ENDOCRINOLOGY  Binding at tissues

 Excretion by the liver into bile

Anabolism
 Ana = upward; Ballein = throw
 Metabolic pathways that construct molecules
from smaller units, requiring energy
Catabolism
 Cata = downward; Ballein = throw
 Metabolic pathways that breakdown
molecules to smaller units, producing energy
 Excretion by the kidneys into urine
 Number and Sensitivity of Receptors
 Number of receptors do not remain constant
 Receptors are often inactivate, destroyed,
reactivated or manufactured by the cell
 UP-REGULATION
 DOWN-REGULATION

Structure & Synthesis of Hormones MSK Symptoms of Endocrine Pathology

 Undiagnosed endocrine problems can present
PROTEINS & POLYPEPTIDES as MSK problems
 From: Ant & Post Pituitary Gl.; Pancreas;
Parathyroid Gl.  Hormone fluctuations can increase MSK
problems
STEROIDS
 From Adrenal Cortex; Ovaries & Testes; Placenta  RA may indicate underlying endocrine disease
(ie DM)
DERIVATIVES OF AMINO ACID TYROSINE
 From Thyroid & Adrenal Medullae Persistent Proximal Muscle Weakness, Atrophy,
Myalgia, Fatigue
 Steroid hormones are usually synthesized from
Cholesterols and not stored ? Early problems with:
 Thyroid
 Thyroid hormones (amine hormones from  PTH
tyrosine) are synthesized and stored in the Thyroid  Acromegaly
Gl.  stored into protein Thyroglobulin  DM
 Cushing’s
Epinephrine is secreted 4x > Norepinephrine in the  Osteomalacia
Adrenal Medulla

Feedback Mechanisms

Negative Feedback  degree of activity of the target Bilat. CTS

tissue feeds back signals to gland to adjust hormone
production ? Early problems:
 Acromegaly
Positive Feedback  biological action of hormone  Myxedema
causes additional secretion of hormone  DM
 Cyclical Variations  Hypothyroidism
 Periodic variations in hormone release are  Pregnancy
influenced by:  Vit B6 Deficiency
 Seasonal Variations (PTH & Vitamin D)
 Stages of development and Aging (GH) Spondyloarthropathies & Osteoarthritis
 Diurnal Cycle (GH and Sleep)
? Early problems with:
 Hemocromatosis (aka Bronze Diabetes/Fe
storage Dse)
Transport and Clearance
Others related to Endoc Pathology:
Transport
 Water Soluble Hormones  Periarthritis

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Peptides and Catecholamines diffuse out of  Shoulder Calcific Tendinitis

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capillaries, into interstitium and into target cells  Calcific Tendinitis

 Chondrocalcinosis
 Steroid & Thyroid Hormones  Gout
o Circulate in the blood bound to plasma CHONs.  FMS
 Hand Stiffness – in DM
 Large amounts of CHON bound hormones act as  Flexor Tenosynovitis – in hypothyroids
reservoir, ready to replenish decreased free
hormones in the circulation.
 Lack of progress in PT may indicate systemic
Clearance of Hormones problems > MSK issues = refer to MD
 Metabolic destruction at tissues
 Note for signs of electrolyte imbalances with  Enhances amino acid transport through cell
diuretic use membrane
 Decreased catabolism of CHONs and Amino
THE HYPOTHALAMUS Acids
 Controls release of Pituitary Hormones:
 Corticotrophin-releasing Hormone  Increases Fat utilization for energy
 Thyrotropin-realeasing Hormone  Increasing fatty acid concentration in the body
 Growth Hormone-releasing Hormone fluids
 Somatostatin  Fats are preferentially used for energy more
than carbs and CHONs
 Ketogenic effect
THE PITUITARY GLAND
 aka Hypophysis  Decreases Carbohydrate utilization

 Rests on the Sella Tursica, under the  Decreased glucose uptake in tissues (muscles
Hypothalamus; connected above via the Pituitary and fats)
(Hypophysial) Stalk  Increased glucose production by the liver
 Increased insulin secretion
2 Physiological Parts:
 Neurohypophysis o Hormone-induced Insulin Resistance
 Adenohypophysis  GH is diabetogenic
 Effects of GH induced DM is the same as in Type
ANTERIOR PITUITARY HORMONES: II DM (NIDDM)
 Follicle Stimulating Hormone
 Adrenocorticotropic Hormone  GH Stimulates Cartilage and Bone Growth
 Thyroid-Stimulating Hormone (Thyrotropin)
 Growth Hormone  Most obvious effect of GH stimulation is growth
 Luteinizing Hormone of skeletal frame
 Prolactin
 Epiphyseal cartilage progressively gets used up
POSTERIOR PITUITARY HORMONES with age—by late adolescence, no further long bone
 Anti-Diuretic Hormone (Vasopressin) growth is possible
 Oxytocin
 Osteoblasts however, gets stimulated by GH and
cause bones to become thicker
 Secretion by the Anterior Pituitary is controlled
by hormones via the Hypothalamic-Hypophyseal REGULATION OF GROWTH HORMONE:
Portal Vessels:  After adolescence GH secretion decreases
slowly and falls to 25% from previous in very old age
 Hypothalamic Releasing Hormones
 Hypothalamic Inhibitory Hormones (or Factors)  Normal GH concentration in the plasma
(Guyton)
 Posterior Pituitary Hormones arise from cell  Adult = 1.6 -3 ng/ml
bodies in the Hypothalamus:  Child/Adolescent = 6 ng/ml
 Magnocellular Neurons in the Supraoptic and  Prolonged starvation = 50 ng/ml
Paraventricular Nuclei
 Acute hypoglycemia is a potent GH stimulator
 Secretion from the Posterior Pituitary is than acute proteinemia
controlled by nerve signals from the Hypothalamus
 There is evidence to show that GH is high in
Growth Hormone (GH) children with Kwashiorkor. GH only returned to
 Apart from the Growth Hormone, all the major normal upon correction of CHON deficiency.
Ant Pituitary hormones are specific to certain target
tissues

 GH affects all if not most of the tissues in the

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body through Somatomedins.

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 GH is also known as Somatotropin

 GH promotes increased size of cells, increased Possible anti-aging effects of GH with multiple tests
mitotic cell activities showing:
 Increased CHON deposition in muscles (anti-
 Soft tissues grow with GH wrinkles)
 Bones lengthen with GH stimulation.  Decreased fat deposits (!)
 Feeling of increased energy

 GH continue to stimulate osteoblasts.

