Stages of general adaptation syndrome
1. Alarm
Initial reaction
Sympathetic nervous system
2. Resistance
Adaptation
Limit stressor
3.
... [Show More] Exhaustion
Adaptation failing
Disease develops
Edema
Excess fluid in the interstitial space
Dehydration (ECF volume deficit)
Can occur independently without electrolyte defects
Decrease in fluid level leads to increase in level of blood solutes
Cell shrinkage
Hypotension
Hypovolemia or fluid volume deficit
Decreased fluid in the intravascular space
Hypotonic Hydration
(fluid overload)
Causes of Fluid Deficit
Inadequate fluid intake
Poor oral intake
Inadequate IV fluid replacement
Excessive fluid or sodium losses:
Gastrointestinal losses Excessive diaphoresis Prolonged hyperventilation Hemorrhage Nephrosis Diabetes mellitus Diabetes insipidus Burns Open wounds Ascites Effusions Excessive use of diuretics Osmotic diuresis
Deydration Manisfestations
thirst, altered level of consciousness, hypotension, tachycardia, weak and thready pulse, flat jugular veins, dry mucous membranes, decreased skin turgor, oliguria, weight loss, and sunken fontanelles
Cancer Benign
Slow, progressive, localized, well defined, resembles host (more differentiated), grows by expansion, does not usually cause death
Cancer Malignant
Rapid growing, spreads (metastasis) quickly, fatal, highly undifferentiated
Sodium
Normal range: 135-145 mEq/L.
• Most significant cation and prevalent electrolyte of extracellular fluid.
• Controls serum osmolality and water balance. Plays a role in acid-base balance.
• Facilitates muscles and nerve impulses.
• Main source is dietary intake.
• Excreted through the kidneys and gastrointestinal tract.
Hypernatremia
Sodium > 145 mEq/L
Serum osmolarity increases
• Results in fluid shifts
Causes of Hypernatremia
Excessive sodium ingestion Hypertonic IV saline (3% saline) administration
Cushing's syndrome
Corticosteroid use
Diarrhea
Excessive sweating
Prolonged episode of hyperventilation
Diuretic use Diabetes insipidus
Decreased water ingestion
Loss of thirst sensation
Inability to drink water
Third spacing
Vomiting
Hypernatremia Manifestations:
increased temperature, warm and flushed skin, dry and sticky mucous membranes, dysphagia, increased thirst, irritability, agitation, weakness, headache, seizures, lethargy, coma, blood pressure changes, tachycardia, weak and thready pulse, edema, and decreased urine output
Hyponatremia
Sodium < 135 mEq/L
Serum osmolarity decreases
Causes of Hyponatremia
Deficient sodium
Diuretic use
Gastrointestinal losses
Excessive sweating
Insufficient aldosterone levels
Adrenal insufficiency
Dietary sodium restrictions
Excessive water
Hypotonic intravenous saline (0.45% saline) Hyperglycemia
Excessive water ingestion
Renal failure
Syndrome of inappropriate antidiuretic hormone Heart failure
Hyponatremia Manifestations:
anorexia, gastrointestinal upset, poor skin turgor, dry mucous membranes, blood pressure changes, pulse changes, edema, headache, lethargy, confusion, diminished deep tendon reflexes, muscle weakness seizures, and coma
Hyponatremia Treatment:
limit fluids and increase dietary sodium
Chloride
Normal range: 98-108 mEq/L
Mineral electrolyte
Major extracellular anion
Found in gastric secretions, pancreatic juices, bile, and cerebrospinal fluid
Plays a role in acid-base balance
Main source is dietary intake
Excreted through the kidneys
Hyperchloremia
Chloride > 108 mEq/L
Hyperchloremia Causes
Increased chloride intake or exchange:
hypernatremia, hypertonic intravenous solution, metabolic acidosis, and hyperkalemia
Decreased chloride excretion:
hyperparathyroidism, hyperaldosteronism, and renal failure
Hypochloremia
Chloride < 98 mEq/L
Hypochloremia Causes
Decreased chloride intake or exchange: hyponatremia, administration of 5% dextrose in water intravenous solution, water intoxication, and hypokalemia Increased chloride excretion: diuretics, vomiting, metabolic alkalosis, and other gastrointestinal losses
Hypochloremia Treatment:
identify and manage underlying cause, sodium replacement (oral or intravenous), ammonium chloride, and saline irrigation of gastric tubes
Potassium
Normal range: 3.5-5 mEq/L.
