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Endocrinology part IIi + Charts by Dr. Sookun Rajeev Kumar
- 1. CHARTS ENDOCRINOLOGY PART II + Dr.Rajeev K Sookun Dept of Physiology Anna Medical College
- 2. CUSHING SYNDROME (HARVERY CUSHING,1932) Definition: An excess secretion of glucocorticoids from adrenal cortex ( zona fasciculata ). Causes : • Excess administration. • Excess secretion from adrenal cortex. • Excess Adrenocorticotropic hormone leading to excess secretion. • Excess Corticotropin-releasing hormone secretion also increases glucocorticoid secretion.
- 3. CUSHING SYNDROME Features : 1. MOON FACE 2. HIRSUITISM (due to T androgen) 3. MENSTRUAL DISTURBANCE 4. OSTEOPOROSIS
- 4. CUSHING SYNDROME 5. PURPLE STRIAE (due to rupture of subcutaneous tissue due to catabolic effect of cortisol). 6. POLYCYTHEMIA. 7. HYPERGLYCEMIA (due to diabetogenic action of cortisol) 8. WOUND HEALING IS POOR 9. HIGH FFA LEVEL IN BLOOD (due to lipolysis) 10. MYOPATHY
- 5. CUSHING SYNDROME 11. THIN LIMBS (redistribution of body fats. Person appears like lemon on toothpicks) 12. MUSCLE WASTING (due to catabolism of proteins) 13. PRONE TO PEPTIC ULCERS
- 6. CUSHING SYNDROME 13. TYPICAL TRUNCAL OBESITY 14. BUFFALO HUMP 15. SYSTOLIC HYPERTENSION 16. PRONE TO INFECTION (due to suppressed immunity) 17. LYMPHOCYTOPENIA and EOSINOPHILIA (due to destruction these cells by cortisol)
- 7. CUSHING SYNDROME 18. Mental changes like EUPHORIA and PSYCHOSIS Treatment: 1. Removal of adrenal gland of it is due to an Adrenal tumour 2. Removal of pituitary if it is due to pituitary tumour. 3. Bilateral adrenalectomy following substitution therapy. 4. Removal of ectopic source of ACTH
- 8. TETANUS Definition : Tetanus is a medical condition characterised by a prolonged contraction of skeletal muscle fibres. It is an infection that generally occurs through wound contamination and often involves a cut or puncture wound. Cause : Gram positive bacteria known as CLOSTRIDIUM TETANI. Clostridium Tetany produces a neurotoxin called TETANOSPASMIN
- 9. TETANUS 4. SPASM AFFECT BREATHING MUSCLES (breathing problems) 5. Prolonged muscular action causes sudden,powerful, and painful contraction of muscle groups known as TETANY Patient suffers from drooling, excessive sweating, fever, hand and foot spasm,irritability, dysphagia and uncontrolled urination and defecation. Treatment : Proper immunisation Post exposure prophylaxis. Features : 1. SPASM IN THE JAW MUSCLE (lockjaw) 2. SPASMS AFFECT CHEST, NECK, BACK, ABDOMINAL MUSCLES, and BUTTOCKS. 3. BACK MUSCLE SPASM cause arching known as OPITHOTONOS
- 10. TROUSSEAU SIGN OF LATENT TETANY Definition : is a medical sign observed in patients with low calcium It appears before other gross manifestations of hypocalcemia such as HYPERREFLEXIA and TETANY. Trousseau sign is more sensitive (94%) than the Chvostek sign.
- 11. MENSTRUAL CYCLE
- 12. MENSTRUAL CYCLE 1. Hypothalamus produces GnRH. 2. GnRH travels to the Anterior Pituitary. 3. GnRH stimulates the production of LH and FSH. 4. During early cycle, more FSH is produced than LH. 5. FSH is a follicular stimulating hormone. It promotes the formation of 6 – 10 follicles. 6. Follicles produce Estrogen. 7. An increase in Estrogen causes a negative feedback. 8. Negative feedback causes a decrease in LH and FSH production.
- 13. MENSTRUAL CYCLE 9. Mature follicle will keep on producing Estrogen despite low level of LH and FSH. 9. This Estrogen will help build the endometrial lining. 10. Decrese LH and FSH causes survival of the fittest. 11. Estrogen level finally reach a threshold. 12. This triggers a positive feedback mechanism which causes the hypothalamus to secrete GnRH and in turn stimulates the anterior pituitary to produce LH and FSH. 13. Now, there is rather increased LH (LH surge) than FSH.(Ovulation phase) 14. Ovum is finally secreted from the follicle.