 Metabolic Effects of GH: ABNORMALITIES OF GROWTH HORMONE
 Promotes Protein deposition in tissues SECRETION:
PANHYPOPITUITARISM
 Decreased Ant Pituitary secretion Hyperpituitarism Post-Op
 Congenital or may occur suddenly or slowly in  Ambulation and Exercise in first 24 hrs
life (results from pituitary tumors)
 Coughing, sneezing and blowing nose =
DWARFISM contraindicated
 Generalized deficiency of Ant Pituitary secretion
(panhypopit.) in childhood  Deep Breathing encouraged
 All physical parts of body develop normally but
in decreased rates  Increased ICP may be due to intracranial bleeds
 Panhypo. dwarves do not pass through normal or edema
puberty, apart from a third (whose GH is the only
deficiency) Watch for signs of increased ICP:
 Rx: hGH (from E.Coli)  Altered LOC
 Visual Acuity changes
PANHYPOPITUITARISM OF ADULTHOOD  Low PR
Results from:  Rising BP
 Craniopharyngiomas,
 Chromophobe Tumors –both impinges on Watch for signs of Meningism:
Pituitary Gland;  Severe H/A
 or Pituitary Thrombosis – seen in mothers  Irritability
developing circulatory shock after child birth  Nuchal Regidity

Effects of Adult Panhypopituitarism:  Monitor blood glucose before and after exercise
 Hypothyroidism
 Depressed prod. of glucocorticoids in the  Visual Field changes
adrenals
 Suppressed gonadotropic hormones Be aware of ortho changes that will not resolve
 OA of extremities or spine
 Results to a lethargic, fat, asexual being  Increased IV Disk
 Rx: Adrenocortical and Thyroid Hormone  Large osteophytes along ALL

Hypopituitarism PT Implications Anti-Diuretic Hormone (ADH or Vasopressin)

 Minute quantities cause decreased water
Observe for: excretion by the Kidneys: Anti-diuresis
 Weakness
 Fatigue  Loss of ADH cause the collecting tubules and
 Lethargy, Apathy ducts of the kidneys to be impermeable to water
 Orthostatic Hypotension  High concentrations of ADH have potent
 Impaired peripheral vision: Bilat Hemianopia vasoconstricting effects throughout the body =
 Nail Bed and Skin changes -- Anemic increased BP

GIGANTISM Stimulus for ADH Secretion :

 Often from Acidophilic Pituitary Tumors
 GH is produced so much
 Occurring before adolescence = Giant (9 ft)
 If untreated, can lead to Panhypopituitarism as
gland eventually fails
 Hyperglycemia leading to DM
 Decreased Blood Volume (decreased by 15-25%,
increased ADH by 50%)
 Circulatory Shock or Severe Hemorrhage
 Related to Atrial Filling and Atrial Stretch
Receptors and Baroreceptors in Carotids, Aorta and
Pulmonary Veins

ABNORMALITIES OF ADH SECRETION:

ACROMEGALY
 Acidophilic tumor after adolescence DIABETES INSIPIDUS
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 Bones become thicker, soft tissues continue to

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grow  imbalance of Water due to ADH deficiency

 Large hands and feet; large membranous bones  Produce large amounts of excreted dilute urine
(forehead, jaw, vertebrae)  Polydipsia, Nocturia & Dehydration
 Hunched Back (Kyphosis)  Possible dehydration
 Tongue, liver, Kidney enlarge (soft tissues)
PT Implication:
 Acromegaly-induced Myopathy – weakness with  With ADH treatment, observe for signs of HTN,
reduced exercise tolerance Diarrhea and Angina/MI
 Observe for signs of water intoxication (edema,
 Anyone with DM with increased CK levels must seizures)
be evaluated for Acromegaly
SYNDROME OF INAPPROPRIATE ANTIDIURETIC
HORMONE
 Excessive release of ADH, can be triggered by
the stress of surgery or systemic disorders
 Lead to severe Hyponatremia (<115 mEq/L)
 Lethargy, nausea, anorexia and weakness
 Mild Hyponatremia (125 – 130 mEq/L)
 Thirst, muscle cramps and lethargy
 Rapid SIADH = coma, convulsions, death
 Water intoxication due to fluid retention
 Edema only when overload exceeds 4L
Neuromuscular S/Sx:
 Brain swelling
 Altered levels of consciousness
 Seizures
 Coma (≤120 mEq/L)
PT Implications:
 Advice not to use NSAIDs or Aspirin without
medical advice
 Monitor fluid balance
 Record changes in mental, motor and energy
status
THE THYROID GLAND
 Located immediately below the Larynx and each
side and in front of the Trachea
Secretes
 Thyroxine (T4)
 Triiodothyronine (T3)
 Calcitonin
 Both T3 & T4 hormones increase the metabolic
rate of the body
 Stimulated by the Thyroid Stimulating Hormone
from the Ant. Pituitary
 Synthesis and Secretion of Thyroid Hormones:
 93% -- Thyroxine; 7% Triiodothyronine
 Almost all of T4 is later converted to T3
 T3 is 4x more potent than Thyroxine but has a
short half-life in body fluids
 T4 and T3 has the same functions
Physiologic anatomy of Thyroid Gland:

