total body water

intracellular fluid and extracellular fluid

intracellular fluid

fluid inside the cells

extracellular fluid

fluid outside the cells

intravascular and interstitial and transcellular and cerebrospinal fluids

sources of water

liquids

foods

cellular metabolism

losses of water

urine

feces

insensible losses (lungs and skin)

balance of water a electrolyets

thirst mechanism in the hypothalamus

antidiuretic hormone

aldosterone

atrial natriuretic peptide

capillary exchange

filtration

diffusion

active transport

osmosis

filtration

movement of fluid from blood to interstitial spaces

hydrostatic pressure (push)

osmotic pressure (pull)

diffusion

solutes down their concentration gradient

active transport

solute moved against their concentration gradient using ATP power

osmosis

movement of water down the "water" gradient, toward higher solute concentration

edema

excess fluid on the interstitial compartment causing swelling or enlargement of the tissues

localized or general

can interfere with venous return, arterial circulation, and cell function in the area

causes of edema

increased capillary hydrostatic pressure

loss of plasma proteins

obstruction of lymphatic circulation

increased capillary permeability

effects of edema

localized swelling

pitting edema

increased body weight

functional impairment of organs or joints

pain

impaired arterial circulation when sustained

poor dental impressions

skin susceptible to ulceration

dehydration

insufficient body fluid resulting from inadequate intake or excessive loss of fluid or a combination of both

fluid loss

measured by change in body weight; adjusted for age, body size, and condition

isotonic dehydration

proportionate loss of fluid and electrolytes

hypotonic dehydration

loss of more electrolytes than water, leaving ECF with lower plasma osmolality

hypertonic dehydration

loss of more fluids than electrolytes, leaving ECF with hight plasma osmolality

causes of dehydration

vomiting and diarrhea

excessive sweating with loss of sodium and water

diabetic ketoacidosis

insufficient water intake

use of concentrated infant formula

direct effects of dehydration

dry mucous membranes in mouth

decreased skin turgor or elasticity

lower blood pressure (low blood volume)

fatigue

increased hematocrit

decreasing mental function

compensation for dehydration

increased thirst

increased heart rate

constricting cutaneous blood vessels

produce less urine that is more concentrated

third-spacing

situation in which fluid shifts out of the blood and into a body cavity or tissue; it is no longer available as circulatory fluid

can occur with peritonitis or burns

sodium imblanaces

primary cation of ECF

active transport with Na+/K+ ATPase in cells maintain high in ECF

active secreted in mucus and body secretion

forms of NaCl and NaHCO3 in body

ingested in with food and fluids; lost in sweat, urine, feces

levels controlled by kidneys

important for maintain ECF volume

involved in nerve conduction and muscle contraction

causes of hyponatremia

Na+

loss: excessive sweating, vomiting, diarrhea

use of certain diuretic drugs and low Na+ diet

low aldosterone, excess ADH, adrenal insufficiency

early chronic renal failure

excess H2O intake

effects of hyponatremia

fatigue, muscle cramps, abdominal discomfort, or cramps with nausea and vomiting

impaired nerve conduction

fluid imbalances between compartments

fluid shift into cells

brain cells may swell

causes of hypernatremia

ingest large amounts of Na+

high H2O losses

insufficient ADH, large volumes of dilute urine

loss of thirst mechanism, not drinking

watery diarrhea

prolonged periods of rapid respiration

effects of hypernatremia

fluid out of cells

weakness, agitation

firm, subcutaneous tissue

increased thirst with dry, rough mucus membranes

decreased urine output due to normal ADH secretion

potassium imbalance

primary cation of ICF

active transport with Na+/K+ ATPase in cells to maintain low in ECF and high in ICF

