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316 Cards in this Set
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1. Anorexia nervosa
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Syndrome with 3 essential criteria:
1. Self-induced starvation to a significant degree 2. Relentless drive for thinness or a morbid fear of fatness 3. Presence of medical signs and symptoms resulting form starvation. DSM: Characterized as a disorder in which persons refuse to maintain a minimally normal weight, intensely fear gaining weight, and significantly misinterpret their body and its shape. |
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2. Prevalence of anorexia nervosa
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Increasing among prepubertal girls and boys; 10 to 20x more common in females than in males.
Most common ages of onset are the midteens, but 5% have the onset early in their 20s. Occurs most freq in developed countries, and seen w/greatest frequency among young women in professions that require thinness |
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3. Comorbidity of anorexia nervosa
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Associated w/depression in 65% of cases, social phobia in 34% of cases and OCD in 26% of cases
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4. MHPG, anorexia nervosa, and depression
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Neurochemically, diminished norepinephrine turnover and activity are suggested by reduced 3-methoxy-4-hydroxyphenylglycol (MHPG) levels in the urine and the CSF of some patients w/anorexia nervosa.
An inverse relation is seen between MHPG and depression in these patients; and increase in MHPG is associated w/a decrease in depression. |
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5. Endogenous opioids and anorexia nervosa
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Endogenous opioids may contribute to the denial of hunger in patients w/this disorder.
Preliminary studies show dramatic weight gains in some patients giver opiate antagonists. |
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6. Starvation and anorexia nervosa
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1. Hypercortisolemia and nonsuppression by dexamethasone
2. Suppression of thyroid function 3. Amenorrhea, due to lowered hormone levels (LH, FSH, GRH) 4. Enlarged CSF spaces (enlarged sulci and ventricles) on CT scans 5. Higher metabolism in the caudate nucleus shown on PET scan |
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7. Corticotropin releasing hormone and starvation
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Increases and causes increased weight loss
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8. Plasma cortisol levels and starvation
Diurnal cortisol levels? |
Mildly increases and causes mildly increased weight loss as well
Diurnal cortisol levels are blunted |
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9. Growth hormone and starvation
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Impaired regulation and increased basal levels; limited response to pharmacological probes
Maintains weight loss |
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10. Somatomedin C and starvation
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Decreases and causes decreased weight loss.
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11. Thyroxine (T4) and starvation
Triiodothyronine (T3)? |
T4: Normal or slightly decreases
Normal or slightly decreases weight loss. T3: Mildly decreases and causes mildly decreases weight loss |
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12. Insulin and starvation
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Delayed release and delays or blunts weight loss
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13. Serotonin and starvation
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Increased function with weight restoration
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14. Dopamine and starvation
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Blunted response to pharmacological probes
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15. Three neurotransmitters involved in regulating eating behavior int eh paraventricular nucleus of the hypothalamus
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1. Serotonin
2. Dopamine 3. Norepinephrine |
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16. Gay and lesbians and anorexia nervosa
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Gay men have strong norms for slimness while lesbians are more tolerant for a normal body shape.
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17. Psychological factors in anorexia nervosa
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Patients w/the disorder substitute their preoccupations (obsessions) with eating and weight gain for other, normal adolescent pursuits.
Many experience their bodies as somehow under the control of their parents, so that self-starvation may be an effort to gain validation as a unique and special person. Only thru acts of self discipline can an anorectic patient develop a sense of autonomy and selfhood. |
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18. Psychodynamic factors in anorexia nervosa
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These patients have been unable to separate psychologically from their mothers. Their body may be perceived as though it were inhabited by the introject of an intrusive and unempathic mother.
Starvation may unconsciously mean arresting the growth of the intrusive internal object and thereby destroying it. Also, many anorectic patients feel that oral desires are greedy and unacceptable; therefore, these desires are projectively disavowed. |
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19. Two types of anorexia nervosa
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1. Restricting type
2. Binge-eating/purging type |
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20. Features of anorexia nervosa
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1. Voluntarily reduces and maintains an unhealthy degree of weight loss or falls to gain weight proportional to growth
2. Intense fear of becoming fat; have a relentless drive for thinness despite starvation 3. Significant starvation related medical symptomatology 4. Behaviors and psychopathology are present for at least three months |
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21. Clinical features of anorexia nervosa
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1. Abnormal reproductive hormone functioning
2. Hypothermia 3. Bradycardia 4. Orthostasis 5. Dependent edema 6. Hypotension 7. Lanugo 8. Amenorrhea (in females) 9. Leukopenia |
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22. Clinical features specific to vomiting or purgative and diuretic abuse in anorexia nervosa
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Hypokalemic or hypochloremic alkalosis
Erosion of dental enamel Siezures, fatigue and weakness Impaired water diuresis |
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23. EKG and cardiac changes in anorexia nervosa
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1. T wave flattening or inversion
2. ST segment depression 3. Lengthening of the QT interval (prolonged His bundle transmission) 4. Loss of cardiac muscle 5. Small heart 6. Atrial and ventricular premature contractions 7. Ventricular tachycardia 8. Bradycardia |
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24. Similarities between anorexic patients that binge and purge with patients that have bulemia nervosa without anorexia nervosa
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Those who binge eat and purge tend to have families in which some members are obese, and they themselves have histories of heavier body weights before the disorder than do persons w/the restricting type.
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25. Suicide rate in anorexics
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Higher in persons with the binge eating/purging type than in those with the restricting type.
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26. Pathology and lab examination of anorexia nervosa
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1. CBC reveals leukopenia w/a relative lymphocytosis in emaciated patients
2. Serum electrolyte determination reveals hypokalemic alkalosis in bing eating and purging types 3. Fasting serum glucose concentrations are often low 4. Serum salivary amylase concentrations are elevated in the patient is vomiting |
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27. Differential Dx of anorexia nervosa
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1. Medical illness that can account for the weight loss (e.g. a brain tumor or cancer)
2. Depressive disorders 3. Somatization disorder 4. Schizophrenia 5. Bulimia nervosa 6. Hyperactivity of the vagus nerve |
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28. Difference btwn depressive disorders and anorexia
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A patient w/a depressive disored has decreased appetitie, whereas a patient with anorexia nervosa claims to have normal appetite and feel hungry; only in sever stages of anorexia do patients actually have decreased appetitie.
Also, the hyperactivity seen in anorexia nervosa is planned and ritualistic (i.e. preoccupation w/recipies, cooking), but is absent in patients with depressive disorder. Lastly, in depressive disorder, patients have no intense fear of obesity or disturbance of body image |
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29. Difference btwn somatization disorders and anorexia
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Share many features w/one another. Patient can fulfill the criteria for both; generally the weight loss is not as severe in somatization disorders as that in anorexia, nor do patients with somatization disorders express a morbid fear of becoming overweight.
Also, amenorrhea for 3+ months is unusual in somatization disorder. |
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30. Difference btwn schizophrenia and anorexia
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In schizophrenics, delusions w/food are seldom concerned w/caloric content.
More likely, they believe the food to be poisoned. They may have bizarre eating habits but not the entire syndrome of anorexia nervosa |
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31. Difference btwn bulimia nervosa and anorexia nervosa
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Bulimia nervosa is a disorder in which episodic binging occurs followed by depressive moods, self-deprecating thoughts, and often self-induced vomiting, all occurs while patients maintain their weight within a normal range.
Patients w/bulimia nervosa seldom lose 15% of their weight, but the two conditions frequently coexist |
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32. Indicators of favorable and poor outcomes of anorexics
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Favorable indicators:
1. Hunger 2. Lessening of denial and immaturity 3. Improved self-esteem Poor indicators: 1. Childhood neuroticism 2. Parental conflict 3. Bulimia nervosa 4. Vomiting 5. Laxitive abuse 6. Various behavioral manifestations |
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33. Hospitalization requirements in anorexia nervosa
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1. Patients with anorexia who are 20% below the expected weight for their height are recommended for inpatient programs.
2. Patients who are 30% below their expected weight require psychiatric hospitalization for 2 to 6 months |
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34. Pharmacotheraphy treatment in anorexia nervosa
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1. Cyproheptadine (Periactin)
-has antihistaminic and antiserotonergic properties beneficial for some patients w/the restricting type 2. Amitriptyline (Elavil) 3. Clomipramine 4. Pimozide (Orap) 5. Chlorpromazine (Thorazine) 6. Fluoxetine -serotonergic agents may yield positive responses in the future 7. Tricyclic drugs -in some patients the depression improves with weight gain and normalized nutritional status. -must be used only in those patients w/an adequate nutritional status. |
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35. Role of water in the human body
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1. Transport of molecules
2. Solubilization of molecules 3. Dissipation of heat 4. Participation in chemical reactions (i.e. hydrolysis) 5. Maintenance of osmolality Molecular interactions and reactions typically occur in an aqueous environment |
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46. Fluid compartments in the body
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Comprises about 50-60% of body weight in adults and 75% of body weight in children.
Total body water: 40 L in an average 70 kg man |
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47. Hydrogen bonds in water
Strength of bonds? |
1. Water is a dipolar molecule
2. One water molecule can form hydrogen bonds with 4 other water molecules. Hydrogen bond -> 4 kcal; approx 1/20th the strength of the covalent O-H bond (80 kcal) |
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48. Hydration shells
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Water forms a hydration shell around both cations and anions
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49. Hydrogen bonds and polar solutes
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Hydrogen bonds between water and polar solutes are dynamic
They continuously dissociate and reform. |
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50. Hydrogen bonds and temp changes
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Water responds to the input of heat by decreasing the extent of hydrogen bonding and to cooling by increasing the boding between water molecules.
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51. Electrolytes in the ECF (plasma and interstitial fluid)
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1. Na+
2. Cl- |
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52. Electrolytes in the ICF (intracellular fluid)
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1. K+
2. Phosphates (HPO4 2-) |
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53. Diabetic ketoacidosis
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When the amount of insulin injected is inadequate, the body remains in a condition similar to a fasting state even though food is ingested.
