Final Flashcards
Total body water for newborn/infant
70% - 80%
Total body water for adult
50% - 60%
Total body water for older adult
55%
Most concerning for dehydration and fluid balance
Total body water comprised of
1/3 Extracellular fluid: interstitial and plasma
2/3 Intracellular fluid
Osmotic pressure
Force that attempts to balance the concentration of solute and water between intracellular and extracellular fluids
Water follows higher concentration of solutes
Isotonic
Solute and water concentration is the same on both sides of cell
Hypertonic
Solute concentration higher outside of cell than inside
Cell will shrink due to water leaving
Hypotonic
Solute concentration is lower outside the cell than inside
Cell will swell due to water entering
Isotonic fluids (IV)
Same osmolarity as body fluids NS 0.9% NaCl Lactated ringers Used for fluid replacement Monitor I and O; hydration status; electrolyte levels
Hypertonic fluids (IV)
Given for sodium and volume replacement
Monitor hydration: lung sounds
Monitor electrolytes, particularly sodium
Hypotonic fluids (IV)
D5W starts as isotonic until glucose is metabolized and becomes hypotonic
Glucose is needed but then must watch for adverse effects of hypotonic solution: edema
Normal serum concentration range for Calcium (Ca)
9 - 11 mg/dl
Normal serum concentration for Magnesium (Mg)
1.5 - 2.5 mEq/L
Normal serum concentration for Potassium (K)
3.5 -5 mEq/L
Normal serum concentration for Sodium (Na)
135 - 145 mEq/L
Sodium
Major extracellular cation
Regulates osmotic forces and water balance
Regulates acid-base balance
Facilitates nerve conduction and neuro-muscular function
Transport of substances across cellular membrane
Potassium
Major intracellular cation Maintains cell electrical neutrality Cardiac muscle contraction Transmission of nerve impulses Maintains acid-base balance
Calcium
Major role in cardiac action potential
Magnesium
Important in women’s health
Suppresses release of acetylcholine (low Mg = too much movement; high Mg = too little movement)
Filtration
Movement of ECF from intravascular space to interstitial space
Reabsorption
Movement of ECF from interstitial space to intravascular
Oncotic pressure
Osmotic pressure exerted by proteins (albumin)
Pulling force
Hydrostatic pressure
Generated by pressure of fluids on capillary walls
Pushing force
What forces favor filtration?
Capillary hydrostatic pressure: pushes fluid out of capillary and into interstitial space
Interstitial osmotic pressure: pulls fluid into interstitial space from capillary
What forces favor reabsorption?
Interstitial hydrostatic pressure: pushes fluid out of interstitial space into capillary
Capillary osmotic pressure: pulls fluid into capillary
Normal pH
7.35 - 7.45
Acid - Base balance
1 Carbonic acid (H2CO3) acid side = 20 bicarbonate ions (HCO3 -) basic side
Acid
Donates Hydrogen ion
Base
Absorbs Hydrogen ion
Relationship between hydrogen ions and pH
Inverse relationship
More H+ = lower pH (acidosis)
Less H+ = higher pH (alkalosis)
Alkalosis
pH above 7.45
Lower H+ Kicks up the pH
Acidosis
pH below 7.35
Higher H+ sliDes down the pH
3 Chemical Acid-Base buffers
Bicarbonate - Carbonic acid buffer (ECF) Protein buffer (ICF): hemoglobin absorbs/releases H+ Phosphate buffer (ICF): sodium phosphate absorbs/releases H+
Carbonic acid/ bicarbonate Buffer
If pH is high (alkalosis/basic), carbonic acid contributes H+ -> H+ increases causing pH to decrease
If pH is low (acidosis/acidic), bicarbonate will absorb H+ -> H+ decreases, causing pH to increase
Respiratory system: 2nd line buffer
Happens quickly If acidic (low pH), breath is faster and deeper to remove carbon dioxide from blood -> lowers H+ and increase pH If basic (high pH), breath is slower and shallower to add carbon dioxide to blood -> increases H+, causing pH to lower
Renal system: 2nd line buffer
Takes longer (hours to days)
- Secretes more or less H+ into renal tubule and out in urine: secreting more H+ lowers H+ in blood and increase pH; secreting less H+ increases H+ in blood and lowers pH
- Reabsorbs more or less bicarbonate: reabsorb more: more base = higher pH; reabsorb less: less base = lower pH
Range for pCO2
35 - 45 mmHg
Respiratory system
Range for HCO3-
22 - 26 mmHg
Kidney system
ROME
Respiratory Opposite
Lower pCO2 = Higher pH
Metabolic Equal
Lower HCO3- = Lower pH
Range for pO2
80 - 100 mmHg
First line of immune defense
Physical barriers Innate Epithelial cells E.g. skin, mucous membranes, cilia, normal flora Not specific/ No memory
2nd line of innate immunity
Inflammation Not specific In response to and proportional to degree of injury Immediate No memory
Adaptive immunity
3rd line: delayed response
Specific toward antigen
Memory
B cells
Humoral: from bone marrow
Antibodies
T cells
Crafted in lymphocytes
Cell mediated
Benefits of inflammation
Prevents infection and further damage
Self limiting
Prepares for healing: 1st step in wound healing
3 steps of inflammation
- Increased vascular permeability
- Recruitment and emigration of leukocytes
- Phagocytosis
What do mast cells release
Histamines: potent vasodilator; leads to itching, pain and swelling
Prostaglandins: vasodilator; chemotic factor, pain
Leukotrienes: chemotaxis
Chemotaxis
Calls other inflammatory cells to injury site
Leukotrienes
Prostaglandins