ingested in with food

insulin promotes movement of K+ into cells

influenced by acid-base balance

abnormal K+ affects contractions of cardiac muscle and causes changes in ECG

causes of hypokalemia

excess losses from diarrhea

diuresis associated with certain diuretic drugs

excessive aldosterone or glucocorticoids in the body

decreased dietary intake

treatment of diabetic ketoacidosis with insulin

effects of hypokalemia

cardiac dysrhythmias and abnormal ECG patterns

fatigue and muscle weakness

paresthesias - pins and needles

decreased digestive tract motility

impaired renal function, failure to concentrate urine

severe deficits, respiratory muscles become weak, shallow respirations

causes of hyperkalemia

renal failure

aldosterone deficit

use of "potassium-sparing" diuretic durgs

leakage of intracellular K+ into ECF in patients with extensive tissue damage

displacement of K+ from cells by prolonged or severe acidosis

effects of hyperkalemia

cardiac dysrhythmias and abnormal ECG patterns

fatigue and muscle weakness

paresthesias - pins and needles

nausea

calcium imbalance

divalent cation of ECF

ingested in food; stored in bone, excreted in urine and feces

balance maintained by PTH and calcitonin

Ca2+ and phosphate ions have reciprocal relationship in the ECF

causes of hypocalcemia

hypoparathyroidism

malabsorption syndrome

deficit serum albumin

increased serum pH - alkalosis

renal failure

effects of hypocalcemia

muscle twitching, carpopedal spasm, hyperactive reflexes

chvostek sign

trousseau sign

laryngospasm

parethesias

weak heart contractions

causes of hypercalcemia

neoplasms; malignant bone tumors

hyperparathyroidism

immobility or decreased stress on bone

increased intake of Ca2+ from more vit D intake

milk-alkali syndrome

effects of hypercalcemia

depress neuromuscular activity

stupor, anorexia, nausea

personality changes

interferes with ADH in kidneys causing polyuria

increased strength of cardiac contractions and dysrhythmias develop

may contribute to kidney stones

magnesium imbalance

divalent cation of the ICF

50% stored in bone

serum levels linked to K+ and Ca2+ levels

imbalances are rare

causes of hypomagnesemia

malabsorption or malnutrition

use of diuretics; diabetic ketoacidosis; hyperparathyroidism; hyperaldosteronism

effects of hypomagnesemia

neuromuscular irritability; tremors of chorea; insomnia; personality changes; increased heart rate with arrhythmias

cause of hypermagnesemia

renal failure

effects of hypermagnesemia

depressed neuromuscular function; decreased reflexes; lethargy; cardiac arrhythmias

phosphate imbalance

divalent anion; located in bone

functions in bone and tooth mineralization; metabolic processes; phosphate buffer system and removal of H+ through kidneys

causes of hypophosphatemia

malabsorption; diarrhea; excessive use of antacids; alkalosis; hyperparathyroidism

effects of hypophosphatemia

tremors; weak reflexes; paresthesias; confusion and stupor; anorexia; dysphagia; poor blood cell function

causes of hyperphosphatemia

renal failure; tissue damage or chemotherapy that releases intracellular phosphate

effects of hyperphosphatemia

same manifestations as that for hypocalcemia

buffer systems

combination of a weak acid and its alkaline salt; components react with acids or alkali in blood

four main buffer pairs

sodium bicarbonate and carbonic acid

phosphate system

hemoglobin system

protein system

bicarbonate - carbonic acid buffer system

catalyzed by carbonic anhydrase in blood, lungs, kidneys

ratio of bicarbonate to carbonic acid must be 20:1 to maintain pH 7.35-7.45

respiratory system

chemoreceptors detect increase in CO2 or decrease in pH, stimulate increased respiratory rate to drive off more CO2; raises blood pH