The liver continues to metabolize fatty acids to the ketone bodies acetoacetic acid and β-hydroxybutyric acid These compounds are weak acids that dissociate to produce anions and hydrogen ions, thereby lower the blood and cellular pH below the normal range. Because the dissociation of the ketone bodies is causing the acidosis, it is classified as a ketoacidosis. |
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54. Osmotic diuresis
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High levels of compounds pass from the blood into the glomerular filtrate in the kidneys and then into the urine.
As a consequence of the high osmolality of the glomerular filtrate, much more water is being excreted in the urine than usual (polyuria). As a result of water lost form the blood into the urine, water passes form inside cells into the interstitial space and into the blood, resulting in an intracellular dehydration. This can result in a coma. |
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55. Why is a 0.9% solution of NaCl via IV used to rehydrate someone instead of water?
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0.9% solution of NaCl is 0.9 g NaCl/100 ml, which is 9 g/L.
NaCl ahs a molar weight of 58 g/mol so the concentration of NaCl is 0.155 M. If all the NaCl were dissociated, the osmolality would by 310 mOsm/kg water. However, b/c NaCl si not completely dissociated, the osmolality of isotonic saline is approximately 290 mOsm/kg water. The osmolality of plasma, interstitial fluids, and ICF is also approx 290 mOsm/kg water, so no large shifts of water or swelling occur when isotonic saline is given via IV. |
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56. pH of water, acids and bases
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Water slightly dissociates into hydrogen ions and hydroxide ions.
Concentration of H+ ions in 10^-7 mol/L (10^-7 M) pH = -log [H+] pH of water = - log [10^-7] = 7 Neutral pH -> [H+] = [OH-] Acidic pH -> [H+] > [OH-] Basic pH -> [H+] < [OH-] |
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57. Bronsted-Lowry Acids
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Any substance that can donate a hydrogen ion (proton)
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58. Bronsted-Lowry Bases
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Any substance that can accept a hydrogen ion (proton)
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59. Conjugate pair
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Acids and bases come in what are called conjugate pairs;
Acids dissociate into a proton and conjugate base when placed in an aqueous environment. HA -> H+ + A- HA is the acid A- is the conjugate base A- + H+ -> HA A- is the base HA is the conjugate acid |
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60. The conjugate acid formed is called?
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________-ic acid (e.g. acetic acid)
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61. The conjugate base formed is called?
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________-ate (e.g. acetate)
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62. Strong acids vs. weak acids
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Strong acids completely dissociate in water (e.g. HCl)
Weak acids incompletely dissociate in water (e.g. acetic acid) |
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63. Ka (Dissociation constant of a weak acid)
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High Ka -> stronger acid
Low Ka -> weaker acid Ka = ([H+][A-])/[HA] |
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64. pKa
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High pKa -> weaker acid
Low pKa -> stronger acid pKa= - log [Ka] |
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65. Kw
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The ion product of water.
Because Kw, the product of [H+] and [OH-], is always constant, a decrease in [H+] must be accompanied by a proportionate increase in [OH-] Kw = [H+][OH-] = 1 x 10^ -14 |
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66. Henderson-Hasselbalch equation
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pH = pKa + log ([base]/[acid])
Used to describe the quantitative relationship between pH, pKa, and the concentrations of a weak acid and its conjugate base in an aqueous solution. Can be used to calculate the ratio of the conjugate base to its un-dissociated weak acid at a given pH if the pKa is known When pH=pKa, the dissociation of a weak acid is 50% (i.e. the concentration of the protonated form is equal to the concentration of the deprotonated form) |
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67. Acetylsalicylic acid
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Aspirin is rapidly converted to salicylic acid in the body. The initial effect of aspirin is to produce a respiratory alkalosis caused by a stimulation of the "metabolic" central respiratory control center in the hypothalamus.
This increases the rate of breathing and the expiration of CO2. This is followed by a complex metabolic acidosis caused partly by the dissociation of salicylic acid (pKa= ~3.5) |
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68. Buffers
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Buffers consist of a weak acid and a conjugate base.
They resist changes in pH when H+ or OH- are added They are most effective within one pH unit of their pKa More concentrated buffers are more effective simply because they contain a greater total number of buffer molecules per unit volume that can dissociate or recombine with hydrogen ions. |
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69. Titration curves
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A plot of pH versus OH- equivalents added
When pH = pKa, the buffer is resistant to changes in pH and the titration curve flattens out. |
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70. Maintenance of body pH
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Normal metabolism produces around 13 to 22 moles of acid per day.
Buffers provide protection against this acidity by resisting changes in pH Neutral pH is maintained by: 1. Buffers 2. Expiration of CO2 thru lungs 3. Excretion of ammonium ion thru the kidneys and into the urine |
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71. Bicarbonate buffer system
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Bicarbonate is the major buffer system in red blood cells (RBC)
In RBCs, carbonic anhydrase catalyzes the formation of carbonic acid, the major acid produced by the body The dissociation of carbonic acid and protonation of bicarbonate acts as a buffer to prevent large changes in pH within RBCs. |
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72. Bicarbonate and hemoglobin in RBCs
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CO2 generated by normal metabolism (TCA cycle) is released into the blood
RBCs take up CO2 and convert it to carbonic acid (H2CO3) via carbonic anhydrase Carbonic acid dissociates into bicarbonate (HCO3−) and a proton (H+) Hemoglobin absorbs protons and thereby buffers changes in pH because of histidine residues present within the hemoglobin molecule (pKa of 6.7) |
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73. Kussmaul's breathing
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Stimulation of the respiratior center in the hypothalamus induced by acidosis leads to deeper and more frequent respiration.
CO2 is expired more easily rapidly than normal and the blood pH rises. |
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74. Intracellular pH
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Bicarbonate is transported out of the RBC in exchange for a Cl− ion
Excess protons inside the RBC or other cells combine with hydrogen phosphate (HPO42−) to form dihydrogen phosphate (H2PO4 −) in order to buffer changes in pH (phosphate buffer system is the 2nd most important in the body) Intracellular proteins that contain histidine act as buffers against changes in pH Metabolic anions are transported out of cells together with protons If the cell is too acidic, more H+ is transported out in exchange for Na+ ions by a different transporter. |
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75. Urinary hydrogen, ammonium, and phosphate ions
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Sulfuric acid is generated from the sulfate-containing AAs and is dissociated into H+ and sulfate anion in the blood an urine.
Urinary excretion of H2PO4- helps to remove acid, Ammonium ions are major contributors to buffering urinary pH, but not blood pH. Cells in the kidney generate NH4+ and excrete it into the urine in proportion to the acidity of the blood. As the renal tubular cells transport H+ into the urine, they return bicarbonate anions to the blood. |
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76. Normal arterial blood pH
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[H+] = 40 nEq/L
pH = -log [0.00000004] pH = 7.4 |
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77. Normal venous blood pH
Why the difference? |
pH = 7.35
B/c of the extra amounts of CO2 released from the tissues to form H2CO3 in these fluids |
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78. Intracellular pH
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Usually slightly lower than plasma pH b/c the metabolism of the cells produces acid, especially H2CO3.
Can range from 6.0 to 7.4 |
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79. pH of urine?
pH of gastric HCl? |
Urine pH = 4.5-8.0
Gastric HCl pH = 0.8 |
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80. Three primary systems that regulate the H+ concentration in the body to prevent acidosis or alkalosis
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1. Chemical acid-base buffer systems of the body fluids
-reacts w/in seconds to minimize changes 2. Respiratory center -reacts w/in a few minutes to eliminate CO2 and, therefore, H2CO3 form the body 3. Kidneys -Slower to respond; takes hours to days, but are the most powerful of the acid-base regulatory systems. |
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81. Addition of a strong acid to the bicarbonate buffer system
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1. Increased H+ is released from the acid and is buffered by HCO3-
2. As a result, more H2CO3 is formed, causing increased CO2 and H2O production. 3. The excess CO2 greatly stimulates respiration, which eliminates CO2 from the extracellular fluid. |
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82. Addition of a strong acid to the bicarbonate buffer system
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1. OH- is released from the base and is buffered by H2CO3 to form additional HCO3-.
2. At the same time, the concentration of H2CO3 decreases (because it reacts with OH-), causing more CO2 to combine with H2O to replace the H2CO3. 3. The net result, therefore, is a tendency for the CO2 level in the blood to decrease, but the decreased CO2 levels in the blood inhibits respiration and decreases the rate of CO2 expiration. |
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83. Calculating the pH of a solution if the molar concentration of HCO3- and the Pco2 are known
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pH = 6.1 + log [HCO3- / (0.03xPco2)]
(For the bicarbonate buffer system, the pK is 6.1) -An increase in the HCO3- concentration causes the pH to rise, shifting the acid-base balance toward alkalosis -An increase in Pco2 causes the pH to decrease, shifting the acid-base-balance toward acidosis |
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84. Where are the bicarbonate and Pco2 concentrations regulated?
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The bicarbonate concentration is regulated by the kidneys, whereas the Pco2 in extracellular fluid is controlled by the rate of respiration
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85. Metabolic acid-base disorder
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Results from a primary change in extracellular fluid bicarbonate concentration
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86. Respiratory acid-base disorder
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Results from a primary change in Pco2 concentration
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87. Effective pH range of the bicarbonate buffer system
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pH = 5.1 - 7.1
Within one unit of 6.1 |
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88. Role of phosphate buffer system
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Important in buffering renal tubular fluid and intracellular fluids
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89. pKa of phosphate buffer system
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pKa = 6.8; this allows the system to operate near its maximum buffering power in the normal pH of blood.
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90. Two reasons why the phosphate buffer system is important in the renal tubular fluids
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1. Phosphate usually becomes greatly concentrated in the tubules, thereby increasing the buffering power of the phosphate system
2. The tubular fluid usually has a considerably lower pH than the extracellular fluid does, bringing the operating range of the buffer closer to the pKa of the system (6.8) |
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91. Importance of the phosphate buffer system in intracellular fluids
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The concentration of phosphate in this fluid is many times that in the extracellular fluid.