- 14. MENSTRUAL CYCLE 15. Rise in Basal body temperature. 16. LH causes the ruptured follicle to become a corpus luteum.(Luteal phase) 17. The corpus luteum produces Estrogen and Progesterone. 18. This rise in Estrogen causes a negative feedback. 19. Results in decrease LH and FSH. 20. Degeneration of corpus luteum causes decrease in Estrogen and Progesterone. 21. Results in sloughing of the endometrial tissue. (Menstrual phase)
- 15. CARDIAC CYCLE
- 16. CARDIAC CYCLE ATRIAL SYSTOLE 1. P wave – Depolarisation of atrial wall – Contraction of the atria. 2. Rise in atrial pressure. 3. Blood goes into ventricles - Slight increase in ventricular volume.
- 17. CARDIAC CYCLE 2. ISOVOLUMETRIC VENTRICULAR CONTRACTION 1. QRS complex is formed – Depolarisation of ventricles – Contraction of ventricles. 2. AV is closed. 3. Increase in ventricular pressure. 4. Ventricular volume is constant.
- 18. CARDIAC CYCLE 3. EJECTION 1. Ventricular pressure > aortic pressure. 2. Causes aortic valve to open. Blood from ventricle goes to aorta. 3. Ventricular pressure decreases slowly. Ventricular volume decreases.
- 19. CARDIAC CYCLE 4. ISOVOLUMETRIC RELAXATION 1. End of T wave – Repolarisation of ventricles (ventricles relax). 2. Ventricular pressure continue to decrease. 3. Ventricular volume stays constant. 4. Aortic valve closes and AV valves open.
- 20. CARDIAC CYCLE 5. RAPID INFLOW 1. Aortic pressure decreases. 2. Increase ventricular volume.
- 21. CARDIAC CYCLE 6. REDUCED VENTRICULAR FILLING (Diastasis) 1. Is the longest phase of the cardiac cycle. 2. Ventricular filling continues, but at a slower rate. 3. The time required for diastasis and ventricular filling depends on the heart rate. Increase in heart rate decrease the time available for ventricular refilling.
- 22. CARDIAC CYCLE 7. PHONOCARDIOGRAM 1. 1st heart sound. Splitting due to MV closes faster than T valve. 2. 2nd heart sound by closure of aortic valve. 3. 3rd heart sound in children , pregnancy and young males. 4. 4th heart sound is pathological.
- 23. SPIROMETRY
- 24. SPIROMETRY LUNG VOLUMES 1. Tidal volume (TV) : - is the volume inspired or expired with each normal breath. 2. Inspiratory reserve volume (IRV) - is the volume that can be inspired over and above the tidal volume. - is used during exercise. 3. Expiratory reserve volume (ERV) - is the volume that can be expired after the expiration of a tidal volume 4. Residual volume (RV) - is the volume that remains in the lungs after a maximal expiration - cannot be measured by spirometry
- 25. SPIROMETRY LUNG VOLUMES 5.Dead space – a.Anatomic dead space - is the volume of the conducting airways. - is normally approximately 150ml. b.Physiologic dead space -is a functional measurement. -is defined as the volume of the lungs that does not participate in gas exchange. -is approximately equal to the anatomic dead space -in normal lungs may be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects.
- 26. SPIROMETRY LUNG CAPACITIES 1.Inspiratory capacity (IC) - is the sum of tidal volume and IRV. 2. Functional residual capacity (FRC) -is the sum of ERV and residual volume. -is the volume remaining in the lungs after a tidal volume is expired. -includes the residual volume, so it cannot be measured by spirometry. 3. Vital capacity ( VC) ,or forced vital capacity (FVC) - is the sum of tidal volume, IRV ,and ERV. - is the volume of air that can be forcibly expired after a maximal inspiration. . 4. TOTAL LUNG CAPACITY (TLC) - is the sum of all four lung volumes - is the volume in the lungs after a maximal inspiration - includes residual volume ,so it cannot be measured by spirometry.
- 28. CYSTOMETROGRAM First sensation of bladder filling is experienced at a volume of 100 – 150 ml in an adult. Then the 1st desire to void/urinate is when the bladder contains about 150-250 ml of urine. A person becomes uncomfortably aware of a full bladder when the volume is 350-400 ml. The volume of urine that normally initiates a reflex contraction is about 300-400 ml. An increase in volume to 700 ml creates pain and loss of control
- 29. STETHOGRAPHY
- 30. STETHOGRAPHY HYPERVENTILATION Periodic breathing occurs following voluntary hyperventilation. There occurs apnea followed by a brief period of hyperpnea. It is seen physiologically in sleep (especially in infants) at high altitude and following voluntary and pathologically in left ventricular failure and brain damage.
