| Normal Pressures in the Heart and Great Vessels | ||
Type of Pressure | Average (mm Hg) | Range (mm Hg) |
Right atrium | 3 | 0–8 |
Right ventricle | ||
Peak-systolic | 25 | 15–30 |
End-diastolic | 4 | 0–8 |
Pulmonary artery | ||
Mean | 15 | 9–16 |
Peak-systolic | 25 | 15–30 |
End-diastolic | 9 | 4–14 |
Pulmonary artery occlusion | ||
Mean | 9 | 2–12 |
Left atrium | ||
Mean | 8 | 2–12 |
A wave | 10 | 4–16 |
V wave | 13 | 6–12 |
Left ventricle | ||
Peak-systolic | 130 | 90–140 |
End-diastolic | 9 | 5–12 |
Brachial artery | ||
Mean | 85 | 70–150 |
Peak-systolic | 130 | 90–140 |
End-diastolic | 70 | 60–90 |
Sunday, December 13, 2009
28 - Normal pressures in the Heart and Great vessels
Monday, October 5, 2009
27 - Vasopressin Receptors
*The cellular effects of vasopressin (ADH) are mediated mainly by interactions of the hormone with the three types of receptors, V1a, V1b, and V2.
*The V1a receptor is the most widespread subtype of Vasopressin receptor; it is found in vascular smooth muscle, the adrenal gland, myometrium, the bladder, adipocytes, hepatocytes, platelets, renal medullary interstitial cells, vasa recta in the renal microcirculation, epithelial cells in the renal cortical collecting-duct, spleen, testis, and many CNS structures.
*V1b receptors have a more limited distribution and are found in the anterior pituitary, several brain regions, the pancreas, and the adrenal medulla.
*V2 receptors are located predominantly in principal cells of the renal collecting-duct system but also are present on epithelial cells in the thick ascending limb and on vascular endothelial cells.
*Although originally defined by pharmacological criteria, vasopressin receptors now are defined by their primary amino acid sequences.
*The cloned vasopressin receptors are typical heptahelical G protein–coupled receptors.
*Manning and coworkers (1999) have synthesized novel hypotensive vasopressin peptide agonists that do not interact with V1a, V1b, or V2 receptors and may stimulate a putative vasopressin vasodilatory receptor. Finally, two additional putative receptors for vasopressin have been cloned.
*A vasopressin-activated Ca2+-mobilizing receptor with one transmembrane domain binds vasopressin and increases intracellular Ca2+. A dual angiotensin II–vasopressin heptahelical receptor activates adenylyl cyclase in response to both angiotensin II and vasopressin. The physiological roles of these putative vasopressin receptors are unclear.
*The V1a receptor is the most widespread subtype of Vasopressin receptor; it is found in vascular smooth muscle, the adrenal gland, myometrium, the bladder, adipocytes, hepatocytes, platelets, renal medullary interstitial cells, vasa recta in the renal microcirculation, epithelial cells in the renal cortical collecting-duct, spleen, testis, and many CNS structures.
*V1b receptors have a more limited distribution and are found in the anterior pituitary, several brain regions, the pancreas, and the adrenal medulla.
*V2 receptors are located predominantly in principal cells of the renal collecting-duct system but also are present on epithelial cells in the thick ascending limb and on vascular endothelial cells.
*Although originally defined by pharmacological criteria, vasopressin receptors now are defined by their primary amino acid sequences.
*The cloned vasopressin receptors are typical heptahelical G protein–coupled receptors.
*Manning and coworkers (1999) have synthesized novel hypotensive vasopressin peptide agonists that do not interact with V1a, V1b, or V2 receptors and may stimulate a putative vasopressin vasodilatory receptor. Finally, two additional putative receptors for vasopressin have been cloned.
*A vasopressin-activated Ca2+-mobilizing receptor with one transmembrane domain binds vasopressin and increases intracellular Ca2+. A dual angiotensin II–vasopressin heptahelical receptor activates adenylyl cyclase in response to both angiotensin II and vasopressin. The physiological roles of these putative vasopressin receptors are unclear.