Also, the pH of intracellular fluid is lower than that of extracellular fluid and therefore is usually closer to the pKa of the phosphate buffer system |
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92. Consequence of the diffusion of CO2 through cell membranes
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This diffusion of the elements of the bicarbonate buffer system causes the pH in intracellular fluid to change when there are changes in extracellular pH.
This is why the buffer systems within the cells help prevent changes in the pH of extracellular fluid, but may take several hours to become maximally effective. |
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93. Importance of intracellular proteins
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Appox 60 to 70% of the total chemical buffering of the body fluids is inside the cells, and most of this results from the intracellular proteins
In addition, another factor that contributes to their buffering power is the fact that they pKas of many of these protein systems are fairly close to 7.4 |
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94. Isohydric principle
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Whenever there is a change in H+ concentrations in the extracellular fluid, the balance of all the buffer systems changes at the same time.
The implication of this principle is that any condition that changes the balance of one of the buffer systems also changes the balance of all the others b/c the buffer systems actually buffer one another by shifting H+ back and forth between them |
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95. Pulmonary expiration of CO2 does what?
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It balances the metabolic formation of CO2 .
If the rate of metabolic formation of CO2 increases, the Pco2 of the extracellular fluid is likewise increased. A decreased metabolic rate lowers the Pco2. If the rate of pulmonary ventilation is increased, CO2 is blown off from the lungs, and the Pco2 in the extracellular fluid decreases. |
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96. Increasing alveolar ventilation does what?
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Decreases the extracellular fluid hydrogen ion concentration and raises pH
The higher the alveolar ventilation, the lower the Pco2; conversely, the lower the alveolar ventilation rate, the higher the Pco2. When CO2 concentration increases, the H2Co3 concentration and H+ concentration also increases, thereby lowering extracellular fluid pH. |
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97. Increased hydrogen ion concentration stimulates what?
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It stimulates alveolar ventilation.
Not only does the alveolar ventilation rate influence H+ concentration by changing the Pco2 of the body fluids, but the H+ concentration affects the rate of alveolar ventilation. |
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98. Effect of blood pH on the rate of alveolar ventilation
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The change in ventilation rate per unit pH change is much greater at reduced levels of pH compared with increased levels of pH.
The reason for this is that as the alveolar ventilation rate decreases, owing to an increase in pH, the amount of oxygen added to the blood decreases and the partial pressure of oxygen in the blood also decreases, which stimulates the ventilation rate. Therefore, the respiratory compensation for an increase in pH is not nearly as effective as the response to a marked reduction in pH. |
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99. Feedback control of H+ concentration by the respiratory system
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B/c increased H+ concentration stimulates respiration, and because increased alveolar ventilation decreases the H+ concentration, the respiratory system acts as a typical negative feedback controller of H+ concentration.
↑[H+] ⇒ ↑Alveolar ventilation ↑Alveolar ventilation ⇒ ↓Pco2 ↓Pco2 ⇒ ↓[H+] |
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100. Efficiency of respiratory control of hydrogen ion concentration
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Respiratory control cannot return the H+ concentration all the way back to normal when a disturbance outside the respiratory system has altered pH.
The respiratory system has an effectiveness between 50 and 75%; corresponding to a feedback gain of 1 to 3. That is, if the H+ concentration is suddenly increased by adding acid to the extracellular fluid and pH fall from 7.4 to 7.0, the respiratory system can return the pH to a value of about 7.2 to 7.3. |
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101. Buffering power of the respiratory system
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Respiration regulation of acid-base balance is a physiologic type of buffer system b/c it acts rapidly and keeps the H+ concentration from changing too much until the slowly responding kidneys can eliminate the imbalance.
One to two times as much acid or base can normally be buffered by this mechanism as by the chemical buffers. |
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102. Respiratory acidosis due to impaired lung function
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Abnormalities of respiration can also cause changes in H+ concentration; for example, an impairment of lung function decreases the ability of the lungs to eliminate CO2; this causes a buildup of CO2 and a tendency towards respiratory acidosis.
Also, the ability to respond to metabolic acidosis is impaired b/c the compensatory reductions in PCo2 that would normally occur by means of increased ventilation are blunted. |
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103. Renal control of acid-base balance
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The kidneys control acid-base balance by excreting either an acidic or basic urine.
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104. Mechanism of kidney excretion of acids or bases
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1. Large numbers of HCO3- are filtered continuously and if they are excreted into the urine, bases are removed from the blood.
2. Large numbers of H+ are also secreted into the tubular lumen by the tubular epithelial cells, thus removing acid from the blood. 3. If more H+ is secreted than HCO3- if filtered, there will be a net loss of acid from the extracellular fluid. 4. Conversely, if more HCO3- is filtered than H+ is secreted, there will be a net loss of base. |
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105. How do kidneys regulate extracellular fluid H+ concentration?
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Through three fundamental mechanisms:
1. Secretion of H+ 2. Reabsorption of filtered HCO3- 3. Production of new HCO3- |
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106. Where does hydrogen ion secretion and bicarbonate reabsorption occur?
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In virtually all parts of the tubules except the descending and ascending thin limbs of the loop of Henle.
About 80-90% of the bicarbonate reabsorption occurs in the proximal tubule, so that only a small amount of bicarbonate flows into the distal tubules and collecting ducts. In the thick ascending loop of Henle, another 10% of the filtered bicarbonate is reabsorbed and the remainder of the reabsorption takes place in the distal tubule and collecting duct. For each bicarbonate reabsorbed, a tubular secretion of H+ must occur. |
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107. Secondary active transport of hydrogen ions
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The epithelial cells of the proximal tubule, the thick segment of the ascending loop of Henle, and the early distal tubule all secrete H+ into the tubular fluid by sodium-hydrogen counter-transport.
This secondary active secretion of H+ is coupled with the transport of Na into the cell at the luminal membrane by the sodium-hydrogen exchanger protein, and the energy for H+ secretion against a concentration gradient is derived from the sodium gradient favoring Na movement into the cell. This gradient is established by the sodium-potassium ATPase pump in the basolateral membrane. More than 90% of the bicarbonate is reabsorbed in this manner, required large amounts of H+ to be secreted each day by the tubules. |
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108. Process of H+ secretion and bicarbonate reabsorption
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1. Active secretion of H+ into the renal tubule
2. Tubular reabsorption of bicarbonate ions by combination with H+ to form carbonic acid, which dissociates to form CO2 and water. 3. Sodium ion reabsorption in exchange for H+ secreted This patten of H+ secretion occurs in the proximal tubule, the thick ascending segment of the loop of Henle, and the early distal tubule. |
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109. Net result of hydrogen secretion and bicarbonate reabsorption
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For every H+ secreted into the tubular lumen, an HCO3- enters the blood.
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110. Can the bicarbonate ions permeate the luminal membranes of the tubular cells?
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Bicarbonate ions do not readily permeate the luminal membranes of the renal tubular cells.
Therefore, the HCO3- that is filtered by the glomerulus cannot be directly reabsorbed. |
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111. How are filtered bicarbonate ions reabsorbed by the tubules?
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1. First, the bicarbonate ion must combine with a H+ to generate H2CO3.
2. The H2CO3 formed then dissociates into CO2 and H2O. 3. The CO2 can then move easily across the tubular membrane; therefore, it instantly diffuses into the tubular cell, where it recombines with H2O under the influence of carbonic anhydrase, to generate a new H2CO3 molecule. 4. This H2CO3 in turn dissociates to form HCO3- and H+ 5. The HCO3- then diffuses thru the basolateral membrane into the interstitial fluid and is taken up into the peritubular capillary blood. |
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112. What two processes facilitate the transport of HCO3 across the basolateral membrane?
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1. Na+_HCO3- co-transport
2. Cl-_HCO3- exchange |
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113. Net result of hydrogen secretion and bicarbonate reabsorption (revised)
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Each time an H+ is formed in the tubular epithelial cells, an HCO3- is also formed and released back into the blood.
The net effect of these reactions is the reabsorption of HCO3- from the tubules, although the HCO3- that actually enters the extracellular fluid is not the same as that filtered into the tubules. |
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114. Titration of bicarbonate ions
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In metabolic alkalosis, the excess HCO3- cannot be reabsorbed; therefore, the excess HCO3- is left in the tubules and eventually excreted into the urine.
In metabolic acidosis, there is excess H+ relative to HCO3-, causing complete reabsorption of the bicarbonate; the excess H+ passes into the urine. Thus, the basic mechanism by which the kidneys correct either acidosis or alkalosis is incomplete titration of H+ of HCO3-; leaving one or the other to pass into the urine and be removed from the extracellular fluid. |
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115. Primary active secretion of H+
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Beginning in the late distal tubules and continuing thru the remainder of the tubular system, the tubular epithelium secreted H+ by primary active transport.
H+ is transported directly across the luminal membrane of the tubular cell by a specific protein, a hydrogen-transporting ATPase. (Uses ATP for pumping H+) The primary active secretion of H+ occurs in a special type of cell called the intercalated cells of the late distal tubule and in the collecting tubules |
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116. Mechanism of primary active secretion of H+
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1. The dissolved CO2 in the cell combines with H2O to form H2CO3
2. The H2CO3 then dissociates into HCO3-, which is reabsorbed into the blood, plus H+, which is secreted into the tubule by means of the hydrogen ATPase mechanism For each H+ secreted, an HCO3- is reabsorbed, similar to the process int he proximal tubules. |
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117. Whats the difference between H+ secretion and HCO3- reabsorption in this later part of the nephron?
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The main difference is that H+ moves across the luminal membrane by an active H+ pump instead of by counter-transport, as occurs in the early parts of the nephron
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118. Significant importance of the later part of the nephron
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This mechanism is important in forming a maximally acidic urine.
In the proximal tubules, H+ concentration can only be increased about 3-4x; in the distal collecting tubules, the H+ concentration can be increased as much as 900x |
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119. What happens where there's an excess of H+ in the urine?
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The H+ combines with buffers other than HCO3- and this results in the genration of new HCO3- that can also enter the blood.
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120. Phosphate buffer system
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Becomes concentrated in the tubular fluid b/c of their relatively poor reabsorption and b/c of the reabsorption of water from the tubular fluid.