- 31. STETHOGRAPHY BREATH-HOLDING TIME (BHT) BHT is the time taken by the subject to hold his breath as long as he can. BHT is greater following inspiration than expiration.
- 32. STETHOGRAPHY DEGLUTITION APNEA During deglutition , respiration stops temporarily. This is called deglutition apnea. It is due to closure of the glottis, which helps in passage of food or water in the esophagus and prevents entry of food materials into the respiratory tract.
- 33. STETHOGRAPHY EXERCISE During exercise, hyperventilation occurs due to stimulation of the respiratory centres by increased discharge from the proprioceptors in the joints, ligaments and muscles.
- 34. ACTION POTENTIAL
Editor's Notes
- FFA – Free fatty acid
- Adrenocorticotropic hormone
- To elicit the sign, a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct. The sign is also known as main d'accoucheur (French for "hand of the obstetrician") because it supposedly resembles the position of an obstetrician's hand in delivering a baby.
- ACTIONS OF ESTROGEN Has both negative and positive feedback effects on FSH and LH secretion. Causes maturation and maintenance of the fallopian tube, uterus, cervix and vagina. Causes the development of female secondary sex characteristics at puberty. Causes the development of the breasts. Up-regulates estrogen, LH and progesterone receptors. Causes proliferation and development of ovarian granulose cells. Maintains pregnancy. Lowers the uterine threshold to contractile stimulus during pregnancy. Stimulates prolacting secretion (but then blocks its action on the breasts). ACTIONS OF PROGESTERONE Has negative feedback effects on FSH and LH secretion during luteal phase. Maintains secretory activity of the uterus during the luteal phase. Maintains pregnancy. Raises the uterine threshold to contractile stimuli during pregnancy. Participate in development of the breasts. MENSTRUAL CYCLE Follicular phase ( days 0-14) A primordial follicle develops to the grafian stage, with atresia of neighbouring follicles. LH and FSH receptors are up-regulated in theca and granulosa cells. Estradiol levels increase and cause proliferation of the uterus. FSH and LH levels are suppressed by the negative feedback affect of estradiol on the anterior pituitary. Progesterone levels are low OVULATION (day 14) Occurs 14 days before menses, regardless of cycle length. Thus, in a 28 days cycle, ovulation occurs on day 14; in a 35 day cycle, ovulation occurs on dat 22. A burst of estradiol synthesis at the end of the follicular phase has a positive feedback effect on the secretion of FSH and LH (LH surge). Ovulation occurs as a result of the estrogen induced LH surge. Estrogen levels decrease just after ovulation (but rise again during the luteal phase). Cervical mucus increases in quantity, it becomes less viscous and more penetrable by sperm. LUTEAL PHASE (day 14-28) The corpus luteum begins to develop and it synthesizes estrogen and progesterone. Vascularity and secretory activity of the endometrium increase to prepare for receipt of a fertilised egg. Basal body temperature increases because of the effects of progesterone on the hypothalamic thermoregulatory centre. If fertilisation does not occur, the corpus luteum regresses at the end of the luteal phase. As a result, estradiol and progesterone levels decrease abruptly. MENSES (days 0-4) The endometrium is sloughed because of the abrupt withdrawal of estradiol and progesterone.