The primary intracellular cation.
Plays a role in electrical conduction, acid-base balance, and metabolism.
Main source is dietary intake.
Excreted through the kidneys and gastrointestinal tract.
Serum potassium cannot fluctuate much without causing serious issue.
Hyperkalemia
Potassium > 5 mEq/L
Hyperkalemia Causes
Deficient excretion: renal failure,
Addison's disease, certain medications, and Gordon's syndrome
Excessive intake: oral potassium supplements, salt substitutes, and rapid intravenous administration of diluted potassium
Increased release from cells: acidosis, blood transfusions, and burns or any other cellular injuries
Hyperkalemia Manifestions:
paresthesia, muscle weakness, flaccid paralysis, bradycardia, dysrhythmias, electrocardiogram changes, cardiac arrest, respiratory depression, abdominal cramping, nausea, and diarrhea
Hyperkalemia Treatment:
Correct acidosis, usually with sodium bicarbonate Calcium gluconate to minimize dysrhythmias
Decrease dietary potassium intake
Increase excretion by Dialysis Kayexalate Intravenous fluids
Potassium-losing diuretics
Facilitate cellular exchange
Insulin
Hypokalemia
Potassium < 3.5 mEq/L
Hypokalemia Causes
Excessive loss: vomiting, diarrhea, nasogastric suctioning, fistulas, laxatives, potassium-losing diuretics, Cushing's syndrome, and corticosteroids Deficient intake: malnutrition, extreme dieting, and alcoholism Increased shift into the cell: alkalosis and insulin excess
Hypokalemia Manifestations:
muscle weakness, paresthesia, hyporeflexia, leg cramps, weak and irregular pulse, hypotension, dysrhythmias, electrocardiogram changes, decreased bowel sounds, abdominal distension, constipation, ileus, and cardiac arrest
Hypokalemia Treatment:
identify and manage underlying cause along with potassium replacement (oral or intravenous)
Calcium
Normal range: 4-5 mEq/L
Mostly found in the bone and teeth
Plays a role in blood clotting, hormone secretion, receptor functions, nerve transmission, and muscular contraction
Has inverse relationship with phosphorus
Has synergistic relationship with magnesium
Main source is dietary intake.
Vitamin D aids absorption.
Regulated by Vitamin K Parathyroid hormone Calcitonin
Hypercalcemia
Calcium > 5 mEq/L
Hypercalcemia Causes:
Increased intake or release: calcium antacids, calcium supplements, cancer, immobilization, corticosteroids, vitamin D deficiency, and hypophosphatemia
Deficit excretion: renal failure, thiazide diuretics, and hyperparathyroidism
Hypercalcemia Manifestations:
dysrhythmias, electrocardiogram changes, personality changes, confusion, decreased memory, headache, lethargy, stupor, coma, muscle weakness, decreased deep tendon reflexes, anorexia, nausea, vomiting, constipation, abdominal pain, pancreatitis, renal calculi, polyuria, and dehydration
Hypercalcemia Treatment:
Identify and manage underlying cause
Manage symptoms
Phosphate Increase mobility
Calcitonin Intravenous fluids Diuretics
Hypocalcemia
Calcium < 4 mEq/L
Hypocalcemia Causes
Excessive losses: hypoparathyroidism, renal failure, hyperphosphatemia, alkalosis, pancreatitis, laxatives, diarrhea, and other medications
Deficient intake: decreased dietary intake, alcoholism, absorption disorders, and hypoalbuminemia
Hypocalcemia Manifestations:
dysrhythmias, electrocardiogram changes, increased bleeding tendencies, anxiety, confusion, depression, irritability, fatigue, lethargy, paresthesia, increased deep tendon reflexes, tremors, muscle spasms, seizures, laryngeal spasms, increased bowel sounds, abdominal cramping, and positive Trousseau's and Chvostek's signs
Нуросalcemia Treatment
Identify and manage underlying cause Calcium replacement (oral or intravenous) Vitamin D Decrease phosphorus
Phosphorus
Normal range: 2.5-4.5 mg/dL.