Therefore, although phosphate is not an important extracellular fluid buffer, it is much more effective as a buffer in the tubular fluid. The one difference between this buffer system and the bicarbonate system is that the HCO3- that is generated in the tubular cell and enters the peritubular blood represents a net gain of HCO3- by the blood, rather than merely a replacement of filtered HCO3-. |
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121. Ammonia buffer system
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This is a second buffer system in the tubular fluid that is even more important quantitatively than the phosphate buffer system.
Composed of ammonia and ammonium ion. Ammonium ion is synthesized from glutamine, which breaks down to form two ammonium ions and two HCO3-. Thus, for each molecule of glutamine metabolized in the proximal tubules, 2 NH4+ are secreted into the urine and 2 HCO3- are reabsorbed into the blood. The HCO3- generated by this process constitutes new bicarbonate as well. |
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122. Mechanism of NH4+ addition to the tubular fluids
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H+ is secreted by the tubular membrane into the lumen, where it combines with NH3 to form NH4+, which is then excreted.
The collecting ducts are permeable to NH3, which can easily diffuse into the tubular lumen. However, the luminal membrane of this part of the tubules is much less permeable to NH4+; therefore, once the H+ has reacted with NH3 to form NH4+, the NH4+ is trapped in the tubular lumen and eliminated in the urine. For each NH4+ excreted, a new HCO3- is generated and added to the blood. |
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123. Chronic acidosis and NH4+
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Increases NH4+ excretion which also generates new bicarbonate
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124. Determination of bicarbonate excretion
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Urine flow rate multiplied by urinary bicarbonate concentration
This number indicates how rapidly the kidneys are removing HCO3- from the blood |
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125. Determining the amount of new bicarbonate contributed to the blood at any given time
|
Calculated by measuring NH4+ excretion
(urine flow rate multiplied by urinary NH4+ concentration) |
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126. Titratable acid
|
This is the value that is used to determine the amount of the nonbicarbonate, non-NH4+ buffer excreted in the urine
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127. Net acid excretion
|
net acid excretion =
(NH4+ excretion + urinary titratable acid - Bicarbonate excretion) |
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128. Regulation of renal tubular hydrogen ion secretion
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The most important stimuli for increasing H+ secretion by the tubules in acidosis are:
1. An increase in Pco2 of the extracellular fluid 2. An increase in H+ concentration of the extracellular fluid (decreased pH) |
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129. Excessive aldosterone secretion
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Increases H+ secretion into the tubular fluid, and thus, increased amounts of bicarbonates added to the blood.
Causes alkalosis |
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130. Increased Angiotensin II
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Also increases H+ secretion and HCO3- reabsorption
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131. Extracellular fluid volume depletion
|
Stimulates sodium reabsorption by the renal tubules and increases H+ secretion and HCO3- reabsorption
Causes alkalosis |
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132. How does extracellular fluid volume depletion causes increased secretion of H+?
|
1. Increased angiotensin II levels, which directly stimulate the activity of the Na+_H+ exchanger in the renal tubules
2. Increased aldosterone levels, which stimulate H+ secretion by the intercalated cells of the cortical collecting tubules. |
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133. Factors that increase H+ secretion and HCO3- reabsorption
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1. ↑Pco2
2. ↑H+, ↓HCO3- 3. ↓Extracellular fluid volume 4. ↓Angiotensin II 5. ↑Aldosterone 6. Hypokalemia |
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134. Factors that decrease H+ secretion and HCO3- reabsorption
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1. ↓Pco2
2. ↓H+, ↑HCO3- 3. ↑Extracellular fluid volume 4. ↓Angiotensin II 5. ↓Aldosterone 6. Hyperkalemia |
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135. Primary compensation for metabolic acidosis
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↑ Ventilation rate to reduce Pco2
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136. Primary compensation for respiratory acidosis
|
↑ Plasma HCO3- concentration by the kidneys
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137. Primary compensation for metabolic alkalosis
|
↓ Ventilation rate to raise Pco2
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138. Primary compensation for respiratory alkalosis
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↓ Plasma HCO3- concentration by the kidneys caused by increased renal excretion of HCO3-
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139. What can cause respiratory alkalosis?
|
1. Person ascending to a high altitude
2. Hyperventilation |
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140. What can cause metabolic acidosis?
|
1. Renal tubular acidosis
-defect in renal secretion of H+ or in reabsorption of HCO3- or both 2. Diarrhea -loss of large amounts of sodium bicarbonate into the feces 3. Vomiting of intestinal contents -deep GI vomiting causes loss of bicarbonate 4. Diabetes mellitus -high blood acetoacetic acid levels 5. Ingestion of acids -aspirin 6. Chronic renal failure |
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141. What can cause respiratory acidosis?
|
Pathological conditions that damage the respiratory centers or that decrease the ability of the lungs to eliminate CO2
This includes pneumonia, emphysema, etc... |
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142. What can cause metabolic alkalosis?
|
1. Administration of diuretics (except the carbonic anhydrase inhibitors)
-all diuretics cause increased flow of fluid along the tubules, which leads to increased resorption of Na+ which is coupled with H+ excretion 2. Excess aldosterone 3. Vomiting of gastric contents -Lose HCl 4. Ingestion of alkaline drugs -Tums |
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143. Treatment of acidosis
|
1. PA administration of Sodium bicarbonate
2. IV administration of sodium lactate and sodium gluconate *careful not to infuse sodium bicarbonate via IV b/c of potentially dangerous side effects |
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144. Treatment of alkalosis
|
1. PO administration of ammonium chloride
-liberates HCl in the body 2. Lysine monohydrochloride |
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145. Expected values for a simple respiratory acidosis
|
↓ plasma pH
↑ Pco2 ↑ plasma concentration of HCO3- after partial renal compensation |
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146. Expected values for a simple metabolic acidosis
|
↓ plasma pH
↓ plasma concentration of HCO3- ↓ Pco2 after partial respiratory compensation |
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147. Expected values for a simple respiratory alkalosis
|
↑ plasma pH
↓ Pco2 ↓ plasma concentration of HCO3- |
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148. Expected values for a simple metabolic alkalosis
|
↑ plasma pH
↑ plasma concentration of HCO3- ↑ Pco2 |
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149. Mixed acid-base disorder
|
In some instance, acid-base disorders are not accompanied by appropriate compensatory responses.
Thus, there are two or more underlying causes for the acid-base disturbance |
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150. Anion gap
|
The difference between unmeasured anions and unmeasured cations.
Will increase if unmeasured anions rise or if unmeasured cations fall. Used mainly in diagnosing different causes of metabolic acidosis. |
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151. Causes of increased anion gap (Normochloremia)
|
1. Diabetes mellitus (ketoacidosis)
2. Lactic acidosis 3. Chronic renal failure 4. Aspirin poisoning 5. Methanol poisoning 6. Ethylene glycol poisoning 7. Starvation |
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152. Causes of normal anion gap (Hyperchloremia)
|
1. Diarrhea
2. Renal tubular acidosis 3. Carbonic anhydrase inhibitors 4. Addison's disease |
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153. Hyperchloremic metabolic acidosis
|
Plasma Cl- increases in proportion to the fall in plasma HCO3-, the anion gap will remain normal but HCO3- has been effectively replaced by Cl-
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154. Most abundant cells in the blood
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Erythrocytes
Necessary for the delivery of O2 |
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155. Major function of erythrocytes
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Transport of hemoglobin
-carries O2 from lungs to tissues -hemoglobin must exist in the blood cell itself to remain in the bloodstream, otherwise it leaks into glomerular filtrate -hemoglobin acts as an acid-base buffer |
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156. Carbonic anhydrase
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Enzyme that catalyzes the reversible reaction between CO2 and H2O to form H2CO3
Contained in the RBCs and it makes it possible for water of the blood to transport massive quantities of CO2 in the form of HCO3- from tissues to lungs where it is converted into CO2 and expelled as a waste product |
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157. Shape of RBCs
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Biconcave; can change shape to squeeze thru capillaries
- normal cell has a great excess of cell membrane compared to the quantity of material inside; therefore deformation does not stretch the membrane greatly and does not rupture the cell as would be the case with other cells. |
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158. Avg # of RBCs
|
5,200,000 per cubic mm for men
4,700,000 per cubic mm for women Persons at high altitude have greater numbers of RBCs |
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159. Hematocrit
|
The percentage of blood that is cells; normally 40-45%
When normal, the quantity of Hb in cells is normal; the whole blood of men contains an average of 15 g of Hb per 100 mL of cells Women - 14 g/100mL |
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160. Production of RBCs in embryonic life
|
Early: primitive nucleated RBCs produced in the yolk sac
Middle trimester: liver (main organ), spleen and lymph nodes Last month of gestation to after birth: bone marrow (exclusively) until age 5 |
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161. RBC production age 20+
|
Majority are produced in the bone marrow of membranous bones and production is less active with increasing age
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162. Blood cell genesis
|
Begin in bone marrow as pluripotential hematopoietic stem cells from which all circulating blood cells are derived
Most pluripotential hematopoietic stem cells differentiate to form other cells types and a portion remains to replenish blood supply later in life |
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163. Committed stem cells
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Form from the pluripotential hematopoietic stem cells committed to specific cell type
A committed stem cell that produces erythrocytes is called a colony-forming-erythrocyte forming unit (CFU-E) |
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164. Control of growth and reproduction of different stem cells
|
Controlled by growth inducers; not by differentiation
IL-3 promotes growth of virtually all stem cell types; some growth inducers induce growth in specific cell types Formation of growth inducers and differentiation inducers is controlled by factors outside the bone marrow. |
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165. Proerythroblasts
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Once formed, divides multiple times, eventually forming an RBC
Early stages = basophil erythroblasts which stain with basophilic dye due to organelles Reticulocyte stages = only a small amount of basophilic material remains and the cell passes from blood to capillaries via diapedesis The remaining basophilic material normally disappears in one to two days post diapedesis |
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166. Destruction of bone marrow
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X-Ray therapy
Drugs Other means Causes hyperplasia of the bone marrow and diminishes the ability to produce RBCs |
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167. Stimulus for RBC production in low O2 states
|
Erythropoietin
90% of erythropoietin is formed in the kidneys the remainder is formed in the liver Sometimes hypoxia in parts of the body other than the kidney stimulate RBC production which suggests there might be some non renal sensor (norepinephrine and epinephrine both stimulate production as well) |
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168. RBC increase post erythropoietin secretion
|
Not immediate; the important effect of Erythropoietin is to stimulate production of proerythroblasts from hematopoietic stem cells in the bone marrow
Once formed, the hormone causes the cells to pass more rapidly thru the erythroblastic stages than they normally do; but they still go thru all the stages |
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169. Final maturation of RBC's
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Vitamin B12 and Folic Acid
Necessary for DNA synthesis b/c each is required for the formation of thymidine triphosphate Common cause of maturation failure |
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170. Common cause of RBC maturation failure
|
Failure of B12 absorption
Gastrin genes secrete intrinsic factor which combines with B12 and makes it available for absorption In the balanced state, B12 is protected from digestion of GI secretion and it binds receptor sites on brush border membranes of mucosal cells of the ileum Post receptor binding, B12 is transported into the blood via pinocytosis It is stored in the liver and then released as needed by the bone marrow |
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171. Life span of RBCs
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Normally circulate for 120 days before being destroyed in the spleen where they self destruct by squeezing thru the red pulp, causing rupture of the older and more fragile cells.