4
Gland is composed of large numbers of closed
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Follicles filled Colloid filled with cuboidal epithelial
cells
 Major constituent of colloid is Thyroglobulin,
which contain thyroid hormones in its molecule
 Thyroid gland has a blood flow 5x the weight of
the gland each minute
 Iodine is needed to form Thyroxine
 Iodide Pump (Iodide Trapping)
 Basal membrane of Thyroid Cells have the
ability to pump iodide actively into the cell (trapping)
 Rate of Trapping is influenced by TSH
 The Iodide Ions need to be oxidized to form
Iodine. This is promoted by Peroxidase
 Without Peroxidase, as in cases of blockage or
hereditary absence, Thyroid formation falls to zero
Thyroid Hormones (TH)
 After synthesis of Thyroid Hormones, each
Thyroglobulin molecule would contain 30 Thyroxine
molecules and a few Triiodothyronine.
 T3 and T4 are then stored in Follicle for 2 to 3
months. Hence, physiologic deficiencies are not seen
for several months.
 Thyroxine and Triiodothyronine are bound to
plasma proteins. They combine mainly with
Thyroxine-binding Globulin and much less with
Thyroxine-Binding Prealbumin and Albumin
 T3 and T4 are released slowly to the tissue cells
 Thyroid Hormones have slow onset and long
duration of action
Physiologic Functions of Thyroid Hormones:
 General effect is to activate nuclear
transcription of large numbers of genes—net result is
generalized increase in functional activity throughout
the body
 Metabolic Rate can increase 60-100% above
normal with TH
 Utilization if food for energy is accelerated
(CHON synthesis and catabolism is increased)
 Growth Rate for the young is increased
 Other endocrine gland activities are also
increased
 Increase Active Transport of Ions through cell
membranes—Na+-K+-ATPase
TH effects on growth:
 With Hypothyroid, growth is retarded
 Hyperthyroid, increased skeletal growth occurs
but the epiphysis close early so the eventual height
as an adult would be short
 If fetus does not secrete enough TH, growth and
dev’t of the brain before and after birth will be
retarded.
 Specific TH effects on Bodily Mechanisms:
 Stimulation of Carbohydrate Metabolism
 Increase: uptake of glucose by cells, Glycolysis,
Gluconeogenesis, GIT absorption, Insulin secretion
 Stimulation of Fat Metabolism
 All aspects of fat metabolism is enhanced.
 Lipids are mobilized more rapidly than fat
tissue.
 Increased TH = decreased cholesterol,
phospholipids and triglycerides in plasma; Increased
free fatty acids
 Decreased TH = increased plasma cholesterol,
phospholipids and triglycerides, fat deposition in
liver; severe atherosclerosis
 Increased Requirements for Vitamins
 Increased Basal Metabolic Rate
 Decreased Body Weight
 Increased Blood Flow and Cardiac Output
 Rapid utilization of oxygen than normal to
release metabolic end products in the tissues
 Vasodilation ensues to increase blood flow to
skin to dissipate heat
 CO increase by 60% or more (50% below normal
in hypothyroidism)
 Increase in Heart Rate
 Increases more than CO
 TH seem to have a more direct effect on heart
excitability
 Increased Heart Strength of Contraction
 Due to increased TH effect on enzymatic activity
 Analogous to increased strength of heart in
fevers and exercise
 With TH marked increase, strength of
contraction is depressed (Cardiac decompensation
due myocardial failure in Thyrotoxic pts)
 Normal Mean Arterial Pressure
 Increased Respiration
 Increased metabolism = utilization of O2 =
formation of CO2
 Increased GI Motility
 Increased food intake, increased digestive juices
and GI motility.
 HyperTH = diarrhea; HypoTH = constipation
 Excitatory effect on CNS
 Increased rapidity of thought processes
 Extreme nervousness in HyperTH, with
psychoneuroses
5
Effect on Muscle Function
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 Slight increase in TH increase muscle vigor
 Marked increase in TH = muscle weakening (due
to CHON catabolism)
 HypoTH = muscle become sluggish and relaxes
slowly after contraction
Muscle Tremor: characteristic Fine Tremors (10-
15x/second); due to increased reactivity of neuronal
synapses
Effect on Sleep
 HyperTH constantly feels tired (due to CNS and
Muscle effects) but finds it difficult to sleep
 HypoTH = extreme somnolence (12-14 hrs/day)
 Effect on other Endocrine Glands
 Increased secretion of hormones but also
increased tissue needs for hormones
Effect on sexual functions
 HypoTH = men and women lose libido
 HyperTH males often become impotent
 HypoTH women = menorrhagia and
polymenorrhea or amenorrhea
 HyperTH women = oligomenorrhea to
amenorrhea
 Thyroid Stimulating Hormone (Thyrotropin)
increases TH secretion
 TSH is regulated by Thyrotropin-Releasing
Hormone form Hypothalamus (TRH)
 Cold temperature stimulates TRH, then TSH and
so stimulate TH
 Emotional stresses, excitement and anxiety has
inverse effects on TRH, TSH and TH
Anti-Thyroid Substances
THIOCYANATE
 Same active pump for Iodide ions used by
thyroid cells can also pump Thiocyanate, which cause
competitive inhibition
 Decreased Iodide in the glandular cells still
continues formation of Thyroglobulin
 TSH senses non-formation of TH and therefore
stimulates the gland further.
 Thyroid gland overgrows under TSH stimulation
but remains incapable of TH production  GOITER
PROPYLTHIOURACIL
 And similar compounds line METHIMAZOLE and
CARBIMAZOLE block Peroxidase enzymes needed for
TH formation
 Side-effects: RA-like arthritis and
Agranulocytosis
HIGH CONCENRATION OF INORGANIC IODIDES
 Cause shrinking of Thyroid Gland and decrease
in its blood supply
DISEASES OF THE THYROID
HYPERTHYROIDISM
 Toxic Goiter, Thyrotoxicosis, Graves’ Dse
 TSH is normal or even zero in the plasma
 T3 Toxicosis; T4 normal
 Thyroid Stimulating Immunoglobulins are often
found in the blood Post-Op Care: observe for signs of
 TSI suppresses TSH Hypoparathyroidism (muscle twitch, tetany,
numbness, tingling around mouth, fingertips or toes)
 An autoimmune reaction to thyroid tissue
Thyroid Storm If on Radioactive Therapy: saliva is radioactive for 24
 Potentially fatal condition due to acute thyroid hrs in Iodine-131 therapy – precautions in coughing
overactivity with: or expectorating patients
 High fever
 Severe Tachycardia
 Delirium Exercise in Hyperthyroidism:
 Dehydration
 Extreme irritability  Exercise Intolerance
 Agitation  Increased HR during exercise, increased muscle
 Stress-induced (surgery, infection, toxemia in blood flow in submax exercise
pregnancy, DKA, MI, PE, drugs overdose)
 Thyrotoxicosis can aggravate pre-existing heart
disease (AF, CHF, worse angina, MI)
Grave’s Disease
 due to Thyroid Stimulating Immunoglobulins  Use RPE instead to monitor response

 TSIs stimulate gland growth and hormone

overproduction HYPOTHYROIDISM
 Likely also due to autoimmune processes
Classic S/Sx:  Gland does not respond to increasing TSH from
 Symmetric but mild goiter Pituitary
 Exophthalmos
 Nervousness  Thyroiditis
 Heat intolerance  Endemic Colloid Goiter
 Weight loss, increased appetite  Idiopathic Nontoxic Colloid Goiter
 Sweating
 Easy breaking hair Type I / Primary Hypothyroidism
 Reduced functional gland mass or impaired
 Diarrhea hormone synthesis
 Tremors
 Palpitations Type II / Secondary Hypothyroidism
 AFs – CHF – inrease CAD/MI  Inadequate stimulation of gland due to pituitary
 Atypical signs in elderly: apathetic but more CV or hypothalamic disease
changes
 Periodic paralysis at rest (Asians)

PT Implications in Hyperthyroidism:

 MD referral if neck inspection reveals: Hypothyroid Symptoms:

 Unusual swelling +/- pain
 Hoarseness  Fatigue and extreme somnolence
 dysphagia  Muscular sluggishness
 Slowed HR
 Overdosage of thyroid hormone replacement:  Decreased CO
nervousness and palpitations; fever, rash, arthralgias  Decreased Blood Volume
 Increased body wt
 Achlorhydia
 Anemia
 Constipation
 Mental Sluggishness
 Trophic changes: depressed hair growth,
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scaliness of skin, frog-like husky voice

