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109 Cards in this Set
- Front
- Back
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What are the components of air?
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Mostly nitrogen
oxygen carbon dioxide water vapor |
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What is Dalton's Law?
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The sum of all the gases in the air which equals atmospheric pressure
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What is partial pressure?
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the separate contribution of each gas in the air
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What variables affect efficiency of alveolar gas exchange?
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-pressure gradients of gases
-solubility of the gases -membrane thickness -membrane area -ventilation-perfusion coupling |
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Pressure gradients of blood entering and leaving the lungs
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Entering:
pp of oxygen: 40 mm Hg pp of carbon dioxide: 46 mm Hg Leaving: pp of oxygen: 95 mm Hg pp of carbon dioxide: 40 mm Hg |
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Alveolar air- what gas does it have a high concentration of?
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higher carbon dioxide, lower oxygen
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Solubility of oxygen and carbon dioxide
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Carbon dioxide is about 20 times more soluble than oxygen
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How does pressure gradient and solubility affect the amount of exchange of oxygen and carbon dioxide?
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***equal amounts of the two gases are exchanged since carbon dioxide is more soluble and oxygen has a higher pressure gradient
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How does membrane thickness affect gas exchange?
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It's very thin- gas exchange is not difficult (in normal healthy conditions)
**however, with heart conditions like left ventricular failure, blood backs up into lungs promoting capillary filtration into connective tissues= causes thickness of respiratory membrane and gas exchange difficult to impossible |
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How does membrane surface area affect affect gas exchange?
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The more membrane surface area, the more gas exchange.
This is decreased by pulmonary disease such as emphysema and lung cancer *decreased membrane surface area of the lungs= low blood partial pressure of oxygen |
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What is ventilation-perfusion coupling and how does it relate to gas exchange?
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It is the ability to match ventilation and perfusion to each other- depending on the amt of oxygen available to one aveoli, the perfusion to that alveoli will adjust- ie: alveoli with great amt of oxygen will have greater perfusion
*a VQ scan measures this to make sure that ventilation and perfusion match -a pulmonary embolis- obstruction of pulmonary artery would affect this |
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What is gas transport?
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The transportation of oxygen and carbon dioxide from the alveoli to the systemic tissues and vice versa
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How is oxygen transported?
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Oxygen is transported by the protein hemoglobin which is present in red blood cells
-Hemoglobin contains 4 protein chains each with 1 heme group- each heme group can carry one oxygen molecule... so 1 hemoglobin= carries 4 oxygen *hemoglobin carrying bound oxygen is called OXYHEMOGLOBIN |
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Explain the Oxyhemoglobin dissociation curve
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It is the relationship btw hemoglobin saturation and partial pressure of oxygen
*@ low pp of oxygen, the curve rises slowly then a rapid increase as oxygen is loading- it plateaus when hemoglobin is full and all 4 heme groups are occupied |
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what form is carbon dioxide transported in?
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In 3 forms:
1. Carbonic acid - 90% 2. Carbamino compounds- 5% 3. Dissolved gas - 5% |
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What is carbonic acid?
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One of the forms that carbon dioxide is transported in (about 90%)
-Carbon dioxide is hydrated to form carbonic acid which dissociates into bicarbonate and hydrogen ions |
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What are carbamino compounds?
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One of the forms that carbon dioxide is transported in (5%)
-Carbon dioxide binds to an amino group of plasma proteins and hemoglobin to for carbamino compounds |
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How is the remaining 5% of carbon dioxide in the blood transported if not by carbonic acid or carbamino compounds?
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The remaining 5% of carbon dioxide is transported as dissolved gas in the blood
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What is the very general breakdown of gas exchange at the alveoli and the systemic tissues?
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@ alveoli- oxygen comes into the blood, CO2 leaves the blood
@ systemic tissues- oxygen leaves the blood to enter tissues, CO2 enters the blood |
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What is carbon dioxide loading?
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Tissue fluid has a relatively high pp of carbon dioxide (since aerobic resp. produces a molecule of CO2 for ever molecule of oxygen it consumes
*Carbon dioxide diffuses into the blood stream from the systemic tissues where it is transported as 3 forms (carbonic acid, carbamino group, dissolved gas) |
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What is oxygen unloading?
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*Oxygen diffuses from the blood into the tissue fluid
-H binds to oxyhemoglobin, reducing the affinity of hemoglobin for oxygen which makes hemoglobin release the oxygen -when blood arrives at the systemic capillaries its oxygen concentration is 20 ml/dl, hemoglobin is 97% saturated -as blood leaves the capillaries of a resting tissue, oxygen conc is 15 ml/dl, hemoglobin is 75% saturated -venous reserve remains in blood |
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What is venous reserve?