- ACTIONS OF ESTROGEN Has both negative and positive feedback effects on FSH and LH secretion. Causes maturation and maintenance of the fallopian tube, uterus, cervix and vagina. Causes the development of female secondary sex characteristics at puberty. Causes the development of the breasts. Up-regulates estrogen, LH and progesterone receptors. Causes proliferation and development of ovarian granulose cells. Maintains pregnancy. Lowers the uterine threshold to contractile stimulus during pregnancy. Stimulates prolacting secretion (but then blocks its action on the breasts). ACTIONS OF PROGESTERONE Has negative feedback effects on FSH and LH secretion during luteal phase. Maintains secretory activity of the uterus during the luteal phase. Maintains pregnancy. Raises the uterine threshold to contractile stimuli during pregnancy. Participate in development of the breasts. MENSTRUAL CYCLE Follicular phase ( days 0-14) A primordial follicle develops to the grafian stage, with atresia of neighbouring follicles. LH and FSH receptors are up-regulated in theca and granulosa cells. Estradiol levels increase and cause proliferation of the uterus. FSH and LH levels are suppressed by the negative feedback affect of estradiol on the anterior pituitary. Progesterone levels are low OVULATION (day 14) Occurs 14 days before menses, regardless of cycle length. Thus, in a 28 days cycle, ovulation occurs on day 14; in a 35 day cycle, ovulation occurs on dat 22. A burst of estradiol synthesis at the end of the follicular phase has a positive feedback effect on the secretion of FSH and LH (LH surge). Ovulation occurs as a result of the estrogen induced LH surge. Estrogen levels decrease just after ovulation (but rise again during the luteal phase). Cervical mucus increases in quantity, it becomes less viscous and more penetrable by sperm. LUTEAL PHASE (day 14-28) The corpus luteum begins to develop and it synthesizes estrogen and progesterone. Vascularity and secretory activity of the endometrium increase to prepare for receipt of a fertilised egg. Basal body temperature increases because of the effects of progesterone on the hypothalamic thermoregulatory centre. If fertilisation does not occur, the corpus luteum regresses at the end of the luteal phase. As a result, estradiol and progesterone levels decrease abruptly. MENSES (days 0-4) The endometrium is sloughed because of the abrupt withdrawal of estradiol and progesterone.
- ACTIONS OF ESTROGEN Has both negative and positive feedback effects on FSH and LH secretion. Causes maturation and maintenance of the fallopian tube, uterus, cervix and vagina. Causes the development of female secondary sex characteristics at puberty. Causes the development of the breasts. Up-regulates estrogen, LH and progesterone receptors. Causes proliferation and development of ovarian granulose cells. Maintains pregnancy. Lowers the uterine threshold to contractile stimulus during pregnancy. Stimulates prolacting secretion (but then blocks its action on the breasts). ACTIONS OF PROGESTERONE Has negative feedback effects on FSH and LH secretion during luteal phase. Maintains secretory activity of the uterus during the luteal phase. Maintains pregnancy. Raises the uterine threshold to contractile stimuli during pregnancy. Participate in development of the breasts. MENSTRUAL CYCLE Follicular phase ( days 0-14) A primordial follicle develops to the grafian stage, with atresia of neighbouring follicles. LH and FSH receptors are up-regulated in theca and granulosa cells. Estradiol levels increase and cause proliferation of the uterus. FSH and LH levels are suppressed by the negative feedback affect of estradiol on the anterior pituitary. Progesterone levels are low OVULATION (day 14) Occurs 14 days before menses, regardless of cycle length. Thus, in a 28 days cycle, ovulation occurs on day 14; in a 35 day cycle, ovulation occurs on dat 22. A burst of estradiol synthesis at the end of the follicular phase has a positive feedback effect on the secretion of FSH and LH (LH surge). Ovulation occurs as a result of the estrogen induced LH surge. Estrogen levels decrease just after ovulation (but rise again during the luteal phase). Cervical mucus increases in quantity, it becomes less viscous and more penetrable by sperm. LUTEAL PHASE (day 14-28) The corpus luteum begins to develop and it synthesizes estrogen and progesterone. Vascularity and secretory activity of the endometrium increase to prepare for receipt of a fertilised egg. Basal body temperature increases because of the effects of progesterone on the hypothalamic thermoregulatory centre. If fertilisation does not occur, the corpus luteum regresses at the end of the luteal phase. As a result, estradiol and progesterone levels decrease abruptly. MENSES (days 0-4) The endometrium is sloughed because of the abrupt withdrawal of estradiol and progesterone.
