Chapter 5
Fluids and Electrolytes,
Acids and Bases
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Distribution of Body Fluids

Total body water (TBW)


Intracellular fluid
Extracellular fluid
• Interstitial fluid
• Intravascular fluid
• Lymph, synovial, intestinal, CSF, sweat, urine, pleural,
peritoneal, pericardial, and intraocular fluids
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2
Distribution of Body Fluids (Cont.)

Pediatrics



75% to 80% of body weight
Susceptible to significant changes in body fluids
• Dehydration in newborns
Aging

Decreased percent of total body water
• Decreased free fat mass and decreased muscle mass
• Renal decline
• Diminished thirst perception
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3
Water Movement
Between Fluid Compartments




Osmolality
Osmotic forces
Aquaporins
Starling forces

Net filtration = forces favoring filtration minus
forces opposing filtration
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4
Fluid Movement Between Plasma
and Interstitial Space
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5
Net Filtration

Forces favoring filtration:



Capillary hydrostatic pressure (blood pressure)
Interstitial oncotic pressure (water-pulling)
Forces favoring reabsorption:


Plasma (capillary) oncotic pressure (water-pulling)
Interstitial hydrostatic pressure
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6
Edema


Accumulation of fluid within the interstitial
spaces
Causes:






Increase in capillary hydrostatic pressure
Decrease in plasma oncotic pressure
Increase in capillary permeability
Lymph obstruction (lymphedema)
Localized vs. generalized
Pitting edema
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7
Edema (Cont.)
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8
Sodium and Chloride Balance

Sodium



Primary ECF cation
Regulates osmotic forces, thus water
Roles
• Neuromuscular irritability, acid-base balance, and cellular
chemical reactions and membrane transport

Chloride

Primary ECF anion
 Provides electroneutrality
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9
Sodium and Chloride Balance (Cont.)

Renin-angiotensin-aldosterone system

Aldosterone—leads to sodium and water
reabsorption back into the circulation and
excretion of potassium
 Natriuretic peptides
 Causes sodium and water excretion
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10
Renin-Angiotensin-Aldosterone
System
Water Balance

ADH secretion


Increases water reabsorption into the plasma
Thirst perception



Osmolality receptors
• Hyperosmolality and plasma volume depletion
Volume receptors
Baroreceptors
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12
Antidiuretic Hormone (ADH) System
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13
Normal Serum Electrolyte Values







Sodium 135-145 mEq/L (mmol/L)
Potassium 3.5-5.0 mEq/L (mmol/L)
Calcium 8.8-10.5mg/dL
Magnesium 1.8-3.0 mEq/L
Chloride 98-106 mEq/L
Bicarbonate 24-28 mEq/L
Phosphous-phosphate 2.5-5.0 mg/dL
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14
Electrolytes Imbalances

Sodium 135-145 mEq/L



Potassium 3.5-5.0 mEq/L



Hypokalemia
Hyperkalemia
Calcium 8.8-10.5 mg/dL



Hyponatremia
Hypernatremia
Hypocalcemia
Hypercalcemia
Magnesium 1.8-3.0 mEq/L


Hypomagnesemia
Hypermagnesemia
Alterations in Na+, Cl, and
Water Balance

Isotonic alterations

Total body water change with proportional
electrolyte and water change (no change in
concentration)
 Isotonic fluid loss
 Isotonic fluid excess
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16
Alterations in Na+, Cl–, and
Water Balance (Cont.)

Hypertonic alterations

Hypernatremia
• Serum sodium >145 mEq/L
• Related to sodium gain or water loss
• Water movement from the ICF to the ECF

Intracellular dehydration
• Manifestations

Clinical
– Thirst, weight gain, bounding pulse, and increased blood
pressure

Central nervous system
– Muscle twitching and hyperreflexia (hyperactive reflexes),
confusion, coma, convulsions, and cerebral hemorrhage
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17
Alterations in Na+, Cl–, and
Water Balance (Cont.)

Hypertonic alterations (Cont.)

Hyperchloremia
• Occurs with hypernatremia or a bicarbonate deficit
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18
Alterations in Na+, Cl–, and
Water Balance (Cont.)

