The Parathyroid Glands

The parathyroid glands are 4 tiny structures embedded in the rear surface of the thyroid gland. They secrete parathyroid hormone (PTH) a polypeptide of 84 amino acids. PTH increases the concentration of Ca²⁺ in the blood in three ways. PTH promotes

• release of Ca²⁺ from the huge reservoir in the bones. (99% of the calcium in the body is incorporated in our bones.)
• reabsorption of Ca²⁺ from the fluid in the tubules in the kidneys
• absorption of Ca²⁺ from the contents of the intestine (this action is mediated by calcitriol, the active form of vitamin D.)

PTH also regulates the level of phosphate in the blood. Secretion of PTH reduces the efficiency with which phosphate is reclaimed in the proximal tubules of the kidney causing a drop in the phosphate concentration of the blood.

Hyperparathyroidism

Elevate the level of PTH causing a rise in the level of blood Ca²⁺ .Calcium may be withdrawn from the bones that they become brittle and break.

 Patients with this disorder have high levels of Ca²⁺ in their blood and excrete small amounts of Ca²⁺ in their urine. This causes hyperparathyroidism.

Hypoparathyroidism

This disorder have low levels of Ca²⁺ in their blood and excrete large amounts of Ca²⁺ in their urine.

Each hormone in the body is unique.  Each one is different in it's chemical composition, structure, and action.  With respect to their chemical structure, hormones may be classified into three groups: amines, proteins, and steroids.

 Amines- these simple hormones are  structural variation of the amino acid tyrosine.  This group includes thyroxine from the thyroid gland and epinephrine and norepinephrine from the adrenal medulla.

Proteins- these hormones are chains of amino acids.  Insulin from the pancreas, growth hormone from the anterior pituitary gland, and calcitonin from the thyroid gland are all proteins.  Short chains of amino acids are called peptides.  Antidiuretic hormone and oxytocin, synthesized by the hypothalamus, are peptide hormones.

Steroids- cholesterol is the precursor for the steroid hormones, which include cortisol and aldosterone from the adrenal cortex, estrogen and progesterone from the ovaries, and testosterone from the testes.

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.

Transport of Carbon Dioxide

A.    Dissolved in Blood Plasma (7-10%)

B.    Bound to Hemoglobin (20-30%)

1.    carbaminohemoglobin - Carb Dioxide binds to an amino acid on the polypeptide chains

2.    Haldane Effect - the less oxygenated blood is, the more Carb Diox it can carry

a.    tissues - as Oxygen is unloaded, affinity for Carb Dioxide increases
b.    lungs - as Oxygen is loaded, affinity for Carb Dioxide decreases, allowing it to be released

C.    Bicarbonate Ion Form in Plasma (60-70%)

1.    Carbon Dioxide combines with water to form Bicarbonate

CO₂ + H₂O <==> H₂CO₃ <==> H⁺ + HCO₃-

2.    carbonic anhydrase - enzyme in RBCs that catalyzes this reaction in both directions

a.    tissues - catalyzes formation of Bicarbonate
b.    lungs - catalyzes formation of Carb Dioxide

3.    Bohr Effect - formation of Bicarbonate (through Carbonic Acid) leads to LOWER pH (H+ increase), and more unloading of Oxygen to tissues

a.    since hemoglobin "buffers" to H⁺, the actual pH of blood does not change much

4.    Chloride Shift - chloride ions move in opposite direction of the entering/leaving Bicarbonate, to prevent osmotic problems with RBCs

D.    Carbon Dioxide Effects on Blood pH

1.    carbonic acid-bicarbonate buffer system
    
low pH       → HCO₃- binds to H⁺
high pH     →   H₂CO₃ releases H⁺
    
2.     low shallow breaths    → HIGH Carb Dioxide    → LOW pH (higher H⁺)
3.     rapid deep breaths     → LOW Carb Dioxide   → HIGH pH (lower H⁺)

Exchange of gases:

• External respiration:
  • exchange of O2 & CO2 between external environment & the cells of the body
  • efficient because alveoli and capillaries have very thin walls & are very abundant (your lungs have about 300 million alveoli with a total surface area of about 75 square meters)

• Internal respiration - intracellular use of O2 to make ATP
• occurs by simple diffusion along partial pressure gradients

HEART DISORDERS

1. Pump failure => Alters pressure (flow) =>alters oxygen carrying capacity.
   1. Renin release (Juxtaglomerular cells) Kidney
   2. Converts Angiotensinogen => Angiotensin I
   3. In lungs Angiotensin I Converted => Angiotensin II
   4. Angiotensin II = powerful vasoconstrictor (raises pressure, increases afterload)
      1. stimulates thirst
      2. stimulates adrenal cortex to release Aldosterone
         (Sodium retention, potassium loss)
      3. stimulates kidney directly to reabsorb Sodium
      4. releases ADH from Posterior Pituitary
2. Myocardial Infarction

    

   1. Myocardial Cells die from lack of Oxygen
   2. Adjacent vessels (collateral) dilate to compensate
   3. Intracellular Enzymes leak from dying cells (Necrosis)
      1. Creatine Kinase CK (Creatine Phosphokinase) 3 forms
         1. One isoenzyme = exclusively Heart (MB)
         2. CK-MB blood levels found 2-5 hrs, peak in 24 hrs
         3. Lactic Dehydrogenase found 6-10 hours after. points less clearly to infarction
      2. Serum glutamic oxaloacetic transaminase (SGOT)
         1. Found 6 hrs after infarction, peaks 24-48 hrs at 2 to 15 times normal,
         2. SGOT returns to normal after 3-4 days
   4. Myocardium weakens = Decreased CO & SV (severe - death)
   5. Infarct heal by fibrous repair
   6. Hypertrophy of undamaged myocardial cells
      1. Increased contractility to restore normal CO
      2. Improved by exercise program
   7. Prognosis
      1. 10% uncomplicated recovery
      2. 20% Suddenly fatal
      3. Rest MI not fatal immediately, 15% will die from related causes
3. Congenital heart disease (Affect oxygenation of blood)
   1. Septal defects
   2. Ductus arteriosus
   3. Valvular heart disease
      1. Stenosis = cusps, fibrotic & thickened, Sometimes fused, can not open
      2. Regurgitation = cusps, retracted, Do not close, blood moves backwards