Sunday, September 6, 2009
26 - Nocturnal Penile Tumescence ( NPT )
Nocturnal penile tumescence (NPT) is the spontaneous occurrence of an erection of the penis during sleep. All men without physiological erectile dysfunction experience this phenomenon, usually three to five times during the night. It typically happens during REM sleep. NPT has been given numerous colloquial names which are typically related to the first time the erection is discovered, namely upon waking in the morning — such an erection is colloquially referred to as morning wood in North America, 'dawn horn' the United Kingdom, whilst in other areas morning glory is used. In the United Kingdom the colloquialism 'piss-proud' is often used to imply a causal relationship between a full bladder and an erection.
The existence and predictability of nocturnal tumescence is used by sexual health practitioners to ascertain whether a given case of erectile dysfunction (E.D.) is psychological or physiological in origin. A patient presenting with E.D. is fitted with an elastic device to wear around his penis during sleep; the device detects changes in girth and relays the information to a computer for later analysis. If nocturnal tumescence is detected, then the E.D. is presumed to be due to a psychosomatic illness such as sexual anxiety; if not, then it is presumed to be due to a physiological cause.
The cause of NPT is not known with certainty. Bancroft (2005) hypothesizes that the noradrenergic neurons of the locus ceruleus are inhibitory to penile erection, and that the cessation of their discharge that occurs during REM sleep may allow testosterone-related excitatory actions to manifest as NPT.
Colloquial naming and anecdotal evidence supporting the possibility that a full bladder can stimulate an erection has existed for some time and is characterised as a 'reflex erection'. The nerves that control a man’s ability to have a reflex erection are located in the sacral nerves (S2-S4) of the spinal cord. A full bladder is known to mildly stimulate nerves in the same region. This mild stimulus which during the day is normally suppressed in adult males by competing stimuli and other distractions, could during sleep with the absence of such factors instigate a reflex erection.
The possibility of a full bladder causing an erection, especially during sleep, is perhaps further supported by the beneficial physiological effect of an erection inhibiting urination, thereby helping to avoid nocturnal enuresis.
The existence and predictability of nocturnal tumescence is used by sexual health practitioners to ascertain whether a given case of erectile dysfunction (E.D.) is psychological or physiological in origin. A patient presenting with E.D. is fitted with an elastic device to wear around his penis during sleep; the device detects changes in girth and relays the information to a computer for later analysis. If nocturnal tumescence is detected, then the E.D. is presumed to be due to a psychosomatic illness such as sexual anxiety; if not, then it is presumed to be due to a physiological cause.
The cause of NPT is not known with certainty. Bancroft (2005) hypothesizes that the noradrenergic neurons of the locus ceruleus are inhibitory to penile erection, and that the cessation of their discharge that occurs during REM sleep may allow testosterone-related excitatory actions to manifest as NPT.
Colloquial naming and anecdotal evidence supporting the possibility that a full bladder can stimulate an erection has existed for some time and is characterised as a 'reflex erection'. The nerves that control a man’s ability to have a reflex erection are located in the sacral nerves (S2-S4) of the spinal cord. A full bladder is known to mildly stimulate nerves in the same region. This mild stimulus which during the day is normally suppressed in adult males by competing stimuli and other distractions, could during sleep with the absence of such factors instigate a reflex erection.
The possibility of a full bladder causing an erection, especially during sleep, is perhaps further supported by the beneficial physiological effect of an erection inhibiting urination, thereby helping to avoid nocturnal enuresis.