Hypotonic alterations


Decreased osmolality
Hyponatremia or free water excess
• Hyponatremia decreases the ECF osmotic pressure, and
water moves into the cell via osmosis
• Cells expand
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19
Hyponatremia



Serum sodium level <135 mEq/L
Sodium deficits cause plasma hypoosmolality
and cellular swelling
Causes:



Pure sodium loss
Low intake
Dilutional hyponatremia
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20
Hyponatremia (Cont.)

Manifestations:

Most life-threatening: cerebral edema and
increased intracranial pressure
 Lethargy, confusion, decreased reflexes, seizures,
and coma
 If leads to loss of ECF and hypovolemia, see
hypotension, tachycardia, decreased urine output
 If dilutional from excess water (hypervolemic
hyponatremia), see weight gain, edema, ascites,
jugular vein distention
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21
Water Excess



Compulsive water drinking
Decreased urine formation
Syndrome of inappropriate ADH (SIADH)


ADH secretion in the absence of hypovolemia or
hyperosmolality
Hyponatremia with hypervolemia
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22
Water Excess (Cont.)

Manifestations: cerebral edema (with
confusion and convulsions), weakness,
muscle twitching, nausea, headache, and
weight gain
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23
Hypochloremia




Usually the result of hyponatremia or
elevated bicarbonate concentration
Develops as a result of vomiting and the
loss of HCl
Occurs in cystic fibrosis
Treatment of underlying cause is required
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24
Potassium




Major intracellular cation
Concentration maintained by Na+/K+ pump
Regulates intracellular electrical neutrality in
relation to Na+ and H+
Essential for transmission and conduction of
nerve impulses, normal cardiac rhythms, and
skeletal and smooth muscle contraction
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25
Potassium Levels

Changes in pH affect K+ balance




Hydrogen ions accumulate in the ICF during
states of acidosis; K+ shifts out to maintain a
balance of cations across the membrane; result is
hyperkalemia
Aldosterone, insulin, and epinephrine
influence serum potassium levels
Kidney is most efficient regulator
Potassium adaptation

Slow changes tolerated better than acute
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26
Hypokalemia



Potassium level <3.5 mEq/L
Potassium balance is described by changes
in plasma potassium levels
Causes: reduced intake of potassium,
increased entry of potassium into cells, and
increased loss of potassium
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27
Hypokalemia (Cont.)

Manifestations (depend on rate and severity)

Membrane hyperpolarization causes a decrease in
neuromuscular excitability, skeletal muscle
weakness, smooth muscle atony, and cardiac
dysrhythmias
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28
Hyperkalemia



Potassium level >5.5 mEq/L
Hyperkalemia is rare because of efficient
renal excretion
Caused by increased intake, shift of K+ from
ICF into ECF, decreased renal excretion,
insulin deficiency, or cell trauma
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29
Hyperkalemia (Cont.)

Mild attacks


Increased neuromuscular irritability
• Restlessness, intestinal cramping, and diarrhea
Severe attacks

Decreases the resting membrane potential
• Muscle weakness, loss of muscle tone, and paralysis
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30
ECG Changes with
Potassium Changes
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31
Calcium and Phosphate

Calcium and phosphate concentrations are
rigidly controlled by parathyroid hormone
(PTH), vitamin D, and calcitonin
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32
Calcium



99% of calcium is located in the bone as
hydroxyapatite
Necessary for structure of bones and teeth,
blood clotting, hormone secretion, cell
receptor function, plasma membrane stability,
transmission of nerve impulses, muscle
contraction
Serum concentration 8.8 to 10.5 mg/dl
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33
Hypocalcemia

Causes:




Inadequate intestinal absorption, deposition of ionized
calcium into bone or soft tissue, blood administration
Decreases in PTH and vitamin D
Nutritional deficiencies occur with inadequate sources of
dairy products or green, leafy vegetables
Effects:

Increased neuromuscular excitability
• Tingling, muscle spasm (particularly in hands, feet, and facial
muscles), intestinal cramping, hyperactive bowel sounds


Severe cases show convulsions and tetany
Prolonged QT interval, cardiac arrest
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34
Hypercalcemia

Causes:






Hyperparathyroidism
Bone metastases with calcium resorption from breast,
prostate, renal, and cervical cancer
Sarcoidosis
Excess vitamin D
Many tumors that produce PTH
Effects:




Many nonspecific: fatigue, weakness, lethargy, anorexia,
nausea, constipation
Impaired renal function, kidney stones
Dysrhythmias, bradycardia, cardiac arrest
Bone pain, osteoporosis
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35
Phosphate