Vasodilation causes
Heat, redness and swelling
Leukotrienes
Chemotaxis: calls other inflammatory cells during phase 1 of inflammation
Antagonist drug: asthma reducer
Margination
Neutrophils stick to vessel wall
Emigration/ Diapedesis
Neutrophil exits blood vessel
4 steps of phagocytosis
- Recognition and adherence
- Engulfment and formation of phagosome
- Fusion with lysosome to form phagolysosome
- Destruction and digestion
Phagocytosis
Phase 3 of inflammation
Digestion of bacteria
By products of phagocytosis
Oxygen (free) radicals: can cause cell damage over long term
Three main hormones in pregnancy
Human chorionic gonadotropin (hCG), estrogen and progesterone
hCG
Produced by conceptus and placenta
Positive pregnancy test
Prevents involution of corpus luteum
Positive feedback loop: causes corpus luteum to secrete larger quantities of sex hormones (estrogen, progesterone)
Estrogen
Produced by corpus luteum and placenta
Helps with enlargement of uterus, breasts, external genitalia
Helps relax pelvic ligaments
Progesterone
Produced by corpus luteum
Role in nutrition of early embryo
Decreases uterine contractility so uterus can expand and not immediately contract back
Helps estrogen prepare breasts for lactation
Formation of placenta
Formed by trophoblastic cells around blastocyst
Fully formed by end of first trimester
Function of placenta
Provides nutrition to fetus and some immunity; excretes waste
All happens by diffusion
Flow of blood through placenta
Fetus has 1 umbilical vein and 2 umbilical arteries
Blood from placenta carried to fetus via umbilical vein to IVC and liver to right atrium to left atrium (bypass lungs) to left ventricle to aorta to body and out through umbilical arteries
Blood volume increase during pregnancy
30% by end of pregnancy
Hematocrit decreased by not anemia
Cardiac output increase during pregnancy
30 - 40 % by 27th week
Macrophages
Phagocyte
Clean up process in inflammation
Three inflammatory mediator cascades
Compliment System
Coagulation/ Clotting system
Kinin system
Complement system
Directs traffic
Destroys directly or indirectly by recruiting others
Activation of complement system
Classical pathway: antibodies
Alternate: infectious organisms
Lectin: other plasma proteins
Results of activation of complement system
Chemotaxis: calls phagocytes to area
Opsonization: Complement tags surfaces of bacteria to mark for phagocytes to destroy
Direct lysis of pathogens: destruction
Degranulation of mast cells: inflammatory mediators
Coagulation/ Clotting system activated by
Extrinsic: tissue injury
Intrinsic: Abnormal vessel wall
Components of kinin system
Coagulation/ Clotting system results in
Clot formation: fibrinogen
Migration of leukocytes
Chemotaxis
Increased permeability
Kinin system
Works closely with clotting system
Initiated by activation factors
Bradykinin (chemical)
Bradykinin
Vasodilation
Vascular permeability
Pain
Cytokines and Chemokins
Signaling molecules
Produced by macrophages and T helper cells
Involved in chemotaxis, recruitment, stimulation of leukocytes
Leukocytes
White blood cells
Which leukocytes are capable of phagocytosis
Neutrophils
Eosinophils
Basophils
Monocytes
Which leukocytes are not capable of phagocytosis
Lymphocytes
Neutrophils
"Early responder" Short lived Phagocytosis Release toxins Destroy bacteria Remove debris and dead cells
Eosinophils
“Fumigator”
Noted in allergic reactions and parasite infections
Regulate inflammatory response
Monocytes
"Disaster response" Macrophages Longer living Phagocytosis Secrete cytokines: signaling molecules Present antigens to activate T cells Clean up
Basophils
"Firefighters" Mast cells Allergic reactions Acute and chronic inflammation Wound healing Tame inflammation
Lymphocytes
"Special forces" Adaptive and innate Longest to mobilize Trained for specific tasks B-cells: able to produce antibodies T-cells: T4 (helper), T8 Natural killer cells: non-specific (innate immunity)
Systemic manifestations of inflammation
Fever: cytokines that are pyrogens
Leukocytosis: increase in circulating WBCs
Lab changes
Lab changes during inflammation
Plasma proteins produced by liver increase
Erythrocyte sedimentation rate
C-reactive protein: opsonin (tagger) to phagocytosis
3 Phases of Wound Healing
Inflammation: filling
Proliferation/new tissue: sealing
Remodeling and maturation: shrinking
Inflammation stage of wound healing
Coagulation Bring cells needed Fibrin mess of blood clot Degranulation of platelets: growth factor Macrophages: clear debris
Proliferation stage of wound healing
“Sealing”
3-4 days after injury, continues up to 2 weeks
Wound is sealed
Fibrin clot replaced by normal or scar tissue
Granulation tissue: new lymphatic vessels and new capillaries
Contraction begins
Remodeling/Maturation stage of wound healing
Begins several weeks after injury Normally complete within 2 years Fibroblast: deposit collagen for strength Tissue continues to regenerate Wound continues to contract
What causes dysfunctional wound healing
Ischemia: low blood supply Obesity: impaired leukocyte function Diabetes: impaired circulation Malnutrition Medications (steroids)
Gate control theory of pain
Only one impulse can make it through at a time
Neuromatrix theory of pain
Brain produces patterns of nerve impulses drawn from various inputs