Sunday, June 7, 2009
25 - AIIMS MAY 2006 mcqs with answers part 2
6q: which of the following organs secrete zinc in large amounts in man ?
a. seminal vesicle
b. prostate
c. epididymis
d. vas
7q: follicular stimulating hormone receptors are present on ?
a. theca cells
b. granulosa cells
c. leydig cells
d. basement membrane of ovarian follicle
8q: the main difference between REM sleep and wakefulness is ?
a. EEG desynchronisation
b. rapid eye movements
c. decreased muscle tone
d. penile erection
9q: on electromyography , all of the following features suggest denervation except ?
a. unregulated firing of individual muscle fibers
b. small short duration polyphasic action potentials
c. presence of positive sharp waves
d. spontaneous firing of motor units
10q: cushing's triad include all except ?
a. hypertension
b. bradycardia
c. hypothermia
d. irregular respiration
a. seminal vesicle
b. prostate
c. epididymis
d. vas
7q: follicular stimulating hormone receptors are present on ?
a. theca cells
b. granulosa cells
c. leydig cells
d. basement membrane of ovarian follicle
8q: the main difference between REM sleep and wakefulness is ?
a. EEG desynchronisation
b. rapid eye movements
c. decreased muscle tone
d. penile erection
9q: on electromyography , all of the following features suggest denervation except ?
a. unregulated firing of individual muscle fibers
b. small short duration polyphasic action potentials
c. presence of positive sharp waves
d. spontaneous firing of motor units
10q: cushing's triad include all except ?
a. hypertension
b. bradycardia
c. hypothermia
d. irregular respiration
24 - AIIMS MAY 2006 mcqs with answers part 1
1q: vanilloid receptors are activated by ?
a. pain
b. vibration
c. touch
d. pressure
2q: the sodium-potassium pump is an example of ?
a. active transport
b. passive transport
c. facilitated diffusion
d. osmosis
3q: which one of the following acts as a second messenger ?
a. Mg++
b. Cl-
c. Ca++
d. PO4+3
4q: all of the following factors influence hemoglobin dissociation curve except ?
a. chloride ion concentration
b. CO2 tension
c. Temperature
d. 2,3 DPG levels
5q: which one of the following is correct statement regarding coronary blood flow ?
a. coronary blood flow is directly related to perfusion pressure and inversely related to resistance
b. coronary blood flow is inversely related to perfusion pressure and directly related to resistance
c. coronary blood flow is directly related to perfusion pressure and also to resistance
d. coronary blood flow is inversely related to perfusion pressure and also resistance
a. pain
b. vibration
c. touch
d. pressure
2q: the sodium-potassium pump is an example of ?
a. active transport
b. passive transport
c. facilitated diffusion
d. osmosis
3q: which one of the following acts as a second messenger ?
a. Mg++
b. Cl-
c. Ca++
d. PO4+3
4q: all of the following factors influence hemoglobin dissociation curve except ?
a. chloride ion concentration
b. CO2 tension
c. Temperature
d. 2,3 DPG levels
5q: which one of the following is correct statement regarding coronary blood flow ?
a. coronary blood flow is directly related to perfusion pressure and inversely related to resistance
b. coronary blood flow is inversely related to perfusion pressure and directly related to resistance
c. coronary blood flow is directly related to perfusion pressure and also to resistance
d. coronary blood flow is inversely related to perfusion pressure and also resistance
Wednesday, April 29, 2009
23 - Faecal osmolar gap
Faecal osmolality is used to determine the faecal osmolar gap. This is defined as the difference between the measured osmolality and an osmolality calculated from 2 x (Na+K).
If the gap is greater than 100 mmol/L this is consistent with an osmotic diarrhoea (eg carbohydrate (poor absorption, eg mannitol, sorbitol, lactulose); monosaccharides; short chain fatty acids; magnesium as used in antacids).
A normal faecal osmolar gap indicates a secretory diarrhoea indicating damage or irritation of the gastro-intestinal mucosa. This test can only be applied to faecal samples which contain a high fluid content.
22 - Urine Osmolality
Urine osmolality is an important test for the concentrating ability of the kidney. Interpretation of urine osmolality must always be made in the light of the appropriate physiological response to the state of hydration of the patient. The test is useful in the following areas:
- For determining the differential diagnosis of hyper- or hyponatraemia.