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 Myxedema
PT Implications in Hyperthyroidism:  Atherosclerosis
 Dry, sparse, hair
 Monitor VS in the involved older adult  Thick, brittle nails
 >100 bpm = check BP, PR, rhythm more
frequently Common Meds:
 Position dyspneic in High-Fowler’s  Levothroid
 Synthroid
 Avoid heat intolerance in Grave’s Disease (no  Levoxyl
aquatx if temp is not monitored)  Euthyrox
Side-effects:  Acute Granulomatous
 AF  Lymphocytic/ Chronic/Hashimoto’s
 Osteoporosis

PT Implications: Hashimoto’s Thyroiditis

 In Myxedema: observe for viscous non-
inflammatory joint effusion that may have
Chondrocalcinosis
 Myofascial Trigger points that do not respond to
PT
 Associated with FMS
 Prone to skin tears and breakdown (ulcers)
PT Implications:
On starting Thyroid replacement:
 Risk of CV disease is increased
 Observe for chest pain and tachycardia
 Observe for signs of hyperthyroidism
Hypothyroidism & Exercise:
 Chronic, affects women more
 Autoimmune basis; genetic predisposition (HLA
DR6)
 Destroys thyroid gland by lymphocytes and
antibodies = Goiter
 Decreased T3 and T4
 stimulates Pituitary TSH
CRETINISM
 Extreme hypothyroidism during fetal life or
childhood
 Congenital Cretinism
 Endemic Cretinism
 Neonate may appear normal due to TH being
supplied by mother in utero, but in a few weeks
sluggishness of mvt and retardation of physical and
mental growth are apparent
 Skeletal growth is more inhibited than soft
tissue growth = disproportionate appearance
 Occasionally the tongue becomes too large that
is induces guttural breathing if not choking

 Increased exercise tolerance once thyroid

therapy initiated The Parathyroids, Calcium, Phosphates & Vitamin D
 ECF Ca normal concentration = 9.4 mg/dL (2.4
 Decreased CO, PVR and ECG changes mmol per L)

Ca is key in:
 Observe for Exercise-Induced Myopathy in  Contraction of skeletal, cardiac and smooth
undiagnosed (may lead to Rhabdomyolysis) = report muscles
to MD  Blood clotting
 Nerve impulses
Goiter
 Enlargement of gland due to lack of iodine,  Nerves are very sensitive to changes in Ca
inflammation or tumors Hypercalcemia = depressed nervous functions

 In hyperthyroidism = Grave’s Disease  Hypocalcemia = Nerve hyperexcitability

 Increased TSH stimulates growth of gland even  Hypocalcemia causes Nervous System
without iodine to complete s Excitability and Tetany

 TSH produces colloid thyroglobulin = Colloid  ECF Ca falls below normal  increased neuronal
Goiter membrane permeability to Na = easy initiation of
Action Potential
 Can ensue dysphagia, hoarseness or
compression of URT  Plasma Ca <50%, peripheral nerves become
very excitable they cause Tetanic Muscle Contraction
 Carpopedal Spasm (tetany in the hand)
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 Tetany occurs in plasma Ca = 6 mg/dL (35%)

 Lethal = 4 mg/dL
 Can cause brain seizures

 Hypercalcemia depresses nerve functions and

Thyroiditis muscle activity
 Inflammation of thyroid gland producing hypo  CNS reflexes become sluggish
or hyperTH  Decreased QT Interval of the Heart
 Lack of appetite and constipation (decreased GI
Types: motility)
 Acute Suppurative
 Plasma Ca >12mg/dL (marked at 15mg/dL)
 17 mg/dL = Calcium Phosphate crystal  Vitamin D in small quantities promote bone
deposition calcification

ABSORPTION AND EXCRETION OF Ca & PO4

 Usual intake of Ca and PO4 is 1000mg/day,
equal to 1L of milk

 Ca ions are normally poorly absorbed in the

intestines. PO4 is easily absorbed in the intestines.

 Vitamin D promotes Ca intestinal absorption

 So 35% (350mg) of Ca is absorbed
 250mg is degraded by GI juices
 Remaining Ca is excreted as feces and urine Parathyroid Hormone (PTH)
 Produced by the Chief Cells of the Parathyroids
BONE, ECF & PO4 (4 bodies located behind the Thyroid Gland)
 Organic Matrix of bone of composed of Ca Salts
Effects of PTH on Ca & PO4
 90-95% of Organic Matrix is Collagen Fibers
 Absorbs Ca and PO4 from bones, increasing
 Bone Salts: Ca and PO4 crystalline salts; major their concentrations in the ECF
crystalline salt is Hydroxyappatite
 Decrease excretion of Ca in kidneys
 Compact Bone is 30% matrix and 70% salts by
weight  Increase PO4 excretion in the Kidneys

 PTH enhances intestinal Ca and PO4 absorption,

PATHOLOGIES OF PTH, VIT.D, & BONES

 Hydroxyapatite does not normally form in the
ECF even in Hypercalcemia and Hyperphosphatemia HYPOPARATHYROIDISM
 due to inhibitors: Pyrophosphates  Insufficient PTH secretion
 Abnormally: Arteriosclerosis
 Osteoclasts are inactive
Calcium Exchange Between Bone and ECF
 Deposition and Absorption of Bone—normally  ECF Ca is depressed  Ca in bones keep bones
in equilibrium strong
 Osteoblasts  Bone deposition cells found on  nerves are hyperexcited (Trousseau &
outer surfaces of bones Chvostek’s Signs of CN VII)
 Osteoclasts = Bone absorbers

Vitamin D  In extremely low plasma Ca levels (6 mg/dL)—

 Has potent effect to increase Calcium muscles are prone to tetany
absorption
 High serum phosphate
 Must first be converted to an active product
1,25-dihydrocholecalciferol (1,25 (OH)2D3) Rx:
 PTH / Vitamin D and Ca
 Cholecalciferol (Vitamin D3) is formed in the  Pseudohypoparathyroidism -- hypocalcemia
skin resistant to PTH; short metacarpals and metatarsals
 Cholecalciferol is converted to 25-
Hydroxycholecalciferol in the Liver
 1,25 (OH)2D3 is formed in the Kidneys PT Implications in Hypoparathyroidism:
 Parathyroid Hormone is required to form 1,25  Monitor for muscle twitching or signs of
(OH)2D3 Laryngospasm (Acute Tetany)
8

 1,25 (OH)2D3 is inversely related to Ca in  Chronic Tetany – less severe, unilateral; gait and
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plasma balance problems