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The oxygen remaining in the blood after oxygen unloading in the systemic tissues (about 15-20% saturation of hemoglobin)
*this can sustain life for 4-5 minutes in the event of respiratory arrest |
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How much water is in the body of a young adult and what are the two percentages?
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40 L
65% intracellular fluid 35% extracellular fluid -water moves osmotically from one fluid compartment to another so that osmolarities of the ECF & ICF seldom differ |
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What is the average amt of water gained and lost on daily basis? How is this water gained and lost?
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2500 mL
gained: metabolism (reabsorbed by large intestine) & by ingestion of food and drink lost: urine, feces, expired breath and sweat |
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How is fluid intake governed?
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By the thirst center in the hypothalamus
-center responds to release of angiotensin II -causes the release of ADH (increases water reabsorption- just water not Na) -signals from osmoreceptor neurons monitor blood osmolarity |
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How is fluid loss governed?
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Mainly by factors that control urine output
-ADH secreted in response to dehydration= reduces urine output |
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What is fluid deficiency?
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when fluid output exceeds fluid input
Occurs with: -Volume depletion (hypovolemia) when total body water is reduced but osmolarity is normal (severe hemorrhage) -Dehydration- volume is reduced and osmolarity is elevated (sweating profusely= losing water AND Na- if only replaced with water, extracellular Na conc becomes very low- water rushes into cells and they lyse) |
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What role does sodium play in electrolyte balance?
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It's the major cation of the ECF
-important in osmotic and fluid balance -nerve and muscle activity (depolarization) -Cotransport (binds with another molecule) -Acid-base balance -Heat generation |
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What is a normal level of sodium and how is it maintained?
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Btw 130-145 mE/L
-Aldosterone promotes Na reabsoption -ADH reduces Na concentration |
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What is Hypernatremia?
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Excess sodium (greater than 145 mE/L)
-Causes water retention, hypertension (high blood pressure) and edema |
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What is Hyponatremia?
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Sodium deficiency (less than 130 mE/L)
results from hypotonic hydration (losing too much water and Na and only replacing it with water- cells lyse) |
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What is Potassium's role in electrolyte balance?
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It is the major cation of the ICF
*excretion of K+ promoted by aldosterone -important in osmotic and fluid balance -nerve and muscle activity (depolarization) -Cotransport (binds with another molecule) -Acid-base balance -Heat generation -cofactor for some enzymes |
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What is Hyperkalemia?
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Excess potassium (greater than 5.5 mE/L)
-can cause nerve muscle dysfunction -cardiac arrest (causes PVCs- resting membrane pot. becomes less neg, heart contracts too soon, looses strength, becomes flaccid) |
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What is Hypokalemia?
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Potassium deficiency (less than 3.5 mE/L
-inhibits nerve function -inhibits muscle function *can be caused by blood pressure medication (diuretic) -causes muscle cramps (sign of K+ deficiency) |
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What is Chloride's role in electrolyte balance?
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It is the major anion of the ECF
*chloride follows Na and is regulated by Na homeostasis Important in: -osmotic balance -formation of stomach acid -respiratory and renal function (chloride shift mechanism) |
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What happens when there is a chloride imbalance?
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pH becomes imbalanced
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What is Ca necessary for?
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-muscle contraction
-nerve transmission -blood clotting -hormone action -bone and tooth formation *regulated by PTH and Calcitonin |
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What is Hypercalcemia?
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excess Ca+ (greater than 5.8 mE/L)
-causes muscle weakness -depressed reflexes -cardiac arrhythmias |
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What is Hypocalcemia?
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Ca+ deficiency (less than 4.5 mE/L)
-Fatal tetany (low Ca causes increased inward flow through Na channels bringing membrane potential closer to threshold causing involuntary contractions of heart) |
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What is normal pH level of the ECF?
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7.4
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What affects the balance of pH?
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The tendency of weak and strong acids to give up H ions and weak and strong bases to absorb H ions
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What is a buffer system?
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any system that resists changes in pH by converting a strong acid or base into a weak one
Physiological systems: urinary (kidneys- most important) and respiratory Chemical systems: bicarbonate, phosphate and protein |
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How does the respiratory system balance acids and bases?
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It buffers pH by adjusting pulmonary ventilation
-reduced ventilation allows carbon dioxide to accumulate in blood, LOWERING pH -increased ventilation expels carbon dioxide too quickly, lowering H concentration and RAISING pH |
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What are the kidneys role in acid-base balance?
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They neutralize more acid and base than any other buffer system
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What is acidosis?
