting Plasma Glucose

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•Normal; 70-100mg/dl,
•IFG “Pre diabetes”: 110-125 mg/dl,
•DM:> 126 mg/dl - confirmed with 2 FPG

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Random Blood Sugar

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Non fasting test
DM= > 200 mg/dl PLUS the presence of classic sx

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OGTT:
Oral Glucose Tolerance Test

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•Used to detect gestational DM or to detect DM-2 in person who has a normal FPG
DM= > 200 mg/dl after 2 hours

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Hemoglobin AIC

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•Normal = 4-6%
•Goal for DM = <7%
•Determines how well DM is being managed
•Reflects average glucose for the preceding 6-12 week period
•Not affected by food intake, stress or exercise

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DKA: Diabetic Ketoacidosis

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•acute complication in DM-1
•When Does it Occur?
Onset of disease (before dx)
Omit insulin or insufficient dose
Illness or Physical-Emotional Stress ==> ↑ BS 2nd to ↑ Counter Regulatory Hormones

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Diabetes Lab findings

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•↓ pH (< 7.35)
•↑ BS (often 600-700)
•↓ HCO3 (< 15 mE/L)
•Ketones in blood and urine
•Glucose in urine
•Compensate = Kussmaul’s respirations

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HHNC:
Hyperglycemic Hyperosmolar Nonketotic Coma

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Acute complication of DM 2
•Lab Findings
BS > 600 mg/dl
Serum osmolarity > 310 mOs/L
No ketoacidosis

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Hypoglycemia or Insulin Reactions

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Occurs in DM-1 or DM-2
BS = < 50 mg/dl

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S/S Hypoglycemia

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↓ Cerebral Function, Autonomic NS Activity; conscience-> injest sugar, unconscience-> HOSPITALIZE

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Somogyi Phenomenon

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Occurs with DM-1
•Morning hyperglycemia 2nd nocturnal hypoglycemia
•Nocturnal hypoglycemia
Occurs because evening dose of insulin too high
•Morning Hyperglycemia = Compensatory response
↑ counter regulatory hormones
↑ Hepatic glucose production
•Confirm Somogyi effect by measuring BS 2-3 am
•Tx: Decrease evening insulin dose

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Dawn Phenomenon

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•Occurs in DM-1 or DM-2
•Morning hyperglycemia without nocturnal hypoglycemia
•Caused by circadian rhythm secretion of growth hormone
•Tx:Increase PM insulin dose
Switch evening NPH to HS

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Retinopathy

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Chronic complication of DM- microvascular disorder
all DM1, 60% DM 2
damage/ruptured blood vessels in eyes

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Nephropathy

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Chronic complication of DM- microvascular disorder
•DM-1: present after 15 years
•DM-2: present at time of dx
•Affects blood vessels that supply glomeruli
•Leading cause of ESRD
•First sign of diabetic nephropathy is an ↑ urinary albumin excretion (microalbuminuria)
•Microalbuminuria defined as urine protein loss between 30-300 mg/day.

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Neuropathy

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Chronic complication of DM- microvascular disorder
•Endothelial thickening of blood vessels that supply nerve -> nerve ischemia
•Demyelinization of Schwann Cells which slows nerve conduction

Peripheral Neuropathy • Most common
•Affects lower extremities
•Numbness / Tingling
•Loss of Sensation

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Chronic Complications of DM-
Macrovascular Disorders

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•DM-2: present at time of dx
•DM-1: onset depends on age & duration of DM
CAD (agina, MI), CVA(stroke), PAD (pain/intermittent claudication)

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Thyroid

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•Small gland located in front of neck just below “adam’s apple”
•Consists of two lateral lobes connected by an isthmus
•Covered by sternomastoid muscle
•Usually NOT palpable

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Thyroid function

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•Takes iodine and converts it to thyroid hormones - T3 & T4
•Iodine Necessary for synthesis of thyroid hormones

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Follicular Cells

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•Functional unit of thyroid gland;
•Tiny sac-like structures that absorb iodine;
•Combine iodine and tyrosine (amino acid) to make T3 and T4.
•Have approximately 2-3 months supply of thyroid hormone stored in gland

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Hypothyroid

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•Insufficient thyroid hormone
•↓ BMR
•Slows down all body activity
•Classification
Congenital
Acquired

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Congenital Hypothyroid

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•Affects approx 1 of 4000 births
•Caused by
-Absent thyroid gland
-Inadequate hormone production
- Deficient TSH
•Cretinism=manifestations of untx congenital hypothyroidism
-Growth retardation
-Mental retardation
Tx: Hormone replacement

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Acquired Hypothyroid

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Primary Hypothyroid = Thyroid Gland Dysfunction
Secondary Hypothyroid = Hypothalmic or Pituitary Dysfunction (less common)

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Causes of Hypothyroidism

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•Hashimoto’s Thyroiditis (most common)
•Surgical-induced hypothyroidism
• Radiation-induced hypothyroidism

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Hashimoto's Thyroiditis

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•Most common
•Primarily affects women (5:1 ratio)
•Autoimmune disorder  form autoantibodies which react with thyroid antigens  destroys gland
•May produce transient hyperthyroid state = leakage of preformed thyroid hormone from damaged cells