 (as Ca affects PTH, its increase inhibits PTH)
 Vitamin D promotes PO4 absorption
 Large Vitamin D quantities results to bone
absorption
 it is related to PTH secretion, and hence bone
absorption
 In it’s absence, PTH is reduced
 Falls Prevention
 Hyperventilation may increase Tetany –
encourage deep breathing during exercise
 Monitor cardiovascular status (arrhythmias,
digitalis toxicity)
 Diet high in Calcium and low in Phosphorus
PRIMARY HYPERPARATHYROIDISM
 Excessive PTH due to Gland abnormality with
Hypercalcemia often due to adenomas
 Common in women more than men or peds
 Thiazide Diuretics and Lithium Carbonate
exacerbates hyper PTH
 Extreme Osteoclastic activity
 Elevated Ca in ECF; PO4 excreted in kidneys
 Often predisposes one to bone fractures
 XRay: Decalcified; Large punched-out cystic
areas of giant-cell Osteoclasts (Osteitis Fibrosa
Cystica)
 Raised Alkaline Phosphatase in the plasma
Osteoblasts still attempt bone formation
but fails. They however secrete large
amounts Alkaline Phosphatase that is a
diagnostic sign of Hyperparathyroidism
 Depressed CNS, PNS due to Hypercalcemia
 Weak muscles
 Constipation
 Abdo pain, peptic Ulcers
 Depressed diastole of heart
 Risk of Parathyroid Poisoning due to elevated Ca
and PO4 levels in blood (>17mg/dL of Ca)
 Kidney Stones formation
SECONDARY HYPERPARATHYROIDISM
 Occurs to compensate for Hypocalcemia and
not due to gland problems
 Vitamin D deficiency or Chronic Renal Disease
are common causes
TERTIARY HYPERPARATHYROIDISM
 In dialysis patients with long-standing secondary
hyperPTH
 Hyperplasic Parathyroid and unresponsive to
Serum Ca Levels
Rickets
 Vitamin D deficiency causes Ca and PO4
deficiency in children
 Occurs in early spring (as summer vit D is used
in winter)
 PTH secretion due to Vit D deficiency further
weakens bones
 Tetany due to depletion of calcium stores in
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bone and blood (<7 mg/dL)
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Osteomalacia (Adult Rickets)
 due to deficiency in Vit D and Ca not from poor
diet but due to failure to absorb fat (Steatorrhea)
 Vit D is fat-soluble
 May also be due to Renal Disease (Renal
Rickets)—failure in conversion of Vit D to active form
 Congenital Hypophosphatemia (Vitamin D
Resistant Rickets) – due to poor PO4 reabsorption
Osteoporosis
 Most common bone disease in adults
 Decreased bone matrix
 Results from diminished organic bone matrix
and not poor calcification
 Less than normal Osteoblastic activity
 In hyperparathyroidism osteoporosis, there is
increased osteoclastic activity
Causes:
 Lack of physical bone stress (Inactivity)
 Malnutrition
 Lack of Vitamin C (needed in osteoid formation)
 Estrogen lack (estrogen decrease osteoclastic
activity)
 Old Age
 Cushing’s Syndrome(decreased CHON
deposition, increased CHON catabolism)
PT Implications in Hyperparathyroidism:
 Chronic LBP
 Easy fractures
 Marked weakness and atrophy of LE
 Osteogenic Synovitis
 Erosion of tendons: Achilles, Triceps, Obturator
Tendons
 Chest PT in acute care
 Monitor if on Digitalis
 Caution with handling Osteopenics
 Falls Assessment
 Schedule ample rest between activities
Post-Op:
 Semi-Fowler’s Positioning
 Look for signs of tetany (hypocalcemia) – report
to MD
 Early ambulation to speed up recalcification
 Use light ankle weights
Calcitonin
 Produced in the C cells or Parafollicular cells of
Thyroid Gland
 Stimulated by increased plasma Ca
 Decreases plasma Ca  opposite action of PTH
 Decreases osteoclastic activity and osteolysis
 Causes reduction in Ca plasma levels but is
often overridden initially by stronger PTH effects on
Ca
THE ADRENOCORTICAL HORMONES
 Adrenal Glands lie at the superior poles of each
Kidney
 Adrenal Cortex secretes Corticosteroids
 Adrenal Medulla secrete catecholamines
Epinephrine and Norepinephrine
 Corticosteroids
Mineralocorticoids
 Affect electrolytes or minerals of the ECF: Na
and K primarily
 Major steroid : Aldosterone
 To note is Cortisol, which has a bit of
mineralocorticoid effect, important to remember in
syndromes of excess Cortisol
 Dexamethasone is such a potent glucocorticoid
with zero mineralocorticoid effect

Aldosterone (Mineralocorticoids)
Glucocorticoids  Deficiency causes Renal NaCl wasting and
 Affect glucose concentration in the blood Hyperkalemia
 Major steroid : Cortisol  Untreated death in 3 days to 2 wks due to K and
Cl loss with ECF fluid and blood volume depletion
Androgenic Hormones
 Affect same effects as testosterone does to  Mineralocorticoids are lifesaving adrenocortical
body hormones
 Synthesis and Secretion of Adrenocortical  Renal and Circulatory Effects of Aldosterone
Hormones
 Increases renal tubular reabsorption of Na and
secretion of K
Layers of the Adrenal Cortex:
 Zona Glomerulosa  Excess Aldosterone increases ECF Volume and
– just beneath the capsule arterial pressure but has little effect on plasma Na
 site of Aldosterone synthesis concentration
 controlled by ECF concentrations of Angiotensin
II and K  If ECF volume is increased by aldosterone >1-2
days, arterial pressure also rises. Kidneys then
 Zona Fasciculata excrete salt and water—PRESSURE NATRIURESIS &
 synthesizes Glucocorticoids Cortisol and DIURESIS
Corticosterone, and some Androgens and Estrogens  This elevated pressure returns renal output of
 controlled by ACTH of Hypothalamus salt and water to normal amidst increased
Aldosterone = ALDOSTERONE ESCAPE
 Zona Reticularis
 adrenal androgens, Dehydroepiandrosterone  After which, salt and water intake and output is
(DHEA) and androstenedione, some estrogens and balanced but Hypertension has now developed due
glucocorticoids synthesis to increased aldosterone still