- For identifying SIADH (urine osmolality > 200 mmol/kg, urine sodium > 20 mmol/L, low serum sodium, patient not dehydrated and no renal, adrenal, thyroid, cardiac or liver disease or interfering drugs)
- For differentiating pre-renal from renal kidney failure (high urine osmolality is consistent with pre-renal impairment, in renal damage the urine osmolality is similar to plasma osmolality).
- For identifying and diagnosing diabetes insipidus (low urine osmolality not responding to water restriction).
21 - Serum Osmolar gap
The osmolar gap is determined by subtracting the calculated osmolality from the measured osmolality. While there are many formulae for the calculated osmolality, the most commonly used is:
Calculated osmolality = 2 x serum sodium + serum glucose + serum urea (all in mmol/L).
The normal osmolar gap is up to 10 mmol/L and values in excess of this usually indicate the presence of an exogenous agent. The most common by far is ethanol, but methanol, ethylene glycol, acetone and isopropyl alcohol can occasionally be present in sufficient quantities to produce an increased osmolar gap. The equation to calculate the osmolar gap when ethanol has been measured, as a sceren for the presence of other substances, is as follows:
Calculated osmolality = 2 x serum sodium + serum glucose + serum urea - 270 x ethanol
(all in mmol/L except ethanol in mg/dL or % ).
Calculated serum osmolality = 2 x sodium + glucose + urea - 1.25 x ethanol
(all in mmol/L including ethanol ).
Clinically significant toxicities, particularly from ethylene glycol, can occur with a normal osmolar gap as the toxic concentrations are quite low. With the passing of time from ingestion of alcohol, methanol or ethylene glycol the osmolar gap falls and the anion gap rises due to conversion to negatively charged substances. In diabetic ketoacidosis an increased osmolar gap may be due to acetone accumulation. * the factor of 1.25, which is included in the factor of 270 in the preceeding equation, is due to ethanol contributing more to the osmolar gap than would be expected from its molecular weight of 46 (Pursell RA et al Ann Emerg Med 2001;38:653-659).
Calculated osmolality = 2 x serum sodium + serum glucose + serum urea (all in mmol/L).
The normal osmolar gap is up to 10 mmol/L and values in excess of this usually indicate the presence of an exogenous agent. The most common by far is ethanol, but methanol, ethylene glycol, acetone and isopropyl alcohol can occasionally be present in sufficient quantities to produce an increased osmolar gap. The equation to calculate the osmolar gap when ethanol has been measured, as a sceren for the presence of other substances, is as follows:
Calculated osmolality = 2 x serum sodium + serum glucose + serum urea - 270 x ethanol
(all in mmol/L except ethanol in mg/dL or % ).
Calculated serum osmolality = 2 x sodium + glucose + urea - 1.25 x ethanol
(all in mmol/L including ethanol ).
Clinically significant toxicities, particularly from ethylene glycol, can occur with a normal osmolar gap as the toxic concentrations are quite low. With the passing of time from ingestion of alcohol, methanol or ethylene glycol the osmolar gap falls and the anion gap rises due to conversion to negatively charged substances. In diabetic ketoacidosis an increased osmolar gap may be due to acetone accumulation. * the factor of 1.25, which is included in the factor of 270 in the preceeding equation, is due to ethanol contributing more to the osmolar gap than would be expected from its molecular weight of 46 (Pursell RA et al Ann Emerg Med 2001;38:653-659).
20 - Serum Osmolality
Serum osmolality is a useful preliminary investigation for identifying the cause of hyponatraemia. If a patient with significant hyponatraemia (serum sodium < 130 mmol/L) has a normal plasma osmolality, the patient may have pseudohyponatraemia due to excess lipids or proteins, or the sample may have been collected from a drip arm containing dextrose.