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Surgical Induced Hypothyroid

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•Thyroidectomy
•Complete or partial removal of thyroid gland

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Radioactive Iodine (RAI)

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• Used to tx hyperthyroid
• Thyroid gland concentrates RAI
•Destroys gland  become hypothyroid

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S/S Hypothyroidism

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Sx Vary ==> May be subtle or overt
Gradual onset, weekness and fatigue, skin dry and course
Hair course and brittle, Accumulation of hydrophilic mucopolysaccharide substance, Puffy appearance especially around eyes, Bradycardia, Decreased RR, Decreased appetite, Menorrhagia, Easy fatigueabiity, Physically/mentally sluggish, Severely hypothyroid, unable to metabolizes sedatives, analgesics and anesthetic drugs, ↓ T3, T4, ↑ TSH, ↑ Cholesterol

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Hyperthyroidism

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•Excess thyroid hormones
•↑ BMR
•Accelerates all body activity

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Primary Hyperthyroid

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Thyroid gland dysfunction

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Secondary Hyperthyroid

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Hypothalamus or Pituitary Dysfunction

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Hyperthyroid Causes

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•Graves’ Disease (most common cause)
other causes not discussed

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Grave's Disease

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•Autoimmune Disorder
Abnormal stimulation of thyroid gland by thyroid stimulating immunoglobulins (TSI)
TSI Bind to TSH receptors on thyroid gland
Competes with TSH
↑ T3,T4
•Affects mostly women (7:1 ratio)
•Onset usually 20-40’s
•Familial Tendency / Genetics
15-20% of pts have close relative with the disorder

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S/S Grave's Disease

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Presentation may be subtle or dramatic ==> Depends on hormone level, Onset: Insidious, heat intolerance, smooth velvety skin, thin fine silky hair, breakable nails, Graves Dermopathy (Rare occurs after many years), Exophthalmos (occurs in 1/3 pts), Goiter (2-3x normal size), Increased CO, Tachycardia, Angina, SOB with exertion, increased appetite, Amenorrhea, muscle protein breakdown= used as fuel, Restless, anxious, nervous, insomnia, difficulty concentrating, Increased sensitivity to catecholamines (epi/norepi)
• ↑ T3, T4
• ↓ TSH
• ↓ Cholesterol

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Adrenal Glands

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located on the top of each kidney; Composed of : Adrenal Medulla & Adrenal Cortex

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Chatecolamines

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Epi and Norepi. Hormones of Adrenal Medulla.
•Increase BP, HR, Respirations
•Increases peripheral vasoconstriction
•Increases sweating

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Glucocorticoid

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Hormone of Adrenal Cortex
•Cortisol (Hydrocortisone) = major Glucocorticoid
•Protects against stress
•Raises Blood Sugar
•Depletes Tissue Protein
•Mobilizes Fatty Acids for Energy (instead of glucose)

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Aldosterone

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Hormone of Adrenal Cortex:
•Regulates Na+, K+, & Water levels

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Sex Hormone

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•Adrenal cortex produces small amounts of sex hormone in both males and females

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Cushing's Syndrome

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•↑ Glucocorticoid / Cortisol
•Syndrome refers to a constellation of clinical features of ↑ cortisol from any cause
•4 x more common in women than men
•Onset = 30-50 YO

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Causes of Cushing's Syndrome

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Pituitary Tumor -> Increased ACTH
Adrenal Tumor -> Increased Cortisol
Lung Cancer -> Increased ACTH
Long term prednisone therapy -> Suppresses ACTH

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S/S of Cushing's Syndrome

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Wide range of emotions, Moon face (full/round), Overt DM develops in approx 20% of pts, Muscle Wasting esp. in extremities, Decreased humoral and cell mediated immunity, Mask infection/inflammation, (Increased Androgen) Acne, Facial hair (hirsutism), Osteoporosis, (loss of collagen) Produces thin/weak integumentary tissue, Peptic ulcers, Increased Na/water retention -> Hypertension, edema, Increased ACTH -> melenocyte stimulating activity

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Primary Adrenal Insufficiency

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•↓ Cortisol,↓ Aldosterone, ↑ ACTH
•Relatively rare
•5 cases / 100,000 persons
•Female:Male = 2:1 ratio
Autoimmunity:
(•Destruction of adrenal gland
•Makes up about 80% of Cases)
Other:
•Metastatic destruction of adrenal gland
•Tuberculosis - common in countries where TB is prevalent
•Adrenal hemorrhage (anticoagulants/trauma)
•Adrenal infarction (thrombosis)

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S/S Primary Adrenal Insufficiency

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Gradual onset, Sx appear when 90% of gland destroyed, (↓ Cortisol) Hypoglycemia
Poor tolerance to stress, infection, trauma, (↓ Aldosterone):• Excrete Na/Water; Retain K+, Hypovolemia, Hyponatremia, Hyperkalemia, Hypotension, Weight loss
↑ ACTH: Melenocyte stimulating activity
↓ Androgen: Females = sparse axillary/pubic hair