Mostly found in the bones; small amounts are in the bloodstream.
Plays a role in bone and tooth mineralization, cellular metabolism, acid base balance, and cell membrane formation.
Main source is dietary intake.
Excreted through the kidneys.
Hyperphosphatemia
Phosphorus > 4.5 mg/dL
Hyperphosphatemia Causes
Deficient excretion: renal failure, hypoparathyroidism, adrenal insufficiency, hypothyroidism, and laxatives Excessive intake or cellular exchange: cellular damage, hypocalcemia, and acidosis
Hypophosphatemia
Phosphorus < 2.5 mg/dL
Hypophosphatemia Causes
Excessive excretion or cellular exchange: renal failure, hyperparathyroidism, and alkalosis Deficient intake: malabsorption, vitamin D deficiency, magnesium and aluminum antacids, alcoholism, and decreased dietary intake
Hypophosphatemia Treatment:
Identify and manage the underlying cause Phosphorus replacement (oral or intravenous)
Magnesium
Normal range: 1.8-2.5 mEq/L.
An intracellular cation. Mostly stored in the bone and muscle.
Plays a role in muscle and nerve function, cardiac rhythm, immune function, bone strength, blood glucose management, blood pressure, energy metabolism, and protein synthesis.
Main source is dietary intake. Excreted through the kidneys.
Hypermagnesemia
Magnesium > 2.5 mEq/L
Hypomagnesemia
Magnesium < 1.8 mEq/L
Hypomagnesemia Treatment:
magnesium replacement (oral or intravenous)
Signs of Inflammation:
redness, heat, swelling, pain, loss of function
Hypersensitivity
Inflated response to antigen Leads to inflammation, which destroys healthy tissue Can be immediate or delayed
Hypersensitivity types:
Type I: IgE mediated
Type II: cytotoxic hypersensitivity reaction
Type III: immune complex-mediated
Type IV: delayed hypersensitivity reaction
Type I, IgE mediated
Produces an immediate response.
Local or systemic.
Allergen activates T-helper cells that stimulate B cells to produce IgE.
-IgE coats mast cells and basophils, sensitizing them to the allergen.
At next exposure, the antigen binds with the surface IgE, releasing mediators and triggering the complement system.
Repeated exposure to large doses of allergen is necessary to cause this response.
Type I, IgE mediated Examples:
Hay fever, food allergies, and anaphylaxis
Type I, IgE mediated Treatment
includes epinephrine, antihistamines, corticosteroids, and desensitizing injections.
Type II, cytotoxic hypersensitivity reaction
IgG or IgM type antibodies bind to antigen on individual's own cells.
Antigen may be intrinsic or extrinsic.
Recognition of these cells by macrophages triggers antibody production.
Lysis of cells occurs because of the activation of the complement and by phagocytosis.
Usually immediate responses.
Type II, cytotoxic hypersensitivity reaction Examples:
Blood transfusion reaction and erythroblastosis
Type II, cytotoxic hypersensitivity reaction Treatment
includes ensuring blood compatibility (transfusion) and administering medication to prevent maternal antibody development (Rho[D]).
Type III, immune complex-mediated hypersensitivity reaction
Circulating antigen
antibody complexes accumulate and are deposited in the tissue.
Triggers the complement system, causing inflammation.