- ACTIONS OF ESTROGEN Has both negative and positive feedback effects on FSH and LH secretion. Causes maturation and maintenance of the fallopian tube, uterus, cervix and vagina. Causes the development of female secondary sex characteristics at puberty. Causes the development of the breasts. Up-regulates estrogen, LH and progesterone receptors. Causes proliferation and development of ovarian granulose cells. Maintains pregnancy. Lowers the uterine threshold to contractile stimulus during pregnancy. Stimulates prolacting secretion (but then blocks its action on the breasts). ACTIONS OF PROGESTERONE Has negative feedback effects on FSH and LH secretion during luteal phase. Maintains secretory activity of the uterus during the luteal phase. Maintains pregnancy. Raises the uterine threshold to contractile stimuli during pregnancy. Participate in development of the breasts. MENSTRUAL CYCLE Follicular phase ( days 0-14) A primordial follicle develops to the grafian stage, with atresia of neighbouring follicles. LH and FSH receptors are up-regulated in theca and granulosa cells. Estradiol levels increase and cause proliferation of the uterus. FSH and LH levels are suppressed by the negative feedback affect of estradiol on the anterior pituitary. Progesterone levels are low OVULATION (day 14) Occurs 14 days before menses, regardless of cycle length. Thus, in a 28 days cycle, ovulation occurs on day 14; in a 35 day cycle, ovulation occurs on dat 22. A burst of estradiol synthesis at the end of the follicular phase has a positive feedback effect on the secretion of FSH and LH (LH surge). Ovulation occurs as a result of the estrogen induced LH surge. Estrogen levels decrease just after ovulation (but rise again during the luteal phase). Cervical mucus increases in quantity, it becomes less viscous and more penetrable by sperm. LUTEAL PHASE (day 14-28) The corpus luteum begins to develop and it synthesizes estrogen and progesterone. Vascularity and secretory activity of the endometrium increase to prepare for receipt of a fertilised egg. Basal body temperature increases because of the effects of progesterone on the hypothalamic thermoregulatory centre. If fertilisation does not occur, the corpus luteum regresses at the end of the luteal phase. As a result, estradiol and progesterone levels decrease abruptly. MENSES (days 0-4) The endometrium is sloughed because of the abrupt withdrawal of estradiol and progesterone.
- 1. ATRIAL SYSTOLE 1. Is preceeded by the P wave,which represents electrical activation of the atria. 2. Contributes to,but is not essential for ventricular filling. 3. The increase in atrial pressure (venous pressure) caused by atrial systole is the Alpha wave on the venous pulse curve. 4. Filling of the ventricle by atrial systole causes the 4th heart sound, which is not audible in normal adults. 2. ISOVOLUMETRIC VENTRICULAR CONTRACTION 1. Begins after the onset of the QRS wave, which represent electrical activation of the ventricles. 2. When ventricular pressure becomes greater than atrial pressure ,the AV valves close.Their closure corresponds to the first heart sound. Because the mitral valve closes before the tricuspid valve, the 1st heart sound may be split. 3. Ventricular pressure increases isovolumetrically as a result of ventricular contraction. However, no blood leaves the ventricle during this phase because the aortic valve is closed. 3. RAPID VENTRICULAR EJECTION 1. Ventricular pressure reaches it’s maximum value during this phase. 2. When ventricular pressure becomes greater than aortic pressure, the aortic valve opens. 3. Rapid ejection of blood into aorta occurs because of the pressure gradient between ventricle and the aorta. 4. Ventricular volume decreases dramatically because most of the stroke volume is ejected during this phase. Atrial filling begins. 5. The onset of the T wave, which represents repolarization of the ventricles, marks the end of both ventricular contraction and rapid ventricular ejection. 4. REDUCED VENTRICULAR EJECTION 1. Ejection of blood from the ventricle continue, but is slower. 2. Ventricular pressure begins to decrease. 3. Aortic pressure also decreases because of the runoff of the blood from large arteries into smaller arterials. 4. Atrial filling continues. 5. ISOVOLUMETRIC VENTRICULAR RELAXATION 1. Repolarization of the ventricles is now complete (end of the T wave). 2. The aortic valve closes, followed by closure of the pulmonary valve. Closure of the semilunar valves corresponds to the 2nd heart sound. Inspiration causes splitting of the 2nd heart sound. 3. The AV valves remains closed during most of this phase. 4. Ventricular pressure rapidly decreases because the ventricle is now relaxed. 5. Ventricular volume is constant ( isovolumetric) because all the valves are closed. 6. A ‘blip’ in the aortic pressure tracing occurs after closure of the aortic valve and is called the dicrotic notch or incisura. 7. When ventricular pressure becomes less than atrial pressure, the mitral valve opens. 6. RAPID VENTRICULAR FILLING 1. The mitral valve is open and ventricular filling from the atrium begin. 2. Aortic pressure continues to decrease because blood continues to run off into the smaller arteries. 3. Rapid flow of blood from the atria into the ventricles causes the third heart sound ,which is normal in children but, in adults, is associated with disease. 7. REDUCED VENTRICULAR FILLING (Diastasis) 1. Is the longest phase of the cardiac cycle. 2. Ventricular filling continues, but at a slower rate. 3. The time required for diastasis and ventricular filling depends on the heart rate. Increase in heart rate decrease the time available for ventricular refilling.
- 1. ATRIAL SYSTOLE 1. Is preceeded by the P wave,which represents electrical activation of the atria. 2. Contributes to,but is not essential for ventricular filling. 3. The increase in atrial pressure (venous pressure) caused by atrial systole is the Alpha wave on the venous pulse curve. 4. Filling of the ventricle by atrial systole causes the 4th heart sound, which is not audible in normal adults.
