NEET MDS Lessons
Physiology
The pituitary gland is pea-sized structure located at the base of the brain. In humans, it consists of two lobes:
- the Anterior Lobe and
- the Posterior Lobe
The Anterior Lobe
The anterior lobe contains six types of secretory cells All of them secrete their hormone in response to hormones reaching them from the hypothalamus of the brain.
Thyroid Stimulating Hormone (TSH)
TSH (also known as thyrotropin) is a glycoprotein The secretion of TSH is
- stimulated by the arrival of thyrotropin releasing hormone (TRH) from the hypothalamus.
- inhibited by the arrival of somatostatin from the hypothalamus.
TSH stimulates the thyroid gland to secrete its hormone thyroxine (T4).
Some develop antibodies against their own TSH receptors making more T4 causing hyperthyroidism. The condition is called thyrotoxicosis or Graves' disease.
Hormone deficiencies
A deficiency of TSH causes hypothyroidism: inadequate levels of T4 (and thus of T3 )..
Follicle-Stimulating Hormone (FSH)
FSH is a heterodimeric glycoprotein Synthesis and release of FSH is triggered by the arrival from the hypothalamus of gonadotropin-releasing hormone (GnRH).
FSH in females :In sexually-mature females, FSH (assisted by LH) acts on the follicle to stimulate it to release estrogens.
FSH in males :In mature males, FSH acts on spermatogonia stimulating (with the aid of testosterone) the production of sperm.
Luteinizing Hormone (LH)
LH is synthesized within the same pituitary cells as FSH and under the same stimulus (GnRH). It is also a heterodimeric glycoprotein
LH in females
In sexually-mature females, LH
- stimulates the follicle to secrete estrogen in the first half of the menstrual cycle
- a surge of LH triggers the completion of meiosis I of the egg and its release (ovulation) in the middle of the cycle
- stimulates the now-empty follicle to develop into the corpus luteum, which secretes progesterone during the latter half of the menstrual cycle.
LH in males
LH acts on the interstitial cells (also known as Leydig cells) of the testes stimulating them to synthesize and secrete the male sex hormone, testosterone.
LH in males is also known as interstitial cell stimulating hormone (ICSH).
Prolactin (PRL)
Prolactin is a protein of 198 amino acids. During pregnancy it helps in the preparation of the breasts for future milk production. After birth, prolactin promotes the synthesis of milk.
Prolactin secretion is
- stimulated by TRH
- repressed by estrogens and dopamine.
Growth Hormone (GH)
- Human growth hormone (also called somatotropin) is a protein
- The GH-secreting cells are stimulated to synthesize and release GH by the intermittent arrival of growth hormone releasing hormone (GHRH) from the hypothalamus. GH promotes body growth
In Child
- hyposecretion of GH produces dwarfism
- hypersecretion leads to gigantism
In adults, a hypersecretion of GH leads to acromegaly.
ACTH — the adrenocorticotropic hormone
ACTH acts on the cells of the adrenal cortex, stimulating them to produce
- glucocorticoids, like cortisol
- mineralocorticoids, like aldosterone
- androgens (male sex hormones, like testosterone
Hypersecretion of ACTH cause of Cushing's disease.
Hypoxia
- Hypoxia is tissue oxygen deficiency
- Brain is the most sensitive tissue to hypoxia: complete lack of oxygen can cause unconsciousness in 15 sec and irreversible damage within 2 min.
- Oxygen delivery and use can be interrupted at several sites
|
Type of |
O2 Uptake |
Hemoglobin |
Circulation |
Tissue O2 Utilization |
|
Hypoxic |
Low |
Normal |
Normal |
Normal |
|
Anemic |
Normal |
Low |
Normal |
Normal |
|
Ischemic |
Normal |
Normal |
Low |
Normal |
|
Histotoxic |
Normal |
Normal |
Normal |
Low |
- Causes:
- Hypoxic: high altitude, pulmonary edema, hypoventilation, emphysema, collapsed lung
- Anemic: iron deficiency, hemoglobin mutations, carbon monoxide poisoning
- Ischemic: shock, heart failure, embolism
- Histotoxic: cyanide poisoning (inhibits mitochondria)
- Carbon monoxide (CO) poisoning:
- CO binds to the same heme Fe atoms that O2 binds to
- CO displaces oxygen from hemoglobin because it has a 200X greater affinity for hemoglobin.