in alkalosis, respiratory rate reduced and more CO2 retained; lowering blood pH

renal system

exchange Na+ with H+ under influence of aldosterone

diagnostic tests for acid-base imbalance

arterial blood gases

base excess or deficit

anion gap

respiratory acidosis

increased CO2 from respiratory problems

acute causes of respiratory acidosis

pneumonia; airway obstruction; chest injuries; patient taking opiates

chronic causes of respiratory acidosis

chronic obstructive pulmonary disease like emphysema

metabolic acidosis

decreased availability of bicarbonate ions

causes of metabolic acidosis

excessive bicarbonate loss from diarrhea, nonvolatile acid production high; renal disease or renal failure, H+ not secreted and bicarbonate not reabsorbed

respiratory alkalosis

hyperventilation caused by anxiety, high fever, or aspirin overdose

re-breathing expired air in a paper bag can help retain CO2 to lower blood pH

metabolic alkalosis

early stage of vomiting, hypokalemia, excessive antacid intake

compensation of acid-base imbalance

the cause of the imbalance determines the first change in the ratio

compensation is assessed by subsequent change in second part of the ratio

decompensation

life-threatening condition

the kidneys and lungs cannot compensate

serum pH moves out of normal range

can result from confounding factors involved such as infection or dehydration

first line of defense

nonspecific mechanical barrier

skin, mucous membranes

body secretions

second line of defense

nonspecific types of inflammation and phagocytosis

third line of defense

specific defense mechanism

stimulates production of unique antibodies or sensitized lymphocytes

inflammation causes

direct, physical damage

caustic chemicals

ischemia or infarction

allergic reactions

extreme temperatures

foreign bodies

infection

basic steps of inflammatory process

injury to capillaries and tissue cells

bradykinin released from injured cells that activates pain receptors

sensation of pain stimulates mast cell and basophils to release histamine

bradykinin and histamine cause capillary dilation, increased blood flow and permeability

break in the skin allows bacteria to enter tissue

neutrophils and macrophages phagocytize bacteria

review of normal capillary exchange

pre-capillary sphincters regulate blood flow to capillary beds

movement of fluid and solutes based on net hydrostatic pressure and relative osmotic pressures of blood and interstitial fluid

arterial end

fluid pushed out due to high hydrostatic pressure in capillary and low hydrostatic pressure of interstitial space

venous end

fluid drawn in due to higher osmotic pressure of blood than that of the interstitial fluid

capillary exchange with inflammation

injured cells release chemical mediators that cause vasodilation

chemical mediators also increase capillary permeability

protein, water, electrolytes leave capillary, from exudate

leukocytes leave capillary and move to site of injury to begin phagocytosis of foreign material

vascular response in acute inflammation

due to chemical mediators released in response to damage

cause local vasodilation and increased capillary permeability

redness and warmth

immediate action in vascular response of acute inflammation

histamine from mast cell granules; kinins and complement system from plasma protein activation

later effects in vascular response of acute inflammation

leukotrienes and prostaglandins synthesized from arachidonic acid in mast cells

cellular response of acute inflammation

white blood cells attracted by chemotaxis

mast cells release chemotactic factors

neutrophils attracted to injury site

phagocytosis of foreign matter

exudate

collection of interstitial fluid formed in inflamed area

serous exudate

watery, fluid with protein and white blood cells

fibrinous exudate

thick and sticky; high cell and fibrin content; increases risk of scar tissue

purulent exudate

thick, yellowish green; leukocytes, cell debris, microbes, bacterial infection; pus

abscess exudate

localize pocket of purulent exudate in solid tissue

hemorrhagic exudate

blood vessels damaged

general manifestations of acute inflammation

mild fever, malaise, fatigue, headache, anorexia

cause of fever

release of pyrogens from macrophages, signaling hypothalamus to reset internal thermostat to hight temperature

leukocytosis

increased number of white blood cells, especially neutrophils

differential count

proportion of each type of white blood cell altered, depending on cause

plasma proteins

increased fibrinogen and prothronmbin

erythrocyte sedimentation rate

elevated plasma proteins increase the rate at which red blood cells settle in a sample

c-reactive protein

a protein not normally found in blood, appears with acute inflammation and necrosis within 24 to 48 hours