Type III, immune complex-mediated hypersensitivity reaction Example:
Autoimmune conditions (e.g., systemic lupus erythematosus)
Type III and Type IV: Treatment
is disease specific.
Type IV, delayed hypersensitivity reaction
Cell-mediated rather than antibody-mediated involving the T cells.
Antigen presentation results in cytokine release, leading to inflammation.
Causes severe tissue injury and fibrosis
Type IV, delayed hypersensitivity reaction Examples:
Tuberculin skin testing, transplant reactions, and contact dermatitis
Immunodeficiency
Diminished or absent immune response
Renders the person susceptible to disease normally prevented
Opportunistic infections
May be acute or chronic Classifications Primary Secondary
HIV
Parasitic retrovirus that infects CD4 and macrophages upon entry
In the US, rates rising among women and African Americans
Transmission Blood and bodily fluids
HIV Type 1
is the most common strain.
HIV Type 2
is more common in West Africa; progresses to disease more slowly.
Verrucae
Warts caused by a number of human papillomaviruses. Can develop at any age and often resolve spontaneously.
Transmitted through direct skin contact between people or within the same person.
The human papillomavirus replicates in the skin cells, causing irregular thickening.
Varying color, shape, and texture depending on type
Herpes simplex type 1
Typically affects the lips, mouth, and face. Usually begins in childhood. Can involve the eyes, leading to conjunctivitis. Can result in meningoencephalitis. Transmitted by contact with infected saliva. The primary infection may be asymptomatic.
After the primary infection, the virus remains dormant in the sensory nerve ganglion to the trigeminal nerve until it is reactivated. Reactivation may be a result of an infection, stress, or sun exposure. When reactivated, causes painful blisters or ulcerations that are preceded by a burning or tingling sensation. The lesions resolve spontaneously within 3 weeks, but healing can be accelerated with administration of oral or topical antiviral agents.
Herpes zoster (shingles)
Caused by the varicella-zoster virus.
Appears in adulthood years after a primary infection of varicella in childhood.
The virus lies dormant on a cranial nerve or a spinal nerve dermatome until it is activated years later.
The virus affects this nerve only, giving the condition its typical unilateral manifestations.
Herpes zoster (shingles) Manifestations:
pain, paresthesia, a red or silvery vesicular rash that develops in a line over the area innervated by the affected nerve (one side of the head or torso), extremely sensitive skin, and pruritis. The rash may persist for weeks to months.
Herpes zoster (shingles) Complications: Treatment:
neuralgia and blindness. antivirals, antidepressants, and anticonvulsants.
Parasitic Infections Tinea
Causes several types of superficial fungal infections. These fungi typically grow in warm, moist places (e.g., showers). Typically manifests as a circular, erythematous rash accompanied by pruritus and burning.
Tinea capitis:
involving the scalp.
Common in school-aged children.
Hair loss at the site is common.
Tinea corporis:
involving the body
Tinea pedis:
involving the feet, especially the toes
Tinea unguium:
involving the nails, typically the toenails
Begins at the tip of one or two nails and then usually spreads to other nails
Turns nails white and then brown, causing them to thicken and crack
Treatment: topical and systemic antifungal agents
Bacterial Infections Impetigo
Common and highly contagious.
Can occur without an apparent skin breach, but typically arises from a break in the skin. Lesions usually begin as small vesicles that enlarge and rupture, forming the characteristic honey-colored crust. Can spread throughout the body through self-transfer of the exudate. Typically caused by staphylococci, which produce a toxin that attacks collagen and promotes spread. Other manifestations: pruritus and lymphadenopathy.
Psoriasis (1
Common chronic inflammatory condition that affects skin cell life cycle. Cellular proliferation is significantly increased, causing cells to build up too rapidly on the skin's surface. Normally takes weeks, but occurs over 3-4 days with psoriasis.