 Excess Aldosterone cause Hypokalemia and

 Adrenocortical Hormones are steroids derived Muscle Weakness; too little cause Hyperkalemia
from Cholesterol and Cardiac Toxicity
 80% from LDL
 Excess Aldosterone increase tubular hydrogen
Synthetic Steroids: ion secretion and Mild Alkalosis
 Mineralocorticocoids:  K is excreted in exchange for Na but also
 Aldosterone – very potent, 90% excretes hydrogen ions alkalosis
mineralocorticoid
Regulation of Aldosterone Secretion:
 Desoxycorticosterone  Increased K in ECF increases Aldosterone*
 Corticosterone  Increased activity of RAS increases Aldosterone*
 9 Alpha Fluorocortisol  Increased Na in ECF very slightly decreases
 Cortisol Aldosterone
 Cortisone  ACTH has little effect on controlling rate of
Aldosterone secretion

Glucocorticocoids:
 Cortisol– very potent glucocorticoid effect The Glucocorticoids
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 95% of Glucocorticoid activity result from

 Corticosterone secretion Cortisol (Hydrocortisone); a small portion is
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 Cortisone provided by corticosterone

 Prednisone  Effects of Cortisol on Carbohydrate
 Methylprednisone  Stimulate Gluconeogenesis
 Dexamethasone  Increases enzymes to convert Amino Acids to
Glucose in the liver
 Mobilizes Amino Acids mainly from muscles
 Hormones both have gluco and
mineralocorticoid effects  Decrease Glucose utilization by Cells
 Cortisol delays rate of glucose utilization
 Elevates Blood Glucose Concentration
 Adrenal Diabetes; AntiInsulin Diabetogenic
Hormone
 Insulin is released but has little effect
 Effects of Cortisol on Protein Metabolism
 Reduction in Cellular CHON except in the liver
 Muscle weakness and decreased immune
responses by the lymphoid tissues
 Increases liver and Plasma CHON
 Increased blood Amino Acids (mobilizes from
tissues), enhanced amino acid transport to liver
 Effects of Cortisol on Fat Metabolism
 Mobilization of Fatty Acids
Obesity
 Amidst mobilization of adipose tissues, excess
deposition of fat in the chest and the head occurs
with increased Cortisol Buffalo-like Torso with
Moon Face
 Cortisol is important in resisting Stress and
Inflammation
Stressors that release Cortisol:
 Trauma of any type
 Infections
 Intense heat or cold
 Injection of sympathomimetics
 Surgery
 Injection of necrotizing substances on skin
 Movement restriction
 Any debilitating disease
 Cortisol has an almost global effect on reducing
inflammation
ABNORMALITIES OF ADRENOCORTICAL SECRETION
HYPOADRENALISM—ADDISON’S DISEASE
Due to:
 primary atrophy of Adrenal Cortex
 Autoimmunity against Cortices
 Gland hypofunction
Effects (mineralocorticoid):
 Decreased ECF volume
 Hyponatremia, Hyperkalemia
 Mild Metabolic Acidosis
 CO decreases  shock
 Arrhythmias (K at 7mEq/L)
Effects (glucocorticoid):
11
 Sluggish energy (decreased gluconeogenesis,
hypoglycemia)
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 Muscle weakness
 Prone to infections; poor immunity
 Melanin pigmentation in mucous membranes
(blotches on the lips or nipples)
 bronzed/tanned appear on extensor surfaces
 ADDISONIAN CRISIS
SECONDARY HYPOADRENALISM
 Caused by other conditions outside the
Adrenals (tumors, rapid withdrawal of steroids)
 Related to Cortisol deficiency only; ACTH lack in
stimulation
 Gland and Aldosterone normal
 No hyperpigmentation
 Not always with Hypotension and Electrolyte
issues
PT Implications in Hypoadrenalism:
 With medical treatment, fatigue and listlessness
will be better
 Gradually increase exercise – too much stress =
Addisonian Crisis
 Dizziness, nausea, sweating, increased HR,
tremors
 Monitor VS closely
 Heat in aquatherapy is contraindicated
 MD may increase dosage in times of stress or
infection
 Assess for signs hypercortisolism
 Must wear ID bracelet and emergency kit with
dexamethasone or hydrocortisone
 Steroids in the late afternoon or evening =
insomnia; increased CNS stimulation
HYPERADRENALISM—CUSHING’S SYNDROME
Due to:
 Adenomas of Ant. Pituitary (increased
ACTHadrenal hyperplasia)
 Abnormal hypothalamus CRH secretion
 ACTH increase from tumor (ie Abdominal CA,
Paraneoplastic for Lung Carcinoma)
 Prolonged use of glucocorticoids for
inflammation
 If syndrome follows excess of ACTH it is called
Cushing’s Disease
Pseudo-Cushings =
depression/ETOH/Estrogen/Eating disorders produce
cushingoid syndrome
Effects of Cushing’s:
 Hypertension
 Hyperglycemia
 Proximal Muscle Weakness
 Osteoporosis
 Pathologic fractures/wedging
 Osteonecrosis of Femoral Head
 Moon Face / Buffalo Torso
 Hirsutism
 Increased blood glucose
 Decreased tissue CHONs in the body  Insulin promotes conversion of excess glucose
 Suppressed immunity into fatty acids and inhibits gluconeogenesis in the
 Purple Striae liver

 Insulin does not intermediate in the brain’s use

of glucose (Hypoglycemic Shock)

PRIMARY ALDOSTERONISM—CONN’S SYNDROME  Insulin deficiency causes lypolysis of storage fat

and release of fatty acids into blood stream—
Due to: increasing plasma cholesterol and phospholipid
 tumor in Zona Glomerulosa (increase (Atherosclerosis)
aldosterone secretion)  Excess use of Fat in insulin lack can cause
 Hyperplastic adrenal cortices Ketosis and Acidosis

Effects: Effects on Protein and Growth

 Hypokalemia/Hypernatremia  Insulin inhibits catabolism of CHON
 Increase in ECF volume & Blood Volume
 Hypertension  Lack of Insulin causes CHON depletion and
 Occasional muscle paralysis due to Hypokalemia increased plasma amino acids--degradation of amino
 Decreased Renin plasma concentration acids lead to Urea excretion in urine
 Metabolic Alkalosis
 DM  Insulin and GH interact synergistically

THE PANCREAS Glucagon

 Pancreas secretes 2 important Hormones:  Increases blood glucose concentration
 Insulin  Opposite of Insulin
 Glucagon  aka Hyperglycemic Hormone

Has 2 tissue types: Glucagon’s Effects on Metabolism:

 ACINI – has digestive function
 ISLETS OF LANGERHANS – has endocrine  Breakdown of liver glycogen (glycogenolysis)
function  Increased gluconeogenesis in liver

Major Cell Types in the Islets:  Activates adipose cell lipase (increasing fatty
acids available for body)
Alpha  Inhibits Triglyceride storage in the liver
 Glucagon
 Enhance heart strength of contraction (in high
Beta concentrations)
 Insulin  Increase blood flow in tissues (esp. Kidneys)
 Amylin  Enhance bile secretion