Like calcium, most phosphate is also located
in the bone
Provides energy for muscle contraction
Parathyroid hormone, vitamin D3, and
calcitonin act together to control phosphate
absorption and excretion
Normal value = 2.5-5.0 mg/dl
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36
Hypophosphatemia

Causes:


Intestinal malabsorption
(vitamin D deficiency, use of
magnesium- and aluminumcontaining antacids, longterm alcohol abuse)
 Malabsorption syndromes
 Respiratory alkalosis
 Increased renal excretion of
phosphate associated with
hyperparathyroidism
Effects:

Reduced capacity for
oxygen transport by red
blood cells, thus disturbed
energy metabolism
 Leukocyte and platelet
dysfunction
 Deranged nerve and muscle
function
 In severe cases, irritability,
confusion, numbness,
coma, convulsions, possibly
respiratory failure,
cardiomyopathies, bone
resorption
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37
Hyperphosphatemia

Causes:





Acute or chronic renal
failure with significant
loss of glomerular
filtration
Treatment of metastatic
tumors with
chemotherapy that
releases large amounts
of phosphate into serum
Long-term use of
laxatives or enemas
containing phosphates
Hypoparathyroidism
Effects:


Symptoms primarily
related to low serum
calcium levels (caused
by high phosphate levels)
similar to the results of
hypocalcemia
When prolonged,
calcification of soft
tissues in lungs, kidneys,
joints
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38
Magnesium




Intracellular cation
Serum concentration 1.8 to 3.0 mEq/L
Acts as a cofactor in intracellular enzymatic
reactions
Increases neuromuscular excitability
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39
Hypomagnesemia

Causes:


Malnutrition
 Malabsorption
syndromes
 Alcoholism
 Urinary losses (renal
tubular dysfunction,
loop diuretics)
Effects:

Behavioral changes
 Irritability
 Increased reflexes
 Muscle cramps
 Ataxia
 Nystagmus
 Tetany
 Convulsions
 Tachycardia
 Hypotension
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40
Hypermagnesemia

Causes:




Usually renal insufficiency or failure
Excessive intake of magnesium-containing antacids
Adrenal insufficiency
Effects:








Skeletal smooth muscle contraction
Excess nerve function
Loss of deep tendon reflexes
Nausea and vomiting
Muscle weakness
Hypotension
Bradycardia
Respiratory distress
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41
Acid-Base Balance

Acid-base balance is carefully regulated
to maintain a normal pH via multiple
mechanisms
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42
pH


Negative logarithm of the H+ concentration
If the H+ are high in number, the pH is low
(acidic); if the H+ are low in number, the pH is
high (alkaline)
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43
pH (Cont.)



Acids are formed as end products of protein,
carbohydrate, and fat metabolism
To maintain the body’s normal pH (7.35-7.45),
the H+ must be neutralized or excreted
The bones, lungs, and kidneys are the major
organs involved in the regulation of acid-base
balance
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44
pH (Cont.)

Body acids exist in two forms:


Volatile
• H2CO3 (can be eliminated as CO2 gas)
Nonvolatile
• Sulfuric, phosphoric, and other organic acids
• Eliminated by the renal tubules with the regulation of
HCO3–
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45
Buffering Systems


A buffer is a chemical that can bind excessive
H+ or OH– without a significant change in pH
The most important plasma-buffering systems
are the carbonic acid–bicarbonate pair
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46
Carbonic Acid–Bicarbonate Pair


Operates in the lung and the kidney
The greater the partial pressure of carbon
dioxide, the more carbonic acid is formed


At a pH of 7.4, the ratio of bicarbonate to carbonic
acid is 20:1
Bicarbonate and carbonic acid can increase or
decrease, but the ratio must be maintained
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47
Carbonic Acid–Bicarbonate Pair
(Cont.)