- Treatment for CO poisoning: move victim to fresh air. Breathing pure O2 can give faster removal of CO
- Cyanide poisoning:
- Cyanide inhibits the cytochrome oxidase enzyme of mitochondria
- Two step treatment for cyanide poisoning:
- 1) Give nitrites
- Nitrites convert some hemoglobin to methemoglobin. Methemoglobin pulls cyanide away from mitochondria.
- 2) Give thiosulfate.
- Thiosulfate converts the cyanide to less poisonous thiocyanate.
- 1) Give nitrites
|
Damage to Spinal Nerves and Spinal Cord |
||
|
Damage |
Possible cause of damage |
Symptoms associated with innervated area |
|
Peripheral nerve |
Mechanical injury |
Loss of muscle tone. Loss of reflexes. Flaccid paralysis. Denervation atrophy. Loss of sensation |
|
Posterior root |
Tabes dorsalis |
Paresthesia. Intermittent sharp pains. Decreased sensitivity to pain. Loss of reflexes. Loss of sensation. Positive Romberg sign. High stepping and slapping of feet. |
|
Anterior Horn |
Poliomyelitis |
Loss of muscle tone. Loss of reflexes. Flaccid paralysis. Denervation atrophy |
|
Lamina X (gray matter) |
Syringomyelia |
Bilateral loss of pain and temperature sense only at afflicted cord level. Sensory dissociation. No sensory impairment below afflicted level |
|
Anterior horn and lateral corticospinal tract |
Amyotrophic lateral sclerosis |
Muscle weakness. Muscle atrophy. Fasciculations of hand and arm muscles. Spastic paralysis |
|
Posterior and lateral funiculi |
Subacute combined degeneration |
Loss of position sense. Loss of vibratory sense. Positive Romberg sign. Muscle weakness. Spasticity. Hyperactive tendon reflexes. Positive Babinski sign. |
|
Hemisection of the spinal cord |
Mechanical injury |
Brown-Sequard syndrome |
|
Below cord level on injured side |
||
|
Flaccid paralysis. Hyperactive tendon reflexes. Loss of position sense. Loss of vibratory sense. Tactile impairment |
||
|
Below cord level on opposite side beginning one or two segments below injury |
||
|
Loss of pain and temperature |
||
Levels of Organization:
CHEMICAL LEVEL - includes all chemical substances necessary for life (see, for example, a small portion - a heme group - of a hemoglobin molecule); together form the next higher level
CELLULAR LEVEL - cells are the basic structural and functional units of the human body & there are many different types of cells (e.g., muscle, nerve, blood)
TISSUE LEVEL - a tissue is a group of cells that perform a specific function and the basic types of tissues in the human body include epithelial, muscle, nervous, and connective tissues
ORGAN LEVEL - an organ consists of 2 or more tissues that perform a particular function (e.g., heart, liver, stomach)
SYSTEM LEVEL - an association of organs that have a common function; the major systems in the human body include digestive, nervous, endocrine, circulatory, respiratory, urinary, and reproductive.
There are two types of cells that make up all living things on earth: prokaryotic and eukaryotic. Prokaryotic cells, like bacteria, have no 'nucleus', while eukaryotic cells, like those of the human body, do.
Reflexes
A reflex is a direct connection between stimulus and response, which does not require conscious thought. There are voluntary and involuntary reflexes.
The Stretch Reflex:
The stretch reflex in its simplest form involves only 2 neurons, and is therefore sometimes called a 2-neuron reflex. The two neurons are a sensory and a motor neuron. The sensory neuron is stimulated by stretch (extension) of a muscle. Stretch of a muscle normally happens when its antagonist contracts, or artificially when its tendon is stretched, as in the knee jerk reflex. Muscles contain receptors called muscle spindles. These receptors respond to the muscles's stretch. They send stimuli back to the spinal cord through a sensory neuron which connects directly to a motor neuron serving the same muscle. This causes the muscle to contract, reversing the stretch. The stretch reflex is important in helping to coordinate normal movements in which antagonistic muscles are contracted and relaxed in sequence, and in keeping the muscle from overstretching.
Since at the time of the muscle stretch its antagonist was contracting, in order to avoid damage it must be inhibited or tuned off in the reflex. So an additional connection through an interneuron sends an inhibitory pathway to the antagonist of the stretched muscle - this is called reciprocal inhibition.
The Deep Tendon Reflex:
Tendon receptors respond to the contraction of a muscle. Their function, like that of stretch reflexes, is the coordination of muscles and body movements. The deep tendon reflex involves sensory neurons, interneurons, and motor neurons. The response reverses the original stimulus therefore causing relaxation of the muscle stimulated. In order to facilitate that the reflex sends excitatory stimuli to the antagonists causing them to contract - reciprocal activation.