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172. Cytoplasmic enzymes of RBCs
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1. Capable of metabolizing glucose and forming small amts of ATP
2. Maintain pliability of the cell membrane 3. Maintain membrane transport ions 4. Keeps iron of the cell's hemoglobin in the ferrous form instead of the ferric form 5. Prevents oxidation of proteins in the RBCs |
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173. Hemoglobin (Hb)
|
Begins in the proerythroblast stage and continues into the reticulocyte stage
Succino-CoA formed in the Krebs cycle binds w/glycine to form pyrole molecules 4 pyroles combine to form protoporphyrin IX which combines w/iron to form heme Each heme combines w/globin synthesized by ribosomes to form the hemoglobin chain 4 chains form the Hb molecule |
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174. Hb and Iron
|
4 iron atoms in each Hb molecule
Each combine loosely w/one molecule of O2; therefore there are four molecules of O2 transported by each Hb molecule; thus there are 8 oxygen atoms total per Hb molecule |
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175. Destruction of Hb
|
When RBCs burst and release their Hb, the Hb is phagocytized by macrophages almost immediately, esp by Kupfer cells in liver and macrophages of the spleen in bone marrow
The porphyrin portion is converted by macrophages into the bile pigment bilirubin which is released into the blood and later released by secretion thru the liver into the bile |
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176. Most important feature of Hb molecule
|
Ability to combine loosely and reversibly with O2
Primary Fx of Hb in body is to combine w/O2 in lungs and release it readily in the tissue capillaries where the gaseous tension is much lower than in the lungs. O2 binds w/coordination bonds of Fe, which is a loose bond and allows O2 to be carried as molecular O2, not as ionic oxygen |
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177. Quantity of iron in body
|
4-5 g
65% in the form of Hb 15-30% stored for later use mainly by reticuloendothelial system and by liver parenchymal cells Stored principally in the form of ferritin |
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178. Five factors that decrease oxygenation
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1. Low blood volume
2. Anemia 3. Low Hb 4. Poor blood flow 5. Pulmonary disease |
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179. Stages of RBC genesis from pluripotential hematopoietic stem cell
|
1. Proerythroblast
2. Basophil erythroblast 3. Polychromatophil erythroblast 4. Reticulocyte 5. Erythrocytes |
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180. Fe absorption from small intestine
|
Immediately combines in the blood plasma with apotransferrin to form transferrin
Transferrin is then transported in the plasma; Fe is loosely bound and can be released to any tissue in the body at this point Transferrin binds strongly w/receptors in the cell membranes of erythroblasts and bone marrow and along w/its bound Fe, it is ingested by the erythroblast via endocytosis and delivered directly to the mitochondria where heme is synthesized |
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181. Fe in the cytoplasm
|
Combines mainly w/apoferritin to form ferritin
May contain only a small amt of Fe or a large amount of Fe and it is called "storage iron" |
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182. Hemosiderin
|
Smaller quantities of Fe in the storage pool and is in the insoluble form.
Collects in the cells in the form of large clusters that can be observed microscopically as large particle |
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183. Fe absorption
|
Liver secretes moderate amts of apotransferrin into the bile, it flows thru the bile duct into the duodenum where it binds w/free Fe and iron compounds
This allows for the formation of transferrin molecules which allows for Fe absorption Total body iron is regulated by altering the rate of absorption |
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184. Blood loss anemia
|
After rapid hemorrhaging, the body replaces the fluid portion of the plasma in 1-3 days, leaving a low concentration of RBCs
Can cause microcytic, hypochromic anemia If second hemorrhage doesn't occur, RBC levels return to normal within three to six weeks. |
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185. Bone marrow aplasia
|
Lack of functioning bone marrow which reduces the production of RBCs
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186. Megaloblastic anemia
|
Loss of B12, folic acid, or intrinsic factor can lead to slow reproduction of erythroblasts in the bone marrow
RBCs grow too large w/odd shapes and are called megaloblast Cells rupture easily |
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187. Hemolytic anemia
|
Different abnormalities of RBCs, many of which are hereditary or acquired, make cells rupture easily as they travel thru capillaries
Life span is so short that cells are destroyed faster than they can be formed |
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188. Three types of hemolytic anemia
|
1. Spherocytosis
-RBC are very small and spherical rather than biconcave -can't withstand compression forces 2. Sickle cell anemia -cells have an abnormal type of Hb called Hb-S which contains faulty beta chains -when exposed to low O2 concentrations, it precipitates into long crystals inside the RBC -precipitated Hb also damages the membrane of the RBC which causes it to rupture and die, causing anemia 3. Erythroblastosis fetalis -Rh positive RBCs in the fetus are attacked by antibodies from the Rh negative mother -This makes Rh positive cells fragile, leading to rapid rupture; causing the child to be born w/anemia |
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189. Effects of anemia
|
1. Greatly increased cardiac output as increased pumping load on the heart which partially offsets the low O2 carrying effects of anemia
2. Heart is unable to pump greater quantities of blood during exercise 3. Extreme tissue hypoxia results; and cardiac failure may ensue |
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190. Secondary polycythemia
|
Whenever tissues become hypoxic b/c of too little O2 in the breatheed air, or because of failure of O2 delivery to the tissues,
Blood forming organs automatically produce large quantities of RBCs Cell count commonly rises about 30% above normal Includes physiologic polycythemia which occurs in natives living at high altitudes |
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191. Polycythemia vera
|
Caused by a genetic aberration in the hematoblastic cells which produce the blood cells
The blast cells no longer stop producing RBCs when too many cells are present Causes excess production of white blood cells and platelets as well and many blood capillaries become plugged by viscous blood. |
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192. Effects of polycythemia on the function of the circulatory system
|
Increased venous return to the heart
2. Arterial pressure is normal in most affected people; blood pressure mechanisms can usually offset the tendency for increased blood viscosity to increase peripheral resistance B/c blood passes sluggishly thru skin capillaries before entering the venous plexus, a larger quantity than normal of Hb is deoxygenated, which leads to a reddy complexion with a bluish tint to the skin. |
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193. Four major functions of respiration
|
1. Pulmonary ventilation
2. Diffusion of O2 and CO2 btwn aveoli and blood 3. Transport of O2 and CO2 in the blood and body fluids 4. Regulation of ventilation and other facets of respiration |
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194. Two ways of expanding and contracting the chest cavity
|
1. Downward and upward movement of the diaphram to lengthen or shorten the chest cavity
-normal quiet breathing 2. Elevation and depression of the ribs to increase or decrease the anteroposterior chest diameter |
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195. Contraction of the diaphragm
|
Pulls lower surface of lungs downward for inspiration, relaxation of diaphragm allows for expiration
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196. Heavy breathing
|
Elastic forces are not powerful enough to cause necessary rapid expiration so extra force is achieved mainly by contraction of the abdominal muscles, the abdominal contents push upward against the diaphragm compressing the lungs
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197. Muscles of inspiration
|
Muscles that elevate the chest cage
1. External intercostals 2. Serratus anterior 3. SCM and scalenes |
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198. Muscles of expiration
|
Muscles that depress the chest cage
1. Internal intercostals 2. Abdominal recti |
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199. Ribs during expiration and inspiration
|
Angle downward during expiration
Pulled upward and forward during inspiration to expand the chest cavity |
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200. Lungs
|
An elastic structure that collapses like a balloon and expel air thru the trachea when there is no force to keep it inflated
They float in the thoracic cavity surrounded by a thin layer of pleural fluid that lubricates their movement in the pleural cavity Continual suction of excess fluid into lymphatic channels maintains a slight suction between the visceral surface of the lung pleural and parietal surface of the thoracic cavity; this holds lungs to the wall |
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201. Pleural pressure
|
The pressure of the fluid in the thin space between the lung pleura and the chest wall
Normally slightly negative; approx -5 cm of H2O During normal inspiration, expansion of the chest cage pulls outward on the lungs with greater force and creates more negative pressure to an avg of -7.5 cm of H2O Events are reversed during expiration |
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202. Alveolar pressure
|
The pressure of the air inside the lung alveoli when glottis is open and no inflow or outflow occurs, the pressure is equal to that of the atm; approx 0 cm H2O
To cause inward flow of air into alveoli during inspiration, pressure in the alveoli must fall to slightly below atm pressure; approx -1 cm H2O During expiration, opposite pressure occurs; approx +1 cm H2O |
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203. Transpulmonary pressure
|
The difference btwn the alveolar pressure and pleural pressure; pressure difference btwn that and the alveoli and that on the outer surface of the lungs, and it is a measure of the elastic forces in the lungs that tend to collapse the lungs at each instant of respiration, called the recoil pressure.