Delta  Inhibits gastric acid secretion

 Somatostatin
Somatostatin
 Secreted by Delta cells of the Islets of
Insulin Langerhans
 Insulin has effects on carbohydrate metabolism
 Same chemical substance as Growth Inhibitory
 Insulin cause excess carbohydrates to be stored Hormone that suppress Ant Pituitary Gland and GH
as glycogen in the liver and muscles or as fats on to secretion
adipose tissues
Effects:
 Insulin inhibits CHON breakdown that are  Depress secretion of Insulin and Glucagon at the
already in the cells Islets
 When insulin binds with membrane receptors,  Decrease GIT motility
12

the tissue will increase uptake of glucose—especially  Decrease secretion and absorption in the GIT
in muscles and adipose but NOT in most neurons
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 Stimulated by almost all factors related to food

 Effects of Insulin on Carbohydrate & Fat ingestion:
Metabolism  Increased blood glucose
 Promotes muscle glucose uptake and  Increased fatty acids
metabolism  Increased GI hormones in the UGIT

 Promotes liver uptake, storage and use of Blood Glucose Regulation

glucose  Normal blood glucose concentrations:
 80-90 mg/100ml = fasting, before breakfast
 120-140 mg/100ml = 1st hour after meal;
returns to normal within 2 hours after last
absorption of carbohydrate
 Liver acts as an important blood glucose buffer
system—storing glucose if it is too highly
concentrated, releases it once blood levels of sugar
& insulin falls
 Both insulin and glucagon act as important
feedback control systems to maintain normal glucose
concentrations
 In severe hypoglycemia, hypothalamus
stimulates sympathetic system to release
Epinephrine to release glucose from liver into the
blood stream
 GH & Cortisol are stimulated in severe
hypoglycemia—both inhibiting rate of glucose
utilization in the cells, calling on fat metabolism to
return glucose concentration in the blood
Diabetes Mellitus
 Syndrome of impaired carbohydrate, fat and
CHON metabolism due to either lack of or decreased
sensitivity to Insulin
Type I DM
 lack of insulin
 Injury to Beta Cells of pancreas – impair insulin
production
 May be due to: Viral Infections or Autoimmune
Disorders
 Usual age of onset (US pop) = 14 y/o, hence aka
Juvenile DM
 Plasma glucose can rise to 300-1200 mg/100ml
 Glycosuria
 Glucose from blood is filtered into the Renal
tubules, spilling into urine
 Occurs when blood concentration is
>180mg/100ml (threshold for glycosuria)
 In 300-500 mg/100ml of glucose in severe DM =
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100 grams or more of glucose is found in urine
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 Dehydration
 Glucose does not diffuse easily into the cell
hence it increases osmotic pressures in ECF—sucking
out water (Sugar loves water).
 Would also trigger Osmotic Diuresis (Polyuria)
 Tissue Injuries
 Vascular wall injuries  risk of cardiac
problems, CVD, HTN, Atherosclerosis, End-Stage
Renal Dse, Retinopathy, Ischemia and gangrene
 Nerve Tissue damage  Peripheral
Neuropathies, Autonomic Nervous System
Dysfunction
 Utilization of Fats and Metabolic Acidosis
 In DM, there is a shift from carbohydrate to fat
metabolism
 Keto Acids like acetoacetic and Beta-
hydroxybutyric Acid, can be released into the plasma
more quickly than they can be used up (more on
Type 1 DM but can seen in uncontrolled Type II)
 Severe Metabolic Acidosis: Kussmaul’s Breathing
(rapid & deep breathing), Acetone Breath
 pH of <7.0 in severe DM = Acidotic Coma
 DM depletes body’s CHON
 Asthenia despite Polyphagia
Brittle DM
 Labile blood glucose in Type I DM
 ‘wide glucose excursions’
Type II (Non-Insulin Dependent)
 insensitivity of tissues to Insulin
 More common than Type I, 90% of all cases
 Usual age of onset 50-60 y/o (Adult Onset)
 Causative Factors:
 Obesity  hyperinsulinemia; fewer insulin
receptors in the obese muscles, liver and adipose
tissues
 Insulin Resistance  compensatory increase in
insulin but impaired receptor sensitivity
Metabolic Syndrome
 Obesity (abdominal fat especially)
 Fasting hyperglycemia
 Lipid abnormalities: increased triglycerides,
decreased HDL
 HTN
Other causes:
 Polycystic Ovary Syndrome
 Excess glucocorticoids (Cushing’s)
 Excess GH (Acromegaly)
 Early Rx: Exercise, Calorific-restriction, Wt.
Reduction.
Hybrid DM / Type 1.5/ Maturity-Onset Diabetes of
the Young (MODY)
 A blur between the two types still being studied
 Antibodies found in Type 2 DM that are obese
Prediabetes / Insulin Resistance Syndrome
 Body unable to utilize glucose as it should
 Glucose in blood rises as less of it is utilized
 Glucose higher than normal but not DM-high
 Also has HTN and dyslipidemia No curative intervention, PT’s role is to provide
risk factor assessments:
 Impaired Glucose Tolerance (IGT) and Impaired  Duration and severity of DM
Fasting Glucose (IFG) = Prediabetic  Elevated triglycerides
 High BMI
Gestational DM  Smoking Hx
 DM at onset of pregnancy; at ~6 wks post-  HTN
partum reclassified into other DM types (often Type  Most common type of neuropathy:
II) Chronic Sensorimotor Distal Symmetric
 Children of Gestational DM = delayed fine and Polyneuropathy (DPN)
motor skills; inattention and hyperactive
Diabetic Amyotrophy: bilateral asymmetrical
proximal muscle weakness
DM Risk Factors:
 TV ≥2 hours daly Charcot’s Joint (Neuropathic Arthropathy)
 Fastfood ≥2x/wk  Severe unilateral swelling (bilat in 20% of cases
 Skipping breakfast but not at the same time)
 Daily carbonated drinks  Increased skin warmth
 Waist girth >35” for women; >40” for men  Redness
 Stress  Impaired eep pressure sensation but less pain
 Normal X-rays initially
 Joint deformity
Medical Treatment of DM
 Regular Insulin has duration of action lasting 3-8  Stable glycemic control is shown to decrease
hours neuropathic pain
 Those with Zinc or other CHON derivatives are
slowly absorbed and can last 10-48 hours
Periarthritis – 5x more common in DM
 IDDM is given a single dose of a longer-acting (IDDM > NIDDM, often bilat)
insulin each day + additional quantities of regular  Global tightness (ER = IR in limitation in
insulin during the day (when blood glucose rise too dominant shoulder); in non-dominant: ER > Hyperext
highly on mealtimes) > IR > Abd more limited