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A pH lower than 7.35
2 types: -Respiratory Acidosis: occurs when pulmonary gas exchange is insufficient and CO2 accumulates faster than the body can expel it -Metabolic acidosis: the result of lactic acid or ketone accumulation, ingestion of acidic drugs (aspirin), loss of bases (diarrhea) |
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What is alkalosis?
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pH greater than 7.45
2 types: -Respiratory alkalosis: results from hyperventilation (stress, anxiety, panic attacks) -Metabolic alkalosis: rare- can be caused by overuse of antacids or loss of stomach acids through vomiting |
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What is uncompensated acidosis or alkalosis?
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when the pH imbalance in the body cannot be corrected by the body's homeostasis
-requires clinical intervention -respiratory compensation: change in pulmonary ventilation -renal compensation: changes in hydrogen secretion |
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What is the definition of pain?
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an unpleasant sensory and emotional experience associated with actual or potential tissue damage
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Is pain subjective or objective?
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It is SUBJECTIVE - different people handle pain in different ways
Multidimensional: biological factors, psychological factors, social factors |
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What are the dimensions of pain?
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Pain is multidimensional: biological factors, psychological factors, social factors
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Is pain difficult to treat?
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Yes. PTs are not pain specialists, we control pain related to movement problems
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What are the Melzack and Casey 3 dimensions of pain?
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-Sensory-discriminative: quality of pain (burning, sharp, aching, dull) location, duration, and intensity
-Motivational-effective: concerned with its unpleasantness and our tendency to escape (become a victim) or attack the pain -Cognitive-evaluative: past experience and the outcome of different response strategies |
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What is acute pain?
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Acute pain: protective- warning sign that body is experiencing actual or potential tissue damage
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What is Allodynia?
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Pain resulting from a stimulus that doesn't usually cause pain
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What is Hyperalgesia?
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an increased response to something that is normally painful
-Primary: occurs at site of tissue damage -Secondary: occurs outside of the site of tissue damage |
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What is Hypoalgesia?
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Diminished pain in response to stimulation that would normally be painful
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What is Referred pain?
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Pain outside the area of tissue damage (ie: heart attack- feel pain in arm or back)
* most important type of pain for PTs to know about |
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What is Radicular pain?
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pain that follows a dermatomal pattern secondary to a nerve compression (ie: sciatica)
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Types of Muscle pain
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-Myofascial pain
-Fibromyalgia -Myositis -Strain |
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Types of Joint pain
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-Acute: after injuries to ligaments or joint capsule
-Chronic: after osteoarthritis or rheumatoid arthritis |
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Where do sprains and strains happen?
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Sprains happen in ligaments
Strains happen in muscle |
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How does pain travel through the peripheral pathways? (starting from injury)
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Following joint or muscle inflammation, sensitization of primary afferent (sensory) fibers occurs
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What is sensitization?
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In response to inflammation of tissues
results in: -an increase in spontaneous activity -decrease in threshold of response to noxious stimuli -an increased response to that same noxious stimuli |
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Substances released by inflammatory cells to sensitize primary afferent fibers
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*all make pain fibers hypersensitive
Serotonin: released from platelets- activates muscle nociceptors and causes pain in humans Bradykinin: released from plasma after tissue injury, sensitizes nociceptors and produces pain Prostaglandins: metabolites of arachadonic acid, produced in response to tissue injury Cytonkines |
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Central pathways of pain
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-Spinal cord
-Ascending facilitatory pathways -Descending facilitatory pathways -Descending inhibitory pathways |
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What is gate control theory?
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Activation of Large Diameter Afferent (sensory) Fibers by pressure, proprioception, touch or vibration- inhibits transmission of pain by small afferent fibers (ie: massage- stops travel of pain)
-this happens by the excitation of an inhibitory interneuron in spinal cord (inhibits c-fibers) |
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What is Chronic pain?
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Chronic pain: non protective, serves no biological purpose (not coming from tissue damage) **has a psychological aspect= the longer the pain is there, the less likely it is to go away
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Types of pain
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Mechanical pain: pain that you can alter w/mvmt (ie: give patient exercises, manipulate patient- does this increase or decrease the pain?)
Chemical pain: inflammatory response (histamine, bradykinin) *treated with rest, ice, massage, heat etc Neurogenic pain: when there is a central component to the pain (CNS becomes hypersensitive to the pain- chronic pain) *body starts to think the pain will always be there |
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What is wound healing?
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The process to restore normal tissue architecture and function with minimal scar tissue
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What are the processes involved in wound healing?