If the patient has an increased osmolality it is likely the patient has reactive hyponatraemia due to an excess of solute pulling water out of cells. Examples of this include glucose in diabetes mellitus or hyperglycinaemia after trans-urethral resection of the prostate. The finding of a hypo-osmolar hyponatraemia ("true hyponatraemia") then leads to further investigation of the cause.
19 - Osmolality clinical uses
Serum osmolality is used in two main circumstances: investigation of hyponatraemia and identification of an osmolar gap. Urine osmolality is an important test of renal concentrating ability, for identifying disorders of the ADH mechanism, and identifying causes of hyper-or hyponatraemia. Faecal osmolality can be used to assist with diagnosis of the cause of diarrhoea.
18 - Osmolality measurement
The osmolality of a solution can be measured using an osmometer. The most commonly used instrument in modern laboratories is a freezing point depression osmometer. This instrument measures the change in freezing point that occurs in a solution with increasing osmolality. Osmolality can be measured in samples of serum (gold top tube) or heparin plasma (lime top tube).
Plasma osmolality can also be calculated from the measured components. While there are many equations, a simple one is as follows:
Osmolality (calc) = 2 x Na + Glucose + urea (all measurements in mmol/L).
The doubling of sodium accounts for the negative ions associated with sodium and the exclusion of potassium approximately allows for the incomplete dissociation of sodium chloride. The difference between the measured and calculated plasma osmolality is known as the osmolar gap and normally is between 0 and 10 mmol/kg.
Plasma osmolality can also be calculated from the measured components. While there are many equations, a simple one is as follows:
Osmolality (calc) = 2 x Na + Glucose + urea (all measurements in mmol/L).
The doubling of sodium accounts for the negative ions associated with sodium and the exclusion of potassium approximately allows for the incomplete dissociation of sodium chloride. The difference between the measured and calculated plasma osmolality is known as the osmolar gap and normally is between 0 and 10 mmol/kg.
17 - Osmolality physiology
The osmolality of plasma is closely regulated by anti-diuretic hormone (ADH). In response to even small increases in plasma osmolality (usually rises in plasma sodium), ADH release from the pituitary is increased causing water resorption in the distal tubules and collecting ducts of the kidney and correction of the increased osmolality. The opposite happens in response to a low plasma osmolality with decreased ADH secretion and water loss through the kidneys. Note that ADH is also secreted in response to hypovolaemia and this stimulus will over-ride any response to serum osmolality.
Urine osmolality may vary between 50 and 1200 mmol/kg in a healthy individual depending on the state of hydration. The urine osmolality is the best measure of urine concentration with high values indicating maximally concentrated urine and low values very dilute urine. The main factor determining urine concentration is the amount of water which is resorbed in the distal tubules and collecting ducts in response to ADH. In a dehydrated patient with normally functioning pituitary and kidneys, a small volume of highly concentrated urine will be produced. In a patient with fluid overload the opposite will be an appropriate response. Note that there is no reference interval ("normal range") for urine osmolality as the interpretation depends on the clinical condition of the patient to determine an appropriate response.
Urine osmolality may vary between 50 and 1200 mmol/kg in a healthy individual depending on the state of hydration. The urine osmolality is the best measure of urine concentration with high values indicating maximally concentrated urine and low values very dilute urine. The main factor determining urine concentration is the amount of water which is resorbed in the distal tubules and collecting ducts in response to ADH. In a dehydrated patient with normally functioning pituitary and kidneys, a small volume of highly concentrated urine will be produced. In a patient with fluid overload the opposite will be an appropriate response. Note that there is no reference interval ("normal range") for urine osmolality as the interpretation depends on the clinical condition of the patient to determine an appropriate response.
16 - Osmolality introduction
Osmolality is a count of the number of particles in a fluid sample. The unit for counting is the mole which is equal to 6.02 x 1023 particles (Avogadro's Number). Molarity is the number of particles of a particular substance in a volume of fluid (eg mmol/L) and molality is the number of particles disolved in a mass weight of fluid (mmol/kg). Osmolality is a count of the total number of osmotically active particles in a solution and is equal to the sum of the molalities of all the solutes present in that solution.