Diabetic Stiff Hand (Limited Joint Mobility)

Insulin Shock & Hyperglycemia  diabetic contracture common in both types
 CNS requires glucose for energy metabolism  Can lead to Sclerodactyly, mimicking
 If high Insulin cause glucose to fall, CNS Scleroderma
metabolism is depressed
 In Insulin-secreting tumors or overdosage of  Strong association with Dupuytren’s contracture
Insulin = Insulin Shock  May also develop CRPS (complex regional pain
syndrome)
 At 50-70 mg/100ml of blood glucose =
hallucinations, extreme nervousness, trembling,
diaphoresis Syndrome of Limited Joint Mobility vs Stiff Hand
Syndrome
 At 20-50 mg/100ml = clonic seizures, LOC
 Even lower blood glucose = coma  SLJM is painless stiffness
 SHS becomes painful
 To differentiate between unconscious Diabetic
Keto Acidosis vs Hyperosmolar, Hyperglycemic States  Prayer Sign for SLJM
(HHS) = Acetone breath is found in DKA
Scleroderma Diabeticorum
 thickening of skin (Peau d’Orange of posterior
neck, upper back and shoulders)
Rehab Considerations in DM
14

 Depression
 Common in Type II DM Diffused Idiopathic Skeletal Hyperostosis (DISH;
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 Prone to take ‘drug holidays’ Ankylosing Hyperostosis; Forestier Dse)

 More likely to miss their health care
appointments for intervention and prevention  Often in Type II DM
 Often right sided osteophytes that form bridges
Diabetic Neuropathy  C/o: stiffness without LOM
 Common chronic complication in DM
 Related to build up of Sorbitol in nerve cells, a  Thoracic spine, Calcaneum, Olecranon common;
by-product of improper glucose metabolism  SI spared
results to electrolyte shifts, ABN fluid balance and
nerve dysfunction

 Medical Intervention to maintain glucose within
80-120 mg/dL in the blood
Recommended preventative care services:
 Yearly eye & foot exams
 Measurement of Glycosylated Hemoglobin
(A1C) at least 2x per year
 an accurate objective measure of chronic
glycemia in DM; normal range 4% to 6%, goal of 7%
in DM (correlates to <170mg/dL of blood glucose)
 PT can conduct careful screening exams
 10-15g of carbohydrate snack for each 30
minutes of activity
 Stop activity in signs of hypoglycemia
 Test blood glucose
 Advice not to exercise alone due to possibility of
hypoglycemia
 If anyone with DM arrives for a visit with a
confused or lethargic state or change in mental
functions, fingerstick glucose test must be done and
immediate GP referral made

Insulin Reaction or Hypoglycemia

 Tissue hypertrophy or atrophy or both at site of
PT Screening (general guidelines): injection
 Insulin allergy
 Screen at time of diagnosis of NIDDM, then  Erratic insulin action
annually thereafter; IDDM every 5 years, annually  Insulin resistance
after for:
S/Sx: (at 70 mg/dL or less)
 Peripheral Neuropathy  H/A
 Check knee & Ankle Reflexes  Weakness
 Sensory function of feet, asking for neuropathic  Irritability
symptoms  Incoordination
 Examine for ulcers, calluses and deformities  Apprehension
 Inability to respond to commands
 APTA & the American Diabetes Association  Psychosis
recommends 30 minutes of moderate exercise at
least 5 days a week (aerobic and/or strengthening) Causes:
 Skipped/late meals
Exercise-related Complications:  Overdose of insulin
 Any exercise can improve insulin use of the  Exercise
body; decreases amount of insulin needed as  Rapid drop in glucose (ex: from 400 to 200)
muscles activity causes glucose uptake
 Must immediately provide carbs (honey, juice,
 When using insulin, exercise may add on to the candy)
effect and may cause dangerous hypoglycemia
 If at start of exercise, plasma glucose is 250 Hospitalize if:
mg/dL  already in insulin deficiency  <50 mg/dL
 exercise is likely to increase glucose further  No change in mental status even after
(remember effects Epinephrine/sympathetic effects treatment
and Growth Hormone during exercise)  Seizures or unconscious
 Carer cannot be with person in the next 12 hrs
 Postpone exercise until <100 mg/dL  Sulfonylurea causes hypoglycemia

 If plasma glucose is <100 mg/dL 

 give 10-15g of carbohydrate snack to increase
glucose; recheck after 15 minutes

 In active retinopathy and nephropathy with DM With use of intermediate/Long-Acting Insulin reports
 avoid high intensity exercise that increase BP of:
 bending (head below waist)  Nightmares
 increasing intrathoracic and intracranial  Unexplained sweating
pressures  H/A during sleep  report these to MD
15

 Avoid insulin injection on active muscles (it  Somogyi Effect

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increases insulin absorption too much)

 Rotate injection sites on area (Lipogenic Effect)
 Know the type, dose, time of insulin injections
so as not to coincide exercise on peak activity times
of insulin
 IDDM may need to reduce insulin dose or
increase food intake when initiating exercise.
Insulin Pumps
 Mostly used by IDDM
 Continuous Subcutaneous Insulin Infusion (CSSI)
 aka Insulin Pump Therapy
 Caution with exercise at it can be cause for DKA
if infusion is physically interrupted
 Perspiration or water over infusion site (skin on
needle)
 Insulin degrades in temperature extremes
 Excessive movement of infusion site

 <100 mg/dL of pre-exercise blood glucose with

CSSI may not need carb snack as they can reduce or
suspend insulin levels during activity

When impossible to differentiate between DKA,

Hyperglycemic State or hypoglycemia in a lethargic
patient...

 give some source of sugar immediately. You are

unlikely to endanger any further with small amount
of sugar if it is hyperglycemia; if it is a hypoglycemia,
sugar will be life-saving

Exercise in Type I DM
 can increase strength and maintain weight and
functions but not proven to provide increased
glycemic control

 Can workout without problems for 30-45 mins

of sustained maximal aerobic exercise

 Greatest risk of hypoglycemia is seen 12-14

hours post exercise

Exercise in Type II DM
 Beneficial for obesity and hyperglycemia
 Effects disappear few days after d/c
 Long-term effects with 80% of peak aerobic
capacity
 Hypoglycemia not often a problem
 Exercise in the morning is best (to avoid glucose
diurnal changes)
 Do not exercise before sleeping or at night

 Menstruating pts need to increase insulin

In aquatx
 DM pt must protect feet (boat shoes to prevent
scarping underwater)
 Temperature rise increases insulin absoprtion by
50-60%
 Increased temp and activity = hypoglycemia
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