The respiratory system compensates by
increasing ventilation to expire carbon dioxide
or by decreasing ventilation to retain carbon
dioxide
The renal system compensates by producing
acidic or alkaline urine
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48
Other Buffering Systems

Protein buffering (hemoglobin)


Proteins have negative charges, so they can serve
as buffers for H+
Renal buffering

Secretion of H+ in the urine and reabsorption of
HCO3–
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49
Acid-Base Imbalances

Normal arterial blood pH



Acidosis


7.35 to 7.45
Obtained by arterial blood gas (ABG) sampling
Systemic increase in H+ concentration or
decrease in bicarbonate (base)
Alkalosis

Systemic decrease in H+ concentration or
increase in bicarbonate
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50
Acidosis and Alkalosis

Four categories of acid-base imbalances:

Respiratory acidosis—elevation of pCO2 as a result
of ventilation depression
 Respiratory alkalosis—depression of pCO2 as a
result of alveolar hyperventilation
 Metabolic acidosis—depression of HCO3– or an
increase in noncarbonic acids
 Metabolic alkalosis—elevation of HCO3– usually
caused by an excessive loss of metabolic acids
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51
Chapter 19
Alterations of Hormonal Regulation
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Mechanisms of
Hormonal Alterations




Failure of feedback systems
Dysfunction of an endocrine gland
Secretory cells are unable to produce, obtain,
or convert hormone precursors
The endocrine gland synthesizes or releases
excessive amounts of hormone
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53
Mechanisms of
Hormonal Alterations (Cont.)



The endocrine gland fails to produce
adequate amounts of hormone
Increased hormone degradation or
inactivation
Ectopic hormone release
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54
Target Cell Failure

Cell surface receptor–associated disorders:






Decrease in number of receptors
Impaired receptor function
Presence of antibodies against specific receptors
Antibodies that mimic hormone action
Unusual expression of receptor function
Intracellular disorders:


Defects in postreceptor signaling cascades
Inadequate synthesis of second messenger
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55
Diseases of the
Posterior Pituitary

Syndrome of inappropriate antidiuretic
hormone secretion (SIADH)



Hypersecretion of ADH
For diagnosis, normal adrenal and thyroid function
must exist
Clinical manifestations are related to enhanced
renal water retention, hyponatremia, and serum
hypoosmolality
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56
Diseases of the
Posterior Pituitary (Cont.)

Diabetes insipidus







Insufficiency of ADH
Polyuria and polydipsia
Partial or total inability to concentrate the urine
Neurogenic
• Insufficient amounts of ADH
Nephrogenic
• Inadequate response to ADH
Psychogenic
Manifestations are related to enhanced water excretion,
hypernatremia, and serum hyperosmolality
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57
Diseases of the Anterior Pituitary

Hypopituitarism

Pituitary infarction
• Sheehan syndrome
• Hemorrhage
• Shock
 Others:
• Head trauma
• Infections
• Tumors
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58
Diseases of the Anterior Pituitary
(Cont.)

Hypopituitarism (Cont.)

Panhypopituitarism
• ACTH deficiency
• TSH deficiency
• FSH and LH deficiency
• GH deficiency
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59
Diseases of the Anterior Pituitary
(Cont.)

Hyperpituitarism


Commonly caused by a benign, slow-growing
pituitary adenoma
Manifestations:
• Headache and fatigue
• Visual changes
• Hyposecretion of neighboring anterior pituitary hormones
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60
Diseases of the Anterior Pituitary
(Cont.)

Hypersecretion of growth hormone (GH)


Acromegaly
• Hypersecretion of GH during adulthood
Giantism
• Hypersecretion of GH in children and adolescents
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61
Diseases of the Anterior Pituitary
(Cont.)
From Patton KT, Thibodeau GA: Anatomy & physiology, ed 8, St Louis, 2013, Mosby.
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62
Diseases of the Anterior Pituitary
(Cont.)

Hypersecretion of prolactin

Caused by prolactinomas
• In females, increased levels of prolactin cause
amenorrhea, galactorrhea, hirsutism, and osteopenia
• In males, increased levels of prolactin cause
hypogonadism, erectile dysfunction
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63
Alterations of Thyroid Function

Hyperthyroidism




Thyrotoxicosis
Graves disease
• Pretibial myxedema
Hyperthyroidism resulting from nodular thyroid
disease
• Goiter
Thyrotoxic crisis (thyroid storm)
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64
Thyrotoxicosis (Graves Disease)
From Belchetz P, Hammond P: Mosby’s color atlas and text of diabetes and
endocrinology, Edinburgh, 2003, Mosby.
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65
Alterations of Thyroid Function

