Physiology | Master Of Medicine

Category Archives: Physiology

GIT hormones,their actions and sites of action.

Cholecystokinin(CCK)

  1. Secreted from I cells
  2. Acts on GB and pancreas
  3. Increase enzyme secretion
  4. Increase contraction

Gastro Intestinal Peptide(GIP)

  1. Secreted from K cells
  2. Acts on Pancreas
  3. Increase insulin
  4. Decrease fluid absorption

Gherlin

  1. Secreted from stomach
  2. Increase food intake
  3. Increase GH secretion

Gastrin

  1. Secreted from G cells
  2. Acts on parietal cells
  3. Increase H+ secretion

Gastrin Releasing Peptide(GRP)

  1. Secreted from vagal nerve end
  2. Acts on G cells
  3. Increase gastrin secretion

Guanylin

  1. Secreted from ileum and colon
  2. Acts on small and large intestines
  3. Increased fluid absorption

Motilin

  1. Secreted from Mo cells
  2. Acts on upper GI
  3. Smooth muscle contraction

Neurotensin

  1. Present all over intestine
  2. Acts  on intestinal smooth muscles
  3. Increase histamine release

Peptide YY

  1. Secreted from ileum and colon
  2. Acts on stomach and pancreas
  3. Decrease acid secretion and increase enzyme fluid

Secretin

  1. From S cells
  2. Acts on pancreas and stomach
  3. Increase bicarbonate and fluid
  4. Decrease acid secretion from stomach

Somatostatin

  1. Secreted from D cells
  2. Acts on stomach,pancreas,intestne,liver
  3. Decrease secretion and increase fluid

Substance -P

  1. From enteric neurons
  2. Acts on enteric neurons

VIP

  1. From ENS neurons
  2. Acts on SI and pancreas
  3. Increase secretion
  4. Decrease smooth muscle relaxation.

Hormone secreting cells of anterior pituitary

Acidophil cells

  1. Somatotroph- Growth Hormone
  2. Lactotroph – Prolactin

Basophil cells

  1. Corticotroph -  ACTH
  2. Thyrotroph – TSH
  3. Gonadotroph - FSH

Physiology of respiration, respiratory centres, effects of transection of brainstem.

Human respiration is controlled by two mechanisms.

  1. Voluntary control
  2. Automatic control

Voluntary control of respiration is by Cerebral cortex.Voluntary control is needed for respiration at one’s will as in whistling,singing etc.

Automatic control of respiration is via the Pontomedullary centers which enable the smooth and unconscious execution of respiratory activities.

Medullary centres of respiration.

  1. Dorsal respiratory group(DRG) -Located in dorsal portion of medulla,and causes spontaneous inspiration.
  2. Ventral respiratory group(VRG) - Located in ventrolateral part of medulla, causes forced expiration.

Pre -Botzinger Complex(pre-BOTC)

Rhythmic respiration is initiated by a small group of pacemaker cells in the pre Botzinger complex on either side of medulla between nucleus ambigus and lateral reticular nucleus.These neurons discharge rhythmically and produce impulse in phrenic nerve to cause respiration.

Medullary centres receive impulses from:

Carotid and aortic bodies(chemoreceptors) via Glossopharyngeal and vagus respectively.Hypoxia,hypercapnia and acidosis stimulate respiration through them.

Afferent impulses from pulmonary stretch receptors,carried by the vagus nerve.When lungs become overstretched, these receptors transmit impulses via vagi to the DRG, and they switch off inspiration.This is also called Hering-Breuer inflation reflex. This reflex also increase the rate of respiration.

Pontine centres of respiration

Pneumotaxic centre – Located dorsally in the nucleus parabrachialis in upper Pons,transmits signals to the inspiratory area. Pneumotxic centre reduces the duration of inspiration,ultimately leading to increased respiratory rate.

Apneustic centre: Excites the DRG and stimulates inspiration. Pnemotaxic centre and vagi send inhibitory impulses to apneustic centre and thus shortens inspiration.

Effects of transection at different brainstem levels:

1.A transection above pons has no effect on respration.

2.Midpontine transection with the vagi cut,inhibits inhibitory influences of both pneumotaxic centre and vagi on the apneustic centre and results in apneusis(Sustained gasping inspiration followed by short,inefficient expiration).

3.In transection at pontomedullary junction, respiration is maintained with slight irregularity.

4.Transection below medulla causes stoppage of respiration,completely.

Hormones and neurotransmitters affecting feeding and satiety.

Feeding and satiety centre in hypothalamus is modulated by several hormones and neurotransmitters. Since this one is a bit confusing it requires lots of revision.

Orexigenic(Increase feeding)

Neuropeptide Y.
Agouti Related Protein (AGRP).
Melanin Concentrating Hormone(MCH).
Orexins A and B.
Endorphins.
Galanin.
Amino acids(Glutamate and GABA).
Cortisol.
Gherlin.
Growth Hormone Releasing Hormone(GHRH).

Anorexigenic( Decrease Feeding)

  1. Alpha melanocyte stimulating hormone
  2. Leptin
  3. Serotonin
  4. Norepinephrine
  5. Corticotropin releasing hormone
  6. Insulin
  7. Cholecystokinin
  8. Glucagon Like peptide
  9. Cocaine and amphetamine regulated transcript(CART)
  10. Peptide YY(PYY)
  11. Bombesin

Kussmaul’s,Cheyne Stoke’s and Bitots breathing

Kussmaul’s breathing/Acidotic breathing

Typically seen in metabolic acidosis

Characterized by rapid and deep breathing due to stimulation by increased H+ concentration

Causes

  1. Metabolic acidosis
  2. Diabetic keto acidosis
  3. Renal failure

Cheyne stokes breathing

Respiration shows alternate waxing and waning of tidal volume

Causes

  1. LVF
  2. Brain Injury
  3. Uremia
  4. In normal children during sleep

Bitot’s /Periodic breathing

Respiration is characterized by alternate eupnea and apnea

Causes

  1. Meningitis
  2. Severe brain damage

Resting Membrane Potential

RMP is the potential difference between the inside of a cell and outside.RMP is maintained by K+ ion.

  1. RMP of neuron   -70mV
  2. RMP of smooth muscle -50mV
  3. RMP of cardiac muscle  -90mV
  4. RMP of skeletal muscle  -90mV

Changes in Na+ ion concentration affects action potential but not RMP.

Renal Tubular acidosis

Type I RTA

DCT- H+ secretion Low

Urine pH cannot be reduced<5.5 even by NH4Cl

Type II RTA

PCT –  HCO3 reabsorption Low

Fanconis syndrome-Swan neck PCT

Type III RTA

Autosomal recessive

Carbonic Anhydrase defect

Type IV RTA

DCT- H+/K+

Hyperkalemic Acidosis

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