- 2. ISOVOLUMETRIC VENTRICULAR CONTRACTION 1. Begins after the onset of the QRS wave, which represent electrical activation of the ventricles. 2. When ventricular pressure becomes greater than atrial pressure ,the AV valves close.Their closure corresponds to the first heart sound. Because the mitral valve closes before the tricuspid valve, the 1st heart sound may be split. 3. Ventricular pressure increases isovolumetrically as a result of ventricular contraction. However, no blood leaves the ventricle during this phase because the aortic valve is closed.
- 3. RAPID VENTRICULAR EJECTION 1. Ventricular pressure reaches it’s maximum value during this phase. 2. When ventricular pressure becomes greater than aortic pressure, the aortic valve opens. 3. Rapid ejection of blood into aorta occurs because of the pressure gradient between ventricle and the aorta. 4. Ventricular volume decreases dramatically because most of the stroke volume is ejected during this phase. Atrial filling begins. 5. The onset of the T wave, which represents repolarization of the ventricles, marks the end of both ventricular contraction and rapid ventricular ejection.
- 4. REDUCED VENTRICULAR EJECTION 1. Ejection of blood from the ventricle continue, but is slower. 2. Ventricular pressure begins to decrease. 3. Aortic pressure also decreases because of the runoff of the blood from large arteries into smaller arterials. 4. Atrial filling continues.
- 5. ISOVOLUMETRIC VENTRICULAR RELAXATION 1. Repolarization of the ventricles is now complete (end of the T wave). 2. The aortic valve closes, followed by closure of the pulmonary valve. Closure of the semilunar valves corresponds to the 2nd heart sound. Inspiration causes splitting of the 2nd heart sound. 3. The AV valves remains closed during most of this phase. 4. Ventricular pressure rapidly decreases because the ventricle is now relaxed. 5. Ventricular volume is constant ( isovolumetric) because all the valves are closed. 6. A ‘blip’ in the aortic pressure tracing occurs after closure of the aortic valve and is called the dicrotic notch or incisura. 7. When ventricular pressure becomes less than atrial pressure, the mitral valve opens.
- 7. REDUCED VENTRICULAR FILLING (Diastasis) 1. Is the longest phase of the cardiac cycle. 2. Ventricular filling continues, but at a slower rate. 3. The time required for diastasis and ventricular filling depends on the heart rate. Increase in heart rate decrease the time available for ventricular refilling.
- 6. RAPID VENTRICULAR FILLING 1. The mitral valve is open and ventricular filling from the atrium begin. 2. Aortic pressure continues to decrease because blood continues to run off into the smaller arteries. 3. Rapid flow of blood from the atria into the ventricles causes the third heart sound ,which is normal in children but, in adults, is associated with disease.
- A.LUNG VOLUMES 1. Tidal volume (TV) is the volume inspired or expired with each normal breath 2. Inspiratory reserve volume (IRV) is the volume that can be inspired over and above the tidal volume is used during exercise. 3. Expiratory reserve volume (ERV) is the volume that can be expired after the expiration of a tidal volume 4. Residual volume (RV) is the volume that remains in the lungs after a maximal expiration cannot be measured by spirometry 5.Dead space a.Anatomic dead space is the volume of the conducting airways is normally approximately 150ml b.Physiologic dead space is a functional measurement is defined as the volume of the lungs that does not participate in gas exchange is approximately equal to the anatomic dead space in normal lungs may be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects. Is calculated by the following equation: Vd=vtxpaco2 – peco2 Paco2 Where vd = physiologic dead space (mL) VT = tidal volume (mL) PACO2 = PCO2 of alveolar gas (mmHg) = PCO2 of arterial blood PECO2 = PCO2 of expired air (mmHg) In words, the equation states that physiologic dead space is tidal volume multiplied by a fraction. The fraction represents the dilution of alveolar PCO2 by dead space air, which does not participate in gas exchange and does not therefore contribute CO2 to expired air. VENTILATION RATE minute ventilation is expressed as follows: minute ventilation = tidal volume x breaths/ min alveolar ventilation is expressed as follows: alveolar ventilation = ( tidal volume – dead space) x breaths/min LUNG CAPACITIES 1.Inspiratory capacity is the sum of tidal volume and IRV 2. Functional residual capacity (FRC) is the sum of ERV and residual volume is the volume remaining in the lungs after a tidal volume is expired includes the residual volume, so it cannot be measured by spirometry 3. Vital capacity ( VC) ,or forced vital capacity (FVC) is the sum of tidal volume, IRV ,and ERV is the volume of air that can be forcibly expired after a maximal inspiration. TOTAL LUNG CAPACITY (TLC) is the sum of all four lung volumes is the volume in the lungs after a maximal inspiration includes residual volume ,so it cannot be measured by spirometry. C.FORCED EXPIRATORY VOLUME (FEV1) FEV1 is the volume of air that can be expired in the first second of a forced maximal expiration. FEV1 is normally 80% of the forced vital capacity ,which is expressed as : FEV1/FVC = 0.8 In obstructive lung disease, as asthma, FEV1 is reduced more than so that FEV1/FVC is decreased. In restrictive lung disease, such as fibrosis, both FEV1 and FVC are reduced and FEV1/FVC is either normal or is increased.