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204. Lung compliance
|
The extent to which the lungs will expand for each unit increase in transpulmonary pressure if allowed enough time to reach equilibrium
Avgs about 200 mL of air for each cm of water transpulmonary pressure Thus, everytime the transpulmonary pressure increases 1 cm of H2O, the lung volume after 10 to 20 secs will expand to 200 mL |
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205. Compliance of the lungs thorax system
|
Almost exactly 1/2 that of the lungs alone; when the lungs are expanded to high vol or compressed to low vol, limitations of the chest become extreme
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206. Compliance diagram
|
Two curves:
1. Inspiratory compliance curve 2. Expiratory compliance curve Characteristics are determined by the elastic forces of the lung, forces of the lung itself, and forces caused by surface tension of fluid that lines lung air space |
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207. Elastic forces of lung tissue
|
Determined by elastin and collagen fibers interwoven in the lung parenchyma
They stretch and exert force during lung expansion |
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208. Elastic forces caused by surface tension
|
More complex than those caused by lung tissue
When lungs are filled w/air, there's an interface btwn alveolar fluid and the air in the alveoli |
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209. Tissue forces and total lung elasticity
|
Tissue forces only represent 1/3 of total lung elasticity
Transpleural pressures required to expand air filled lungs are three times as great as those required to expand saline solution filled lungs in which surface tension effect is not present |
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210. Inner surface of alveoli
|
Water surface is attempting to contract, results in an attempt to force the air out of the alveoli thru the bronchi and causes the alveoli to collapse
Net effect is to cause an elastic contractile force of the entire lungs, which is called the surface tension elastic force |
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211. Surfactant
|
Greatly reduces the surface tension of H2O; secreted by Type II alveolar epithelial cells which constitutes 10% of the alveoli
Cells are granular containing lipid inclusions and surfactant is a complex mixture of several phospholipids, proteins and ions. |
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212. Dipalmitoylphosphatidylcholine
|
Most important phospholipid of surfactant
Along w/several less important phospholipids, it's responsible for reducing surface tension; part of the molecule dissolves while the remainder spreads over the surface of the water in the alveoli. |
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|
213. Surface tension pressure in the alveoli
|
Inversely affected by the radius of the alveolus
The smaller the alveolus the greater the alveolar pressure caused by surface tension Esp significant in small premature babies, many of whom have alveoli with a radius less than one quarter of an adult person Additionally, surfactant does not begin to be secreted until the sixth and seventh month of gestation, and sometimes even later than that |
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214. Fractions of work performed by inspiratory muscles under resting conditions
|
1. That required to expand the lungs against lung and chest elastic forces (compliance work)
2. That required to overcome the viscosity of the lung and chest wall structures (tissue resistance work) 3. That required to overcome airway resistance to movement of air into the lungs (airway resistance work) |
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215. Spirometry
|
Record of the volume movement of air into and out of the lungs
Consists of a drum inverted over a chamber of H2O with the drum counterbalanced by a weight In the drum is a breathing gas and a tube connects the mouth with the gas chamber Drum rises and falls with inspiration/expiration and records levels |
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216. Pulmonary volumes
|
When added together, they equal the max volume to which the lungs can be expanded.
1. Tidal volume 2. Inspiratory reserve volume 3. Expiratory reserve volume 4. Residual volume |
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|
217. Tidal volume
|
The volume of air inspired or expired with each normal breath
Amounts to about 500 mL in the adult male |
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|
218. Inspiratory reserve volume
|
Extra volume of air that can be inspired over and above the normal tidal volume when the person inspires w/full force
3,000 mL |
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|
219. Expiratory reserve volume
|
The maximum extra volume of air that can be expired by forceful expiration after the end of a normal tidal expiration
1,100 mL |
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|
220. Residual volume
|
Volume of air remaining in the lungs after the most forceful expiration
1,200 mL |
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|
221. Pulmonary capacities
|
Combining two or more of the pulmonary volumes to describe events in the pulmonary cycle:
1. Inspiratory capacity 2. Functional residual capacity 3. Vital capacity 4. Total lung capacity |
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|
221. Inspiratory capacity
|
Is the tidal volume + inspiratory reserve volume
This is the amount of air a person can breathe in beginning at the normal expiratory level and distending the lungs to the maximum amount 3,500 mL |
|
|
222. Functional residual capacity
|
Equals the expiratory reserve volume + residual volume
The amount of air that remains in the lungs at the end of normal expiration 2,300 mL |
|
|
223. Vital capacity
|
Equals the inspiratory reserve volume + tidal volume + expiratory reserve volume
This is the maximum amount of air a person can expel from the lungs after first filling the lungs to the maximum extent and then expiring to the maximum extent 4,600 mL |
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224. Total lung capacity
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Vital capacity + residual volume
Maximum volume to which the lungs can be expanded with the greatest possible effort 5,800 mL |
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225. Men vs. women
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20-25% less in women for pulmonary volumes and capacities
Greater in large and athletic people than in small and asthenic people |
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226. Minute respiratory volume
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Total amount of new air moved into the respiratory passages each minute
Equal to tidal volume multiplied by the respiratory rate per min |
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227. Ultimate importance of pulmonary ventilation
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To continually renew air in the gas exchange areas of the lungs, where air is in the proximity to the pulmonary blood
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228. Dead space air
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Air a person breathes in that never reaches the gas exchange sites but simply fills respiratory passages where gas exchange does not occur such as the nose, pharynx and trachea
It is expired first before any of the air from the alveoli reaches the atm Normal dead space air in a young adult male is about 150 mL and increases slightly w/age |
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229. Anatomic dead space
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Volume of all the space of the respiratory system other than the alveoli and their other closely related gas exchange areas
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230. Physiologic dead space
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Anatomic dead space but includes the alveolar dead space in the total measurement of dead space
In a normal person, anatomic and physiologic dead spaces are nearly equal; this is not the case with partially functional alveoli; the physiological dead space may be 10x that of the anatomic dead space |
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231. Alveolar ventilation per minute
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Total volume of new air entering the alveoli and adjacent gas exchange areas each minute
Equal to the respiratory rate times the amount of new air that enters these areas with each breath Approx 4,200 mL/min One of the major factors determining the concentrations of O2 and CO2 in the alveoli |
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232. Bronchioles vs. respiratory bronchioles
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Wall of bronchioles are almost entirely made of smooth muscle; respiratory bronchioles function in gas exchange and are composed of mainly pulmonary epithelium and underlying fibrous tissue
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233. Greatest amt of air resistance flow occurs where?
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Larger bronchioles and bronchi near the trachea
Due to relatively few of the larger bronchi in comparison with the many terminal bronchioles, so greater quantities of air have to pass thru the larger vs. smaller ones (normal conditions) In disease conditions, the smaller bronchioles play a larger role in airway resistance b/c they are easily occluded |
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234. Nervous control of bronchiolar musculature
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Norepinephrine and epinephrine released in the blood thru sympathetic stimulation stimulate beta receptors and caused dilation of the bronchiole tree
Parasympathetic nerves secrete ACh which causes mild to moderate constriction of bronchioles |
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235. Three distinct normal
respiratory functions are performed by the nasal cavities |
1. Warm the air by the conchae, septum
2. Almost complete humidification 3. Partially filter particles Air conditioning function is the combined result |
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236. Turbulent precipitation
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The air passing thru the nasal passageways hit many obstructing vanes, the conchae, septum, and the pharyngeal wall.
Each time air hits one of these obstructions, it must change direction; particles suspended int he air have more mass and cannot change direction as rapidly causing them to be entrapped in the mucus coating and then is transported by the cilia to be excreted. |
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237. Gravitational precipitation
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Particles between 1 and 5 micrometers settle in the small bronchioles due to inability to be removed by the turbulence mechanism
These particles become entrapped in the alveoli and are removed by alveolar macrophages |
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238. Neurological causes of speeh
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1. Specific speech nervous control centers in cerebral cortex
2. Respiratory control centers of the brain 3. Articulation and resonance structures of the mouth and nasal cavities |
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239. Mechanical functions of speech
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1. Phonation acheived by larynx
2. Articulation acheived by structures of the mouth |
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240. Respiratory center
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Composed of several groups of neurons located bilaterally in the medulla oblongata and the pons of the brainstem
Three major collections of neurons: 1. Dorsal respiratory group 2. Ventral respiratory group 3. Pneumotaxic center |
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241. Dorsal respiratory group
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Dorsal portion of medulla; mainly causes inspiration
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242. Ventral respiratory group
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Located in the ventrolateral part of the medulla; mainly causes expiration
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243. Pneumotaxic center
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Located dorsally in the superior portion of the pons; controls rate and depth of breathing
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242. Nucleus of the tractus solitarius
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Location of most of the dorsal respiratory neurons
Sensory termination of both vagal and glossopharyngeal nerves with sensory signals into respiratory center from peripheral chemorecepters, baroreceptors, and receptors found in the lungs |
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243. Basic rhythm of respiration generated by what?
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Mainly dorsal respiratory group of neurons
Emits repetitive births of inspiratory neuronal action potentials |
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244. Inspiratory ramp signal
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In normal respiration, nervous signal begins weakly and increases steadily in a ramp manner for about two seconds, then ceases abruptly for the next three seconds which turns off the excitation of the diaphragm and allows elastic recoil of the chest wall and lungs to cause expiration
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245. Two qualities of the inspiratory ramp signal that are controlled
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1. Rate of increase of the ramp signal so that during heavy respiration, the ramp increases rapidly and therefore fills the lungs rapidly
2. Limiting point at which the ramp suddenly ceases. The earlier the ramp ceases, the shorter the duration of inspiration and expiration |
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246. Primary effect of the pneumotaxic center
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To control the switch off point of the inspiratory ramp; thus controlling the duration of the filling phase of the lung cycle
Signal strong = short inspiration time frame Signal weak = long inspiration time frame Function is primarily to limit inspiration |
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247. Nucleus ambiguus and nucleus retroambiguus
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Located within the ventral respiratory group of neurons
1. They remain inactive during normal quiet respiration 2. Do not participate in basic rhythmical oscillation that controls respiration 3. Contributes extra respiratory drive when respiratory drive for increased pulmonary ventilation becomes greater than normal 4. Stimulation of ventral neurons causes both inspiration and expiration and are especially important in providing powerful expiratory signals to abdominal muscles during very heavy expiration |
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248. Hering-Breuer inflation reflex
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Stretch receptors throughout lungs transmit signals thru the vagi into dorsal respiratory group of neurons when lungs become overstretched.