For most biological systems the molarity and the molality of a solution are nearly exactly equal because the density of water is 1 kg/L. There is a slight difference between molality and molarity in plasma because of the non-aqueous components present such as proteins and lipids which make up about 6% of the total volume. Thus serum is only 94% water and the molality of a substance in serum is about 6% higher than its molarity. Except in unusual circumstances this difference is unimportant and the terms molarity to the molarity are often used interchangeably. Note that the size of the particle is unimportant so that a single ion, eg sodium, contributes as much to the serum osmolality as a single large protein molecule, eg albumin.
The osmolality of physiological fluids tends to be dominated by small molecules which are present in high concentrations. For example in serum, sodium, potassium, chloride, bicarbonate, urea and glucose are the only components present in high enough concentrations to individually affect the osmolality. Together these make up over 95% of total osmolality of serum. Large serum components contribute little to the overall osmolality. For example the molar concentration of albumin, the most abundant serum protein, is only about 0.6 mmol/L. Only a few exogenous compounds such as ethanol, methanol, ethylene glycol and manitol can be present in the blood at high enough quantities to significantly affect the osmolality.
For most biological systems the molarity and the molality of a solution are nearly exactly equal because the density of water is 1 kg/L. There is a slight difference between molality and molarity in plasma because of the non-aqueous components present such as proteins and lipids which make up about 6% of the total volume. Thus serum is only 94% water and the molality of a substance in serum is about 6% higher than its molarity. Except in unusual circumstances this difference is unimportant and the terms molarity to the molarity are often used interchangeably. Note that the size of the particle is unimportant so that a single ion, eg sodium, contributes as much to the serum osmolality as a single large protein molecule, eg albumin.
The osmolality of physiological fluids tends to be dominated by small molecules which are present in high concentrations. For example in serum, sodium, potassium, chloride, bicarbonate, urea and glucose are the only components present in high enough concentrations to individually affect the osmolality. Together these make up over 95% of total osmolality of serum. Large serum components contribute little to the overall osmolality. For example the molar concentration of albumin, the most abundant serum protein, is only about 0.6 mmol/L. Only a few exogenous compounds such as ethanol, methanol, ethylene glycol and manitol can be present in the blood at high enough quantities to significantly affect the osmolality.
Monday, April 20, 2009
15 - Basal Metabolic Rate Mcqs with notes
1q: which of the following statements is true regarding basal metabolic rate ?
a. increased in starvation
b. it is not influenced by hormonal changes
c. it is not affected by dietary changes
d. decreased by 40 % in starvation
e. it is not affected by energy expenditure
Some important points about basal metabolic rate :
1. the energy expended by an individual during resting post-absorptive state is called Basal Metabolic Rate. It represents the energy required for normal body functions .
2. in starvation it is decreased by 40 % .
3. it is influenced by hormones like thyroid hormones and catecholamines .
4. it is affected by dietary component . eg: diet containing protein increases metabolic rate than same amount of carbohydrate and fat .
5. from 50 % to 70 % of the daily energy expenditure in sedentary individuals is attributable to BMR until very old age .
Factors affecting BMR are :
1. Age : BMR is higher in children than adults. With advancing age BMR gradually falls and in neonate BMR is high .
2. Sex : women have lower BMR than male
3. Surface area : BMR is directly proportional to body surface area .
4. Exercise : increases BMR .
5. Climate : in colder climates BMR is higher than in tropical climates.
6. Nutrition : BMR decreases 20-30 % in malnutrition ,starvation, wasting disease .
7. Body temperature : BMR rises by 14 % for each Celsius degree of elevation .
8. Hormones : circulating levels of hormones secreted by thyroid ,adrenal medulla ,anterior pituitary ( eg: GH ) , male sex hormones increase BMR .