cell enzymes

released from necrotic cells and enter tissue fluids and blood; specific enzymes may indicate the site of inflammation

potential complications of acute inflammation

ulcers, local complications, infections, skeletal muscle spasms

chronic inflammation

develops from unresolved acute episode

less swelling and exudate

more lymphocytes, macrophages, and fibroblasts

more tissue destruction

more collagen production

complications of chronic inflammation

arthritis in joints

deep ulcers that may perforate the viscera

extensive scar tissue

aspirin

acetylsalicylic acid

decreases prostaglandin synthesis at site of inflammation; reduces pain and fever

never for children

some people are allergic

gastrointestinal distress and interferes with blood clotting

acetaminophen

tylenol or paracetamol

analgesic, antipyretic, not anti-inflammatory

NSAIDS

analgesic, antipyretic, anti-inflammatory

ibuprofen

some are allergic, delays blood clotting, risk of gastrointestinal distress and gastric ulcers

NSAID COX-2 inhibitor

anti-inflammatory; analgesic

similar negative effects as aspirin and NSAIDS

edema/increased blood pressure

corticosteroids

anti-inflammatory drugs

decrease capillary permeability; enhancement of epinephrine and norepinephrine to stabilize vasculature

reduce number of leukocytes and mast cells at site, decreasing release of histamine and prostaglandins

adverse effects of corticosteroids

atrophy of lymphoid tissue; catabolic effects on tissues; delayed healing; delayed growth in children; retention of sodium and water leading to high BP and edema

anti-inflammatory herbs and spices

turmeric

black pepper

ginger root

rosemary

RICE

rest ice compression elevation

first aid measures

RICE

mold, moderate exercise can help blood flow

elevation and compression can help mediate swelling

types of healing

resolution

regeneration

replacement

healing by first intention

healing by second intention

resolution

minimal tissue damage; damaged cells recover and tissue returns to normal after a short period

regeneration

cells of damaged tissue can undergo mitosis; damaged tissue replaced by identical cells generated by cells

replacement

extensive tissue damage, cells not capable of mitosis; replaced by connective tissue

healing by first intention

clean wound, no necrotic tissue, edges held together with minimal gap and minimal scar

healing by second intention

large wound, more inflammation, longer healing period, more scarring

healing process

blood clot forms and seals area

inflammation develops in surrounding area

granulation tissue grows into gap

epithelial cells undergo mitosis

fibroblasts and connective tissue cells enter area

scar tissue remains

factors promoting healing

youth

good nutrition

adequate hemoglobin

effective circulation

clean, undisturbed wound

no infection

factors delaying healing

advanced age; reduced mitosis

poor nutrition, dehydration

anemia

circulatory problems

certain chronic diseases

irritation

infection

chemotherapy treatment

prolonged use of glucocorticoids

complications due to scar formation

loss of function

contractures and obstruction

adhesions

hypertrophic scar tissue

ulcerations

burn

a thermal or non-thermal injury that causing acute inflammation and tissue destruction

classification of burns

classified by depth of skin damage and percentage of body surface area involved

first-degree burn

superficial burn

damage to epidermis

heals without scar; sunburn, mild scald

second-degree burn

partial thickness burn

destruction of epidermis and part of dermis

red, edematous, blistered, hypersensitivity

easily infected; cause scarring

third-degree burn

destruction of all skin layers

wound coagulated and charred

damaged tissue shrinks causing pressure on edematous tissue beneath

escharotomy

requires skin grafting for healing

effects of burn injury

shock

respiratory problems

pain

infection

metabolic needs

healing of burns

immediate covering; nonstick dressing

large areas - stretch skin graft

synthetic or biosynthetic substitutes

goal to minimize scar tissue formation

physiotherapy and occupational therapy to reduce effects of scar tissue

burns in children

growth of children effected during hyper-metabolism of burn recovery

thin skin easily burned in hot water for baths

additional surgery for grafts required to accommodate growth