When this occurs, stretch receptors activate appropriate feedback response that switches off the inspiratory ramp and thus stops further inspiration Also increases the rate of respiration Not activated until the tidal volume increases to more than three times normal ( > 1.5 L per breath) |
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249. Excess CO2 or H+ in blood
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Mainly act directly on the inspiratory center itself causing greatly increases strength of both inspiratory and expiratory signals to the respiratory muscles
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250. O2 effects on respiration
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Does not have significant direct effect on the respiratory center of the brain in controlling respiration;
Acts almost entirely on peripheral chemoreceptors in the carotid and aortic bodies which transmit signals to the respiratory center. |
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251. Chemosensitive area
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Located bilaterally beneath the ventral surface of the medulla; area that is highly sensitive to changes in either blood, Pco2, or H+ concentration
Excites the other portions of the respiratory center |
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252. Sensory neurons of the chemosensitive area
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Especially excited by H+ ions; however, H+ ions do not easily cross the blood-brain barrier. For this reason, changes in H+ ion concentration in the blood have less effect in stimulating the chemosensitive neurons than do changes in blood CO2
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253. CO2 stimulation of chemosensitive area
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Indirect effect on the chemosensitive area reacts w/water of the tissue to form carbonic acid which dissociates into H+ and HCO3- ions
The H+ ions have a potent direct stimulatory effect on respiration |
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254. Blood brain barrier and H+ ions
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Not overly permeable to H+ ions; extremely permeable to CO2
When blood Pco2 increases, so does Pco2 of the interstitial fluid of the medulla and CSF. In both these fluids, CO2 reacts w/water to form H2CO3 which splits to form HCO3- and new H+ ions which directly act on chemosensitive neurons. |
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255. Adaptation to increases in CO2
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Excitation of the respiratory center by CO2 increase is initially great, but gradually declines over the next 1-2 days
Part of this decline results from renal adjustment of H+ ion concentration of the circulating blood back towards normal after the CO2 first increases H+ concentration Kidneys achieve this by increasing blood HCO3- which binds H+ in the blood and CSF |
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256. Peripheral Chemoreceptor
System |
Chemoreceptors located in several areas located outside of the brain specialized for sensing O2 levels
Also respond to changes in CO2 and H+ to a lesser degree Transmit nervous signals to respiratory signals in brain to help regulate respiratory activity Cranial nerves IX and X associated thru the carotid and aortic bodies *Chemoreceptors are exposed to arterial blood only* |
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257. Glomus cells
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Multiple highly characterist glandular-like cells found in the carotid and aortic bodies that synapse directly or indirectly w/associated nerve endings (IX and X)
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258. Acclimatization
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At higher altitudes, within 2 to 3 days the respiratory center in the brain stem loses the majority of sensitivity to changes in Pco2 and H+ ions.
Therefore, excess ventilatory blowoff of CO2 that would normally inhibit and increase in respiration fails to occur and low O2 can drive the respiratory system to a much higher level of alveolar ventilation than under acute conditions |
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259. Cause of intense ventilation during exercise
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1. Brain
On transmitting motor impulses to exercising muscles, it is believed to transmit collateral impulses into the brain stem to excite the respiratory center; causes a simultaneous increase in arterial pressure |
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260. Changes in alveolar and arterial Pco2 during initial period of exercise
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Direct nervous signals stimualte the respiratory center almost the proper amount to supply the extra O2 required for exercise and blow off extra CO2
If signals, are too weak or strong, chemical factors bring about the final adjustment of respiration required to keep O2, CO2 and H+ concentrations as nearly normal as possible |
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261. Increase in ventilation at beginning of exercise
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Usually great enough so that at first, it actually decreases arterial Pco2 below normal due to the increased ventilation causing a buildup of blood CO2 so that the brain provides an "anticipatory stimulation" of respiration at the onset of exercise.
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261. 30-40s into exercise
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The amount of CO2 released into the blood from active muscles approx matches the increased rate of ventilation and arterial Pco2 returns to normal even as exercise continues
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262. Voluntary control of respiration
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1. Hypoventilate
2. Hyperventilate Person can do this intentionally to such an extent that serious derrangements in Pco2, pH, and Po2 can occur in the blood |
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263. Irritant receptors in the airways
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Sensory nerve endings that cause coughing and sneezing and may also cause bronchial constriction in diseases such as asthma and emphysema
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264. J receptors
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Sensory nerve endings in alveolar walls in juxtaposition to the pulmonary capillaries stimulated when capillaries become engorged w/blood or with pulmonary edema may give a person a feeling of dyspnea
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265. Effect of brain edema on respiration
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Respiratory center may be depressed or inactivated by acute brain edema
Occasionally can be relieved temporarily by IV solution of hypertonic solutions which osmotically remove some fluids of the brain to remove intracranial pressure and re-establic respiration |
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266. Anesthesia and respiration
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Causes respiratory depression and respiratory arrest when overdose occurs with anesthetics or narcotics
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267. Periodic breathing (Cheyne-Stokes Breathing)
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Person overbreathes and blows off too much CO2 from pulmonary blood while at same time increasing blood O2.
Takes several seconds before changed pulmonary blood can travel to the brain to inhibit the excess ventilation. By this time, the person has already over ventilated for a few seconds and when the overventilated blood reaches the brain, the respiratory center becomes depressed in an excessive amount, and the cycle repeats. |
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268. Causes of Cheyne-Stokes Breathing
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1. Long delay of blood transport from lungs to brain
2. Increased negative feedback gain in the respiratory control areas *Mainly occurs in patients w/brain damage |
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269. Sleep apnea
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Apnea means absence of spontaneous breathing; sleep apneas occur during normal sleep and can be caused by obstruction of the upper airways or by impaired CNS respiratory drive
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270. Obstructive sleep apnea
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Individuals w/especially narrow pharyngeal passages experience complete closure of the pharynx due to relaxation of the muscles that normally keep this passageway open
Normally occurs in older obese person; most common treatment is surgery to remove excessive fat, enlarged tonsils or adenoids, or to create an opening in the trachea, or continuous positive airway pressure |
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271. Neuronal sleep apnea
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In few people w/sleep apnea, the CNS drive to the ventilatory muscles transiently ceases
Caused by damage to the respiratory centers or abnormalities of the respiratory neuromuscular apparatus Treatment includes meds that stimulate the respiratory centers and continuous positive airway pressure |
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272. Fundamental tests of pulmonary performance
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1. Blood PO2
2. CO2 3. pH |
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273. Determination of blood pH
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Measured using a glass pH electrode; the voltage generated by the glass electrode is a measure of pH and is read by a voltmeter
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274. Determination of blood CO2
|
Glass electrode pH meter can be used to determine CO2
When a weak solution of HCO3- is exposed to CO2 the CO2 dissolves in the solution until an equilibrium state is established In this equilibrium state, the pH of the solution is a Fx of the CO2 and the HCO3- ion concentrations in accordance w/Henderson Hasselbach |
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275. Determination of blood PO2
|
Measured by polarography
Electric current is made to flow btwn small negatie electrode and the solution If the voltage of the electrode is more than -.6 V different from the voltage of the solution, O2 will deposit on the electrode. Rate of current flow thru electrode will be directly proportional to concentration of O2 |
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276. Maximum expiratory flow
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When a person expires w/great force, the expiratory airflow reaches a maximum flow beyond which the flow cannot be increased, even with greatly increased additional force
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277. Constricted lungs
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Have both total lung capacity and reduced residual volume
b/c lung cannot expand to the normal max volume even w/the greatest respiratory effort, the maximal expiratory flow cannot rise to that of normal |
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278. Constricted lung diseases
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1. Fibrotic diseases of lung itself
-tuberculosis -silicosis 2. Diseases that constrict the chest cage such as -kyphosis -scoliosis -fibrotic pleural disease |
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279. Diseases w/airway obstruction
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Usually much more difficult to expire than to inspire b/c the closing tendency of the airways is greatly increased w/extra positive pressure required in the chest to cause expiration
By contrast, the neg extra pleural pressure that occurs during inspiration actually pulls the airways open at the same time it expands the alveoli allowing air to enter easily and become trapped in lungs |
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280. Forced expiratory vital capacity
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Pt inspires maximally to the total lung capacity
Exhales into spirometer w/maximum expiratory effort as rapidly and completely as possible Total volume changes are not greatly different btwn normal lungs and partial airway obstruction; major difference is in the amt of air the person can expire each second |
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281. Pulmonary emphysema
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Literally means excess air in lungs
Usually used to describe complex obstructive and destructive processes of the lungs caused by many years of smoking |
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282. Pathophysiologic changes associated w/emphysema
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1. Chronic infection
-due to smoking; causes excessively thick mucus blocking it from moving out 2. Chronic obstruction of smaller airways 3. Entrapment of air in the alveoli and overstretching of them -leads to destruction of as much as 50-80% of the alveolar walls |
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283. Physiologic changes associated w/emphysema
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Depends on severity of disease and relative degree of bronchiolar obstruction vs lung parenchymal destruction
1. Increased airway resistance which causes increased work of breathing 2. Decreased diffusing capacity of lungs b/c of loss of alveolar walls 3. Extremely abnormal ventilation/perfusion ratios resulting in poor aeration of the blood -poor aeration in blood can vary btwn people b/c of differing abnormalities in ventilation/perfusion ratios 4. Pulmonary hypertension which eventually causes right sided heart failure Net result of all these effects is severe prolonged devastating air hunger that can last for years until hypoxia and hypercapnia cause death |
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284. Pneumonia
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Any inflammatory condition in the lung in which some or all of the alveoli are filled w/fluid or blood cells.