Hypothyroidism


Primary hypothyroidism
• Autoimmune thyroiditis (Hashimoto disease)
• Subacute thyroiditis
• Painless thyroiditis
• Postpartum thyroiditis
• Myxedema coma
Congenital hypothyroidism
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66
Manifestations of
Thyroid Alterations
From Damjanov I: Pathology for the health professions, ed 4, St Louis, 2012, Saunders.
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67
Alterations of
Parathyroid Function

Hyperparathyroidism

Primary hyperparathyroidism
• Excess secretion of PTH from one or more parathyroid
glands


Secondary hyperparathyroidism
• Increase in PTH secondary to chronic hypocalcemia
Manifestations:
• Hypercalcemia
• Hypophosphatemia
• Hypercalciuria: kidney stones
• Pathologic fractures
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68
Alterations of
Parathyroid Function (Cont.)

Hypoparathyroidism



Abnormally low PTH levels
Usually caused by parathyroid damage in thyroid
surgery
Manifestations:
• Hypocalcemia

Chvostek and Trousseau signs
• Hyperphosphatemia
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69
Type 1 Diabetes Mellitus

Types:





Idiopathic type 1
Autoimmune type 1
Pancreatic atrophy and specific loss of beta
cells; hyperglycemia when 80%-90% cells
lost
Macrophages, T-cytotoxic cells, antibodies
Alterations in insulin, amylin, glucagon
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70
Type 1 Diabetes Mellitus (Cont.)




Genetic susceptibility
Environmental factors
Immunologically mediated destruction of beta cells
Manifestations:






Hyperglycemia
Polydipsia
Polyuria
Polyphagia
Weight loss
Fatigue
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71
Type 2 Diabetes Mellitus




Ranges from insulin resistance with relative
insulin deficiency to insulin secretory defect
with insulin resistance
Caused by genetic-environmental interaction
Risk factors are age, obesity, hypertension,
physical activity, and family history
Metabolic syndrome
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72
Type 2 Diabetes Mellitus (Cont.)


Initial insulin resistance
Later loss of beta cells

Manifestations (nonspecific): fatigue, pruritus,
recurrent infections, visual changes, or symptoms
of neuropathy; often overweight, dyslipidemic,
hyperinsulinemic, and hypertensive
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73
Other Types of Diabetes Mellitus

Maturity onset diabetes of youth (MODY)


Beta-cell function or insulin action affected by
autosomal dominant mutations
Gestational diabetes mellitus (GDM)

Any degree of glucose intolerance with onset or
first recognition during pregnancy
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74
Acute Complications of
Diabetes Mellitus



Hypoglycemia
Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycemic nonketotic
syndrome (HHNKS)
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75
Diabetic Ketoacidosis
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76
Chronic Complications of Diabetes
Mellitus

Microvascular disease




Macrovascular disease




Diabetic retinopathy
Diabetic nephropathy
Diabetic neuropathies
Cardiovascular disease
Stroke
Peripheral vascular disease
Infection
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77
Alterations of Adrenal Function

Disorders of the adrenal cortex:


Cushing disease
• Excessive anterior pituitary secretion of ACTH
Cushing syndrome
• Manifestations resulting from chronic excess cortisol
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78
Cushing Disease
Cushing Disease
From Zitelli BJ et al: Zitelli and Davis’ atlas of pediatric physical diagnosis, ed 6, London, 2012, Saunders.
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80
Alterations of Adrenal Function

Disorders of the adrenal cortex


Congenital adrenal hyperplasia
Hyperaldosteronism
• Primary hyperaldosteronism (Conn disease)
• Secondary hyperaldosteronism
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Alterations of Adrenal Function
(Cont.)

Disorders of the adrenal cortex (Cont.)

Hypersecretion of adrenal androgens and
estrogens
• Feminization
• Virilization
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82
Virilization
From Thibodeau GA, Patton KT: The human body in health & disease, ed 4,
St Louis, 2010, Mosby.
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83
Alterations of Adrenal Function
(Cont.)

Disorders of the adrenal cortex (Cont.)

Adrenocortical hypofunction
• Addison disease (primary adrenal insufficiency)

Addisonian crisis
• Secondary hypocortisolism
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84
Alterations of Adrenal Function
(Cont.)

Disorders of the adrenal medulla

Adrenal medulla hyperfunction
• Caused by tumors derived from the chromaffin cells of
the adrenal medulla

Pheochromocytomas
• Secrete catecholamines on a continuous or episodic
basis
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85