- A.LUNG VOLUMES 1. Tidal volume (TV) is the volume inspired or expired with each normal breath 2. Inspiratory reserve volume (IRV) is the volume that can be inspired over and above the tidal volume is used during exercise. 3. Expiratory reserve volume (ERV) is the volume that can be expired after the expiration of a tidal volume 4. Residual volume (RV) is the volume that remains in the lungs after a maximal expiration cannot be measured by spirometry 5.Dead space a.Anatomic dead space is the volume of the conducting airways is normally approximately 150ml b.Physiologic dead space is a functional measurement is defined as the volume of the lungs that does not participate in gas exchange is approximately equal to the anatomic dead space in normal lungs may be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects.
- A.LUNG VOLUMES 1. Tidal volume (TV) is the volume inspired or expired with each normal breath 2. Inspiratory reserve volume (IRV) is the volume that can be inspired over and above the tidal volume is used during exercise. 3. Expiratory reserve volume (ERV) is the volume that can be expired after the expiration of a tidal volume 4. Residual volume (RV) is the volume that remains in the lungs after a maximal expiration cannot be measured by spirometry 5.Dead space a.Anatomic dead space is the volume of the conducting airways is normally approximately 150ml b.Physiologic dead space is a functional measurement is defined as the volume of the lungs that does not participate in gas exchange is approximately equal to the anatomic dead space in normal lungs may be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects.
- LUNG CAPACITIES 1.Inspiratory capacity is the sum of tidal volume and IRV 2. Functional residual capacity (FRC) is the sum of ERV and residual volume is the volume remaining in the lungs after a tidal volume is expired includes the residual volume, so it cannot be measured by spirometry 3. Vital capacity ( VC) ,or forced vital capacity (FVC) is the sum of tidal volume, IRV ,and ERV is the volume of air that can be forcibly expired after a maximal inspiration. TOTAL LUNG CAPACITY (TLC) is the sum of all four lung volumes is the volume in the lungs after a maximal inspiration includes residual volume ,so it cannot be measured by spirometry.
- Lister’s perimetry is used to map the peripheral visual field
- When the urinary bladder is empty, the intravesical pressure is zero. When about 50 mL of fluid is collected, the pressure rises sharply (Ia)to about 10 cm H2O (Ia in the cystometrogram). The pressure in the bladder remains more or less constant with further addition of about 350 mL of urine (Ib) in an adult. This is in accordance with law of Laplace. In the bladder tension increases as the urine is filled. At the same time, the radius also increases due to relaxation of the detrusor muscle. Because of this, the pressure rise is almost nil. When bladder wall stretches during filling it will initiate a reflex contraction which has lower threshold. That does not trigger micturition reflex. When bladder is filled about 300 – 400 mL of urine, there will be sharp rise in the intravesical pressure as the micturition reflex is triggered. When, urine of about 400 mL is collected, the contraction of detrusor muscle becomes intense, increasing the consciousness and the urge for micturition. At this point also voluntary control is possible. Beyond 600 – 700 mL of urine voluntary control starts failing.