9. Emotional state : sympathetic stimulation .
10. Pregnancy , lactation
11. Race
12. Sleep , drugs , barometric pressure etc .
Download and read this article by American journal of nutrition which discusses about the various factors affecting the BMR on priority basis.
The MCQ above was asked in the PGIMER ( PGI ) chandigarh 2001 december paper .
a. increased in starvation
b. it is not influenced by hormonal changes
c. it is not affected by dietary changes
d. decreased by 40 % in starvation
e. it is not affected by energy expenditure
Some important points about basal metabolic rate :
1. the energy expended by an individual during resting post-absorptive state is called Basal Metabolic Rate. It represents the energy required for normal body functions .
2. in starvation it is decreased by 40 % .
3. it is influenced by hormones like thyroid hormones and catecholamines .
4. it is affected by dietary component . eg: diet containing protein increases metabolic rate than same amount of carbohydrate and fat .
5. from 50 % to 70 % of the daily energy expenditure in sedentary individuals is attributable to BMR until very old age .
Factors affecting BMR are :
1. Age : BMR is higher in children than adults. With advancing age BMR gradually falls and in neonate BMR is high .
2. Sex : women have lower BMR than male
3. Surface area : BMR is directly proportional to body surface area .
4. Exercise : increases BMR .
5. Climate : in colder climates BMR is higher than in tropical climates.
6. Nutrition : BMR decreases 20-30 % in malnutrition ,starvation, wasting disease .
7. Body temperature : BMR rises by 14 % for each Celsius degree of elevation .
8. Hormones : circulating levels of hormones secreted by thyroid ,adrenal medulla ,anterior pituitary ( eg: GH ) , male sex hormones increase BMR .
9. Emotional state : sympathetic stimulation .
10. Pregnancy , lactation
11. Race
12. Sleep , drugs , barometric pressure etc .
Download and read this article by American journal of nutrition which discusses about the various factors affecting the BMR on priority basis.
The MCQ above was asked in the PGIMER ( PGI ) chandigarh 2001 december paper .
Friday, March 27, 2009
14 - AIIMS may 2005 physiology mcqs with answers part 3
10q: there is a mutation of gene coding for the ryanodine receptors in malignant hyperthermia . which of the following statements best explains the increased heat production in malignant hyperthermia ?
a. increased muscle metabolism by excess of calcium ions
b. thermic effect of food
c. increased sympathetic discharge
d. mitochondrial thermogenesis
11q: which of the following conditions lead to tissue hypoxia without alteration of oxygen content of blood ?
a. CO poisoning
b. Meth Hb
c. Cyanide poisoning
d. Respiratory acidosis
12q: which of the following hormones is an example of peptide hormone ?
a. parathormone
b. adrenaline
c. cortisol
d. thyroxine
13q: which of the following methods is not used for measurement of body fluid volumes?
a. antipyrin for total body water
b. inulin for extracellular fluid
c. evan’s blue for plasma volume
d. I 125 albumin for blood volume
14q: which of the following is not a transportor binding protein ?
a. erythropoietin
b. ceruloplasmin
c. lactoferrin
d. transferrin
13 - AIIMS may 2005 physiology mcqs with answers part 2
6q: all of the following enzymes are active with in a cell except?
a. trypsin
b. fumarase
c. exokinase
d. alcohol dehydrogenase
7q: exercise is also prescribed as an adjuvant treatment for depression . most probably this acts by ?
a. increasing pulse pressure
b. improving hemodynamics
c. raising endorphin levels
d. inducing good sleep
8q: the intrapleural pressure is negative both during inspiration and expiration because ?
a. intrapulmonary pressure is always negative
b. thoracic cage and lungs are elastic structures
c. transpulmonary pressure determines the negativity
d. surfactant prevents the lungs from collapse
9q: the velocity of blood is maximum in the ?
a. large veins
b. small veins
c. venules
d. capillaries
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