Buildup leads to thickening of the dermis and epidermis because dead cells cannot shed fast enough. The exact cause is unknown, but it is thought to be multifactorial (environmental, genetic, and immunological factors play a role). It can also be a result of an autoimmune in which T lymphocytes mistake process normal skin cells as foreign.
family tendency is observed. Onset is most frequently between 15 and 35 years of age, and may be sudden or gradual. Patient usually experiences remissions and exacerbations. Factors that trigger an exacerbation: bacteria or viral infections in any location, dry air or dry skin, skin injuries, certain medicines (e.g., antimalaria agents, beta-blockers, and lithium), stress, too little or too much sunlight, and excessive alcohol consumption.
Severity varies. May also have arthritis-psoriatic arthritis. May be severe in persons who have a weakened immune system. Begins as a small, red papule. Papules most often occur on the elbows, knees, and trunk, but they can appear anywhere.
Papules develop into one of the following lesions: Erythrodermic: intense erythema that covers a large area Guttate: small, pink-red spots Inverse: erythema and irritation that occurs in the armpits, groin, and skin folds Plaque: thick, red patches covered by flaky, silver-white scales (the most common type) Pustular: white blisters surrounded by red, irritated skin
Other manifestations: genital lesions in males, joint pain or aching, nail changes (e.g., thickening, yellow-brown spots, pits on the nail surface, and separation of the nail from the base), and dandruff
Atopic Dermatitis
Also called eczema
Chronic inflammatory condition triggered by an allergen
Has an inherited tendency
May be accompanied by asthma and allergic rhinitis Most common in infants and usually resolves by early adulthood
Characterized by remissions and exacerbations
Exact cause unknown, but may result from an immune system malfunction (similar to hypersensitivity reaction, i.e., IgE elevation present)
Atopic march theory
Atopic Dermatitis Complications
secondary bacterial skin infections, neurodermatitis (permanent scarring and discoloration from chronic scratching), and eye problems (e.g., conjunctivitis) May affect any area, but typically appears on the arms and behind the knees
Atopic Dermatitis Manifestations
Red to brownish-gray skin patches Pruritus, which may be severe, especially at night Vesicles Thickened (lichenified), cracked, or scaly skin Irritated, sensitive skin from scratching
Systemic Lupus Erythematosus
Chronic inflammatory autoimmune condition. May affect connective tissue of any body organ. Remission and exacerbations- -stressors tend to trigger. • Disease progression varies from mild to severe. More common in women, Asians, and African Americans. Cause is unclear, but it's thought that B cells are activated to produce autoantibodies and autoantigens that combine to form immune complexes, which attack the body's own tissues.
Systemic Lupus Erythematosus manifestations
Immunological phenomena Antinuclear antibody Neurological disorders (seizures/psychosis) - Malar rash (butterfly rash over cheeks) - Discoid rash (patchy redness that can cause scarring)
Systemic Lupus Erythematosus treatment
No cure only symptom management Stress management and health promotion behaviors - Pharmacological • NSAIDS, antimalarials, corticosteroids, immunosuppressants, and DMARDS Plasmapheresis Prognosis improves with early diagnosis and treatment.
Yeast infection candidiasis
A fungal infection typically on the skin or mucous membranes caused by candida.
Syphilis
is a bacterial infection usually spread by sexual contact. The disease starts as a painless sore - typically on your genitals, rectum or mouth. Syphilis spreads from person to person via skin or mucous membrane contact with these sores.
Parasitic Infections Scabies
Result of a mite infestation. Male mites fertilize the females and then die. Female mites burrow into the epidermis, laying eggs over a period of several weeks through a series of tracts. After laying the eggs, the female mites die. Larvae hatch from the eggs and migrate to the skin's surface.
Larvae burrow in search of nutrients and mature to repeat the cycle. Burrowing appears as small, light brown streaks on the skin. Burrowing and fecal matter left by the mites triggers the inflammatory process, leading to erythema and pruritus. Mites can only survive for short periods without a host, so transmission usually results from close contact. Treatment: topical treatments. [Show Less]