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*similar in all types of wounds
Molecular processes Cellular processes Vascular processes |
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Phases of wound healing
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*these phases are not exclusive of each other, they overlap
-Inflammatory response: acute or chronic -Repair phase (proliferation) -Remodeling phase |
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What is Acute Inflammatory Response?
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Essential component of healing
Vasoconstriction, vasodilation, edema Platelets, Neutrophils, Monocytes/Macrophages, Lymphocytes -allows for recruitment of leukocytes (WBCs) for phagocytosis of pathogens and damaged tissue Typically lasts 24-48 hours -usually complete in 2 weeks -Cardinal signs: redness, swell, heat & pain -Redness swelling and heat are secondary reactions to vasodilation and increases permeability -Pain (caused by swelling) |
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What are the signs of infection?
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FEVER
also: Puss, oozing, odor at wound |
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What happens during the acute inflammatory response on a cellular level?
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-swelling allows for recruitment of leukocytes (WBCs) for phagocytosis of pathogens and damaged tissue
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What is the vascular reaction to the acute inflammatory response?
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Immediately after injury:
-vasconstriction to slow bleeding & allow platelets to gather -vasoconstriction stimulates release of NE and seratonin -vasodilation occurs= increased permeability and edema- brings WBCs to wound site |
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What substances mediate the Vascular Reaction of acute inflammatory response?
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Kinins
Prostaglandins Leukotrines Histamine Bradykinins *Medications (anti-inflammatory) often over-prescribed by Dr., patients suppress inflammatory response too much |
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Transudate vs. Exudate
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Transudate is fluid from the wound that is clear, no cells
Exudate is puss, lymph and WBCs (infection) |
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Platelets
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Part of the cellular response to acute inflammatory response
-first cells to appear when wound occurs -bind to exposed fibrillar collagen to initiate coagulation *clotting begins as prothrombin is converted to thrombin--> fibrinogen ---> fibrin *fibrin forms matrix of mesh which forms clot |
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Neutrophils/Monocytes
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Neutrolphils are the first WBCs to site of wound
-appear 1 hours after wound and peak at 24-48 hours after -pick up dead cells to fight infection Monocytes are drawn to wound 48-96 hours after injury -quickly transform into macrophages (eat debris) |
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Macrophages
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*Most important cells for healing
-main cells responsible for removing dead tissue -recycle important amino acids (to use in synthesis of new collagen) |
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Lymphocytes
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Various types of Lymphocytes- immunological component of healing
-T-lymphocytes & B-lymphocytes play small role -more prominent in chronic inflammation, not acute -arrive 5 days after wound -peak in number by 7th day -not required for initiation of wound healing but essential for normal repair |
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What is Chronic inflammation?
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Caused by
-repetitive microtrauma (overuse) -autoimmune response *not associated with cardinal signs of inflammation (redness, swelling, heat) *predominant cell types found: lymphocytes and macrophages |
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Steps of Repair Phase
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1. Granulation Tissue Formation
2. Fibroplasia 3. Angiogenesis 4. Re-Epithelialization |
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What happens during Granulation Tissue Formation?
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Fibrin matrix is replaced by granulation tissue
-formed by: fibroplasia (collagen produces fibroblasts- go to wound site) & angiogenesis (re-oxygenation) -Granulation tissue: macrophages, fibroblasts, myofibroblasts (collagen formation) |
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What does Granulation Tissue consist of?
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Collagen
Ground Substance Hyaluronic Acid Proteoglycans -has a cobbled appearance due to underlying angiogenic (re-oxygenation) capillary beds |
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What is Fibroplasia?
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A step in Repair Phase
-formation of fibrous tissue -Begins as fibroblasts draw to wound (5-7 days after) -fibroblasts ---> myofibroblasts (major role: contain actin filaments & huge amts of RER for protein synthesis) |
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What role does Type III collagen play in wound healing?
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-Type III collagen first appears 48-72 hours after injury
-stimulated by hypoxic conditions (low amts of blood) = chronic wounds have excess fibrosis -highly unorganized -yields poor wound strength -replaced by Type I collagen during remodeling phase |
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Angiogenesis
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growth of new blood vessels
Occurs in response to: -tissue hypoxia -cytokine release during injury moist environment is essential= KERATINOCYTES migration is the main factor in this stage -keratinocytes draw moisture to environment |
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What are Cytokines
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chemicals released in response to low oxygen
-stimulatory cytokines for angiogenesis synthesized by: platelets, macrophages, fibroblasts |
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Re-Epithelialization
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concurrent with formation of granulation tissue (as granulation tissue forms it undergoes re-epithelialization
*keratinocyte transformation takes place at free edge of wound -migration occurs over framework or granulation tissue and cells move from periphery to center of wound -cells slide over one another to center of wound to close it up -complete re-epithelialization is crucial for continuation of repair and remodeling phases |
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What is the Remodeling phase?