The stretch and tendon reflexes complement one another. When one muscle is stretching and stimulating the stretch reflex, its antagonist is contracting and stimulating the tendon reflex. The two reflexes cause the same responses thus enhancing one another.
The Crossed Extensor Reflex -
The crossed extensor reflex is just a withdrawal reflex on one side with the addition of inhibitory pathways needed to maintain balance and coordination. For example, you step on a nail with your right foot as you are walking along. This will initiate a withdrawal of your right leg. Since your quadriceps muscles, the extensors, were contracting to place your foot forward, they will now be inhibited and the flexors, the hamstrings will now be excited on your right leg. But in order to maintain your balance and not fall down your left leg, which was flexing, will now be extended to plant your left foot (e.g. crossed extensor). So on the left leg the flexor muscles which were contracting will be inhibited, and the extensor muscles will be excited
-
Partial Pressures of O2 and CO2 in the body (normal, resting conditions):
- Alveoli
- PO2 = 100 mm Hg
- PCO2 = 40 mm Hg
- Alveolar capillaries
- Entering the alveolar capillaries
- PO2 = 40 mm Hg (relatively low because this blood has just returned from the systemic circulation & has lost much of its oxygen)
- PCO2 = 45 mm Hg (relatively high because the blood returning from the systemic circulation has picked up carbon dioxide)
- Entering the alveolar capillaries
-
While in the alveolar capillaries, the diffusion of gasses occurs: oxygen diffuses from the alveoli into the blood & carbon dioxide from the blood into the alveoli.
- Leaving the alveolar capillaries
- PO2 = 100 mm Hg
- PCO2 = 40 mm Hg
- Blood leaving the alveolar capillaries returns to the left atrium & is pumped by the left ventricle into the systemic circulation. This blood travels through arteries & arterioles and into the systemic, or body, capillaries. As blood travels through arteries & arterioles, no gas exchange occurs.
-
- Entering the systemic capillaries
- PO2 = 100 mm Hg
- PCO2 = 40 mm Hg
- Body cells (resting conditions)
- PO2 = 40 mm Hg
- PCO2 = 45 mm Hg
- Entering the systemic capillaries
- Because of the differences in partial pressures of oxygen & carbon dioxide in the systemic capillaries & the body cells, oxygen diffuses from the blood & into the cells, while carbon dioxide diffuses from the cells into the blood.
-
- Leaving the systemic capillaries
- PO2 = 40 mm Hg
- PCO2 = 45 mm Hg
- Leaving the systemic capillaries
- Blood leaving the systemic capillaries returns to the heart (right atrium) via venules & veins (and no gas exchange occurs while blood is in venules & veins). This blood is then pumped to the lungs (and the alveolar capillaries) by the right ventricle.
Clinical Physiology
Heart Failure : Heart failure is inability of the heart to pump the enough amount of blood needed to sustain the needs of organism .
It is usually called congestive heart failure ( CHF) .
To understand the pathophysiology of the heart failure , lets compare it with the physiology of the cardiac output :
Cardiac output =Heart rate X stroke volume
Stroke volume is determined by three determinants : Preload ( venous return ) , contractility , and afterload (peripheral resistance ) . Any disorder of these factors will reduce the ability of the heart to pump blood .
Preload : Any factor that decrease the venous return , either by decreasing the intravenous pressure or increasing the intraatrial pressure will lead to heart failure .
Contractility : Reducing the power of contraction such as in myocarditis , cardiomyopathy , preicardial tamponade ..etc , will lead to heart failure .
Afterload : Any factor that may increase the peripheral resistance such as hypertension , valvular diseases of the heart may cause heart failure.
Pathophysiology : When the heart needs to contract more to meet the increased demand , compensatory mechanisms start to develope to enhance the power of contractility . One of these mechanism is increasing heart rate , which will worsen the situation because this will increase the demands of the myocardial cells themselves . The other one is hypertrophy of the cardiac muscle which may compensate the failure temporarily but then the hypertrophy will be an additional load as the fibers became stiff .
The stroke volume will be reduced , the intraventricular pressure will increase and consequently the intraatrial pressure and then the venous pressure . This will lead to decrease reabsorption of water from the interstitium ( see microcirculation) and then leads to developing of edema ( Pulmonary edema if the failure is left , and systemic edema if the failure is right) .