- DEGLUTITION APNEA During deglutition respiration stops temporarily. This is called deglutition apnea. It is due to closure of the glottis, which helps in passage of food or water in the esophagus and prevents entry of food materials into the respiratory tract. BREATH-HOLDING TIME (BHT) BHT is the time taken by the subject to hold his breath as long as he can. BHT is greater following inspiration than expiration. Respiration can be voluntarily held for some time, but eventually the voluntary control is overridden. The point at which breathing can no longer be voluntarily inhibited us called a breaking point. The breaking is due to rise in arterial pCO2 and fall in pO2, as body tissues continue to utilise oxygen and produce carbon dioxide. The rise in arterial pCO2 and the fall in pO2 stimulate central and peripheral chemoreceptors that stimulate respiration. Generally, breaking point reaches at alveolar pO2 of 56mmHg and alveolar pCO2 of 49 mmHg. It has been suggested that proprioceptive impulses from respiratory muscles and joints may be involved in breaking point. Factors affecting Breaking point Breathing 100 % oxygen increases BHT. Breathing 100 % oxygen before holding breath increases alveolar pO2 so that the breaking point is delayed. Hyperventilation at room air increases BHT. This is because hyperventilation removes CO2 from the blood and therefore delays breaking point. Psychological factors play a role. Encouragement delays breaking point. HYPERVENTILATION Periodic breathing occurs following voluntary hyperventilation. There occurs apnea followed by a brief period of hyperpnea. The apnea occurs due to removal of carbon dioxide during hyperventilation, so respiration stops temporarily. This causes accumulation of carbon dioxide that stimulates respiration; as a result there is hyperventilation. Periodic breathing (cheyne- stokes breathing) is characterised by alternating apnea and hyperventilation. It is seen physiologically in sleep (especially in infants) at high altitude and following voluntary hyperventilation, and pathologically in left ventricular failure and brain damage. EXERCISE During exercise, hyperventilation occurs due to stimulation of the respiratory centres by increased discharge from the proprioceptors in the joints, ligaments and muscles. Though the increase in respiration is proportionate to the increase in oxygen consumption, the role of oxygen in stimulation of hyperventilation is still not clear. Increased body temperature, increases K+ level and lactic acid concentration play role in hyperventilation. But, as the exercise is mild to moderate here, hyperventilation is mainly due to increased proprioceptive information from the exercising muscles and joints. Hyperventilation persists after intense exercise due to increased arterial H+ concentration that occurs due to lactic academia. Sometimes, a pattern of periodic breathing is also observed following exercise.
- HYPERVENTILATION Periodic breathing occurs following voluntary hyperventilation. There occurs apnea followed by a brief period of hyperpnea. The apnea occurs due to removal of carbon dioxide during hyperventilation, so respiration stops temporarily. This causes accumulation of carbon dioxide that stimulates respiration; as a result there is hyperventilation. Periodic breathing (cheyne- stokes breathing) is characterised by alternating apnea and hyperventilation. It is seen physiologically in sleep (especially in infants) at high altitude and following voluntary hyperventilation, and pathologically in left ventricular failure and brain damage.
- BREATH-HOLDING TIME (BHT) BHT is the time taken by the subject to hold his breath as long as he can. BHT is greater following inspiration than expiration. Respiration can be voluntarily held for some time, but eventually the voluntary control is overridden. The point at which breathing can no longer be voluntarily inhibited us called a breaking point. The breaking is due to rise in arterial pCO2 and fall in pO2, as body tissues continue to utilise oxygen and produce carbon dioxide. The rise in arterial pCO2 and the fall in pO2 stimulate central and peripheral chemoreceptors that stimulate respiration. Generally, breaking point reaches at alveolar pO2 of 56mmHg and alveolar pCO2 of 49 mmHg. It has been suggested that proprioceptive impulses from respiratory muscles and joints may be involved in breaking point. Factors affecting Breaking point Breathing 100 % oxygen increases BHT. Breathing 100 % oxygen before holding breath increases alveolar pO2 so that the breaking point is delayed. Hyperventilation at room air increases BHT. This is because hyperventilation removes CO2 from the blood and therefore delays breaking point. Psychological factors play a role. Encouragement delays breaking point.
- DEGLUTITION APNEA During deglutition respiration stops temporarily. This is called deglutition apnea. It is due to closure of the glottis, which helps in passage of food or water in the esophagus and prevents entry of food materials into the respiratory tract.
- EXERCISE During exercise, hyperventilation occurs due to stimulation of the respiratory centres by increased discharge from the proprioceptors in the joints, ligaments and muscles. Though the increase in respiration is proportionate to the increase in oxygen consumption, the role of oxygen in stimulation of hyperventilation is still not clear. Increased body temperature, increases K+ level and lactic acid concentration play role in hyperventilation. But, as the exercise is mild to moderate here, hyperventilation is mainly due to increased proprioceptive information from the exercising muscles and joints. Hyperventilation persists after intense exercise due to increased arterial H+ concentration that occurs due to lactic academia. Sometimes, a pattern of periodic breathing is also observed following exercise.