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balance btw tissue synthesis and degradation
****collagen conversion from type III to type I- most important part of remodeling phase -wound contraction -scar formation |
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What is collagen conversion?
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part of remodeling phase
-collagen converts from type III to type I -converted via enzyme released by fibroblasts and macrophages -oxygen necessary -conversion won't happen without stress/strain on tissue (PTs responsible for applying stress/strain) |
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What is wound contraction?
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process by which wounds close
*mediated by Epi, NE, Bradykinins -contraction of actin filaments brings collagen fibers closer together -effector cell myofibroblasts bind to adjacent collagen -this process reduces wound size by about 40% |
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Stages of scar formation
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Stage I: weak scar, prone to rupture, initial stage (days 2-4)
Stage II: (*btw repair & remodeling phase) -inc. fibroplasia -conversion of collagen -wound contraction begins -GREATEST responsiveness to intervention* most important phase for PTs to make change to tissue -Days 5-21 Stage III: scar consolidation, remodeling begins to decrease, responsiveness to intervention diminishes, days 21-60 Stage IV: scar maturation, remodeling begins to cease, least responsive time, 60-360 days |
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What type of cartilage is most frequently injured?
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Hyaline cartilage (bc its in all synovial joints)
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Types of collagen
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Type I- most common in body- strongest- type III converts to this
Type II- type of collagen in articular cartilage Type III- initial collage laid down in wound healing- converts to type I |
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How does articular cartilage heal?
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intervention- will not heal on its own due to avascular quality (gains nutrition through osmosis and diffusion from bone- mvmt needed to increase diffusion
*when wb is not allowed, motion must occur to preserve art cartilage -during immobilization, art. cart. begins to degrade- most of the time braced in extension to maintain neutral allignment (however, bracing in extension may lead to irreversible and progressive Osteoarthritis) *Remobilization-moderate activity promotes cartilage thickening (strenuous can cause damage) |
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Articular cartilage healing time
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-48 Hours fibrin clot forms
-5 days fibroblasts combine w/collagen to replace clot -2 weeks fibroblasts differentiate, chondrocytes appear -1 month fibroblasts completely differentiated -2 months satisfactory repair type I collagen -6 months type I and type II collagen ***6 months to a year for full healing to take place |
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How do ligaments heal?
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ligaments remodel based on the mechanical demands placed on them
-during immobilization bone-ligament junction is at increased risk for injury rather than midsubstance |
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MCL injuries
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most MCL injuries heal on their own w/o surgery
-immobilization at 30 degrees flexion -immediate wb and motion to prevent creep and loss of cross-sectional area -same for LCL injury |
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ACL injuries
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*never heals on its own
-increased risk for damage after immobilization -after reconstruction, graft site is WEAKEST btw 3-7 weeks |
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Healing time of ligaments
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**1 year healing time (90% strength back)
-first hours- RBCs WBCs -24 hours- macrophages, fibroblasts -2-3 days- fibroblasts produce matrix -1-2 weeks- collagen present -2 days-6 weeks- cellular structures replace blood clot -6 weeks-12 months- macrophages and fibroblasts diminish -up to 12 months- type I collagen replaces type III -from 1 year on- near normal tensile strength |
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Remobilization of ligaments
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-healing of bone-ligament junction SLOWER than midsubstance healing
-must consider the nontraumatized ligaments (they get tight) |
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Muscle immobilization
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1st affect of muscle immobilizaton is loss of strength (loss of cross-sectional area)
-rate of loss most rapid during initial days of immobilization -atrophy slows after first week |
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How do you rehab different muscle fiber types?
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Type I- slow twitch- meant for endurance- low weight, high reps
Type II- fast twitch- meant for power- high weight, low reps |
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What is reflexive inhibition?
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When muscle automatically shuts itself down & becomes weak due to:
-pain -surgery -swelling -joint angle -duration of immobilization |
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Muscle imbalances
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Cross patterns in body
-tight muscle on anterior, long muscle on posterior and vice versa |
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Muscle healing time
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** 6 months healing time
-6 hours- fragmentation of injured muscle fibers begins -1-4 days- fibroblasts appear -1 week- loss of muscle strength -7-11 days- tensile strength near normal -6 weeks- 6 months- contraction ability 90% |
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Muscle Remobilization
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-Overload principle- to make muscle larger increase weight or reps
-neuromuscular stim- used with active exercise to increase results |