Common type is bacterial pneumonia caused by pneumococci Begins w/infection in the alveoli; then the pulmonary membrane becomes inflamed and highly porous so that fluid and blood cells leak out of the blood and into the alveoli. Infection spreads by extension of bacteria or virus from alveolus to alveolus |
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285. Pneumonia and gas exchange functions
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Changes in different stages of disease
Early disease process may be localized to only one lung w/alveolar ventilation reduced while blood flow thru lung continues normally. This results in 1. Reduction of the total available surface area of the membrane 2. Decreased ventilation perfusion ratio |
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286. Ventilation/perfusion ratio (or V/Q ratio)
|
In respiratory physiology, the ventilation/perfusion ratio (or V/Q ratio) is a measurement used to assess the efficiency and adequacy of the matching of two variables
"V" - ventilation - the air which reaches the lungs "Q" - perfusion - the blood which reaches the lungs |
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287. Atelectasis
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Means collapse of alveoli
Can occur in localized areas or in the entire lung Most common causes are total obstruction of airway or lack of surfactant |
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288. Atelectatic lung
|
When an entire lung becomes collapsed; a condition called massive collapse of the lung
Effects are: 1. Collapse of lung tissue not only occludes the alveoli but almost always increases the resistance to blood flow thru pulmonary vessels in the collapsed lung 2. Hypoxia in the collapse alveoli cause additional vasoconstriction 3. Vasoconstriction causes blood flow to become slight, however the V/Q ratio is only moderately compromised b/c most of the blood is routed thru the ventilated lung |
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289. Surfactant disorder
|
Called hyaline membrane disease AKA respiratory distress syndrome
Quantity of surfactant secreted by the alveoli is so low that the surface tension causes the lungs to collapse |
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290. Asthma and IgE antibodies
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Allergic persons have a tendency to form abnormally large amts of IgE
These antibodies react w/specific antigens and then become attached to mast cells and then the mast release: 1. Histamine 2. Slow reacting substance of anaphylaxis 3. Eosinophilic chemotactic factor 4. Bradykinin |
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291. Effects of factors released by mast cells in asthma
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1. Localized edema in the walls of small bronchioles as well as secretion of thick mucus into the bronchiolar lumens
2. Spasm of bronchiolar smooth muscle |
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292. Clinical measurements of asthmatic person
|
1. Greatly reduced max expiratory rate
2. Reduced timed expiratory volume 3. Functional residual capacity and residual volume of the lung become increased during the acute attack b/c of the difficulty in expiring the air. Results in dyspnea |
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293. Tuberculosis
|
Tubercle bacilli cause tissue reaction in the lungs :
1. Invasion of the infected tissue by macrophages 2. Walling off of the lesion by fibrous tissue to form the so called tubercle -helps to limit further transmission of the bacilli in the lungs but can cause significant destruction of lung tissue w/formation of large abscess cavities |
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294. Effects of tuberculosis
|
1. Increased work on the part of respiratory muscles to cause pulmonary ventilation and reduced vital capacity and breathing capacity
2. Reduced total respiratory membrane surface area and increased thickness of surface membrane causing diminished diffusing capacity 3. Abnormal ventilation perfusion ratio in the lungs, further reducing overall pulmonary diffusion of O2 and CO2 |
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295. Causes of hypoxia
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1. Inadequate oxygenation of blood due to extrinsic reasons (i.e. atmosphere)
2. Pulmonary disease 3. Venous to arterial shunts (right to left cardiac shunts) 4. Inadequate O2 transport to the tissues by blood 5. Inadequate tissue capability of using O2 |
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296. Inadequate tissue capability of using O2
|
Caused by cyanide poisoning in which action of cytochrome oxidase is blocked by cyanide
The disease beriberi, in which several important steps in tissue utilization of O2 due to vitamin B12 deficiency *Cannot be corrected by O2 therapy |
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297. Effects of hypoxia on the body
|
1. Depressed mental activity sometimes culminating in coma
2. Reduced work capacity of muscles |
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298. Cyanosis
|
Means blueness of the skin and is caused by excessive amts of deoxygenated Hb in the skin and blood vessels, esp in the capillaries
Generally appears when arterial blood contains more than 5g of deoxygenated Hb per 100 mL blood Not usually w/anemia but does occur w/polycythemia vera |
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299. Hypercapnia
|
Means excessive CO2 in body fluids which occurs w/hypoxia only when it is caused by hypoventilation or circulatory deficiency
At higher levels of Pco2, excess CO2 actually begins to depress respiration rather than stimulate it; causing more CO2 to accumulate and cause further depression of respiration and results in respiratory death |
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300. Dyspnea
|
Means mental anguish associated w/the inability to ventilate enough to satisfy the demand for air
AKA air hunger Three factors: 1. Abnormality of respiratory gases in the body fluids, esp hypercapnia 2. Amt of work that must be performed by respiratory muscles to provide adequate ventilation 3. State of mind (called neurogenic dyspnea or emotional dyspnea) -hyperventilation due to anxiety |
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301. Artificial respiration
|
1. Resuscitator
2. Tank respirator (AKA iron lung) *Both can reduce the cardiac output b/c of inadequate venous return b/c the pressure inside the lungs become greater than everywhere else |
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302. Pleural disease
|
In certain systemic illnesses or diseases of the thorax, the pleural space if violated by an accumulation of air, fluid, blood, as well as tumors or traumatic disruption
Pleural inflammation increases the permeability of pleural vessels and causes excessive fluid to enter the space for a given driving force Additionally, protein concentration in the fluid increases, and creates and increased oncotic force that favors fluid accumulation |
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303. Disturbance of fluid turnover in the pleural space
|
Due to central lymphatic obstruction or obstruction of channels at the pleural surface by tumor or exudates
Dynamics are altered by increased hydrostatic pressure as observed w/congestive heart failure, decreased blood oncotic pressure, increased permeability, increased negative pleural pressure, or impaired lymphatic drainage |
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304. Symptoms of pleural disease
|
1. May be asymptomatic or exhibit dyspnea and/or pleuritic chest pain
2. Fever may be present depending on origin of problem 3. Physical exam may reveal splinting, limited hemithorax excursion, and friction rub 4. Decreased breath sounds, egophony and dullness to percussion are expected in pleural effusion, atelectasis, consolidation, or lung mass |
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305. Radiography of pleural disease
|
XRay may show a # of findings:
1. Homogeneous density with meniscus formation at the lateral chest wall 2. Blunted costophrenic angle and thickened fissure lines US is used to localized effusion CT allows eval of pleural space and adjacent structures that may be involved |
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306. Pleural effusion
|
Most common cause is CHF
Parapneumonic effusions also common and malignancy, result of a primary tumor or metastatic lesion due to lymphatic spread |
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307. Development of transudate and exudate
|
Osmotic and hydrostatic forces are responsible for the devel of transudate
Altered vascular permeability causes exudate formation |
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308. Distinguishing exudate from transudate
|
Three criteria in pleural fluid:
1. Serum protein ratio 2. Serum lactate dehydrogenase ratio 3. Lactate dehydrogenase |
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309. Exudate
|
Has high levels of
1. Serum protein ratio > .5 2. Serum lactate dehydrogenase ratio > .6 3. Lactate dehydrogenase > 200 Transudate has lower values |
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310. Complicated effusion
|
Refers to fluid accumulation as a result of infection; evacuation is necessary and can be obtained by the insertion of a thoracostomy tube
pH < 7.2 usually is complicated effusion but is not definitive |
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311. Copes or Abram's needle
|
Used for blind biopsy of pleura; may also be used under video assisted thoracoscopy
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312. Transudative effusions
|
Typically small and rarely require draining to improve symptoms
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313. Exudative effusions
|
Require drainage to avoid sepsis and prevent development of loculation, cutaneous fistulas, lung abscess, and bronchopleural fistulas
Injection of fibrolytic agents into interpleural space may be necessary to prevent fibrothorax in these cases |
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314. Pneumothorax types
|
1. Spontaneous pneumothorax
2. Complicated (result of underlying lung disease- pneumocytic carini infection) 3. Catamenial pneumothorax which develops menstruation in women between ages of 30-40 w/pelvic endometriosis 4. Tension pneumothorax |
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315. Malignant mesothelioma
|
Caused by exposure to absestos in the distant past
May exhibit dyspnea, chest pain, weight loss Chest imaging shows pleural effusion and mass; Dx requires pleural biopsy; prognosis is poor |
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316. Mediastinitis
|
Rapidly progressive and inflammatory process that occurs as a result of trauma and necrotic tumor or iatrogenic during invasive procedures
Infection leads to fever, sepsis, pain, and subcutaneous emphysema Imaging reveals widening of mediastinum, pneumothorax or hydrothorax; treatment requires antibiotics, pleural drainage, and mediastinal evacuation |
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317. Mediastinal masses
|
Major cause = neurogenic neoplasms, thymomas, congenital cysts, lymphomas, and germ cell tumors
Medistinoscopy can be used to eval Treatment depends on type of mass |
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318. Chest wall diseases
|
Any disease that restricts motion of the chest, wall, distorts its symmetry, or interferes w/neuromuscular function
May produce hypoventilation Total lung and vital capacities are decreased but residual volume is usually normal or even increased |
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319. Vertebral disease
|
Disorders of the chest wall that are associated w/the vertebrae; i.e. scoliosis and kyphosis
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320. Obesity
|
Classified as a chest wall disease; causes decrease in expiratory reserve volume, decreased ventilation of basilar portion of lungs, and hypoxia of V/Q inequality
Abnormalities increase in supine position |
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321. Unilatera diaphragmatic paralysis
|
-may be asymptomatic
-encroachment of abdominal contents in supine position may worsen symptoms -causes include injury of phrenic nerve, viral neuropathy, systemic lupus, or other neuropathic diseases Dx made by pleuroscopic observation and nerve conduction studies |
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322. Bilateral diaphragmatic paralysis
|
Causes significant dyspnea and orthopnea
Paradoxic inward motion of the abdominal wall during inspiration is classic finding Max inspiratory force is decreased Usually the manifestation of acute or chronic generalized neuromuscular disease and is usually irreversible. |
