Question

1. Graves' disease is a condition in which some of the body's antibodies mimic the function of thyroid-stimulating hormone and cause over activity of the thyroid gland. what consequences would this have on a patient's overall metabolic rate and their ability to maintain a healthy weight? would you expect someone with Graves' disease to have a higher or lower average core body temperature compared to someone who was unaffected?

2. when fatty acids are metabolized for cellular respiration, the first step involves breaking two carbons at a time off the chain to form of acetyl - CoA. This acetyl- CoA than:

3. Stenosis (constriction) of the pyloric sphincter would interfere with:

4. Any organ which helps break down food but is not part of the tube through which the foodstuffs pass is referred to as a(n):

5. At the corners of each hepatic lobule are three vessels, collectively known as the portal triad. what vessels make up this group?

6. The main part of the stomach is called the:

Answer 1

1. GRAVES DISEASE

Graves disease is the most common cause of endogenous hyperthyroidism. It is characterized by a triad of manifestations:
• Thyrotoxicosis, caused by a diffusely enlarged, hyper- functional thyroid
• An infiltrative ophthalmopathy with resultant exophthal- mos, noted in as many as 40% of patients
• A localized, infiltrative dermopathy (sometimes desig- nated pretibial myxedema), seen in a minority of cases

Pathogenesis of Graves Disease

Many manifestations of Graves disease are caused by autoantibodies against the TSH receptor that bind to, and stimulate, thyroid follicular cells independent of endogenous trophic hormones. Multiple autoantibodies are produced in Graves disease, including the following:

• Thyroid-stimulating immunoglobulin (TSI). This IgG antibody binds to the TSH receptor and mimics the action of TSH, stimulating adenyl cyclase, with resultant increased release of thyroid hormones. Almost all indi- viduals with Graves disease have detectable amounts of this autoantibody, which is relatively specific for Graves disease.

• Thyroid growth-stimulating immunoglobulins. Also directed against the TSH receptor, these antibodies have been implicated in the proliferation of thyroid follicular epithelium.

• TSH-binding inhibitor immunoglobulins. These anti-TSH receptor antibodies prevent TSH from binding to its receptor on thyroid epithelial cells and in so doing may inhibit thyroid cell function. The coexistence of stimulat- ing and inhibiting immunoglobulins in the serum of the same patient is not unusual, and may explain why some patients develop episodes of hypothyroidism.

Morphology of Graves Disease

In the typical case of Graves disease, the thyroid gland is enlarged (usually symmetrically) due to diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells. The gland is usually smooth and soft, and its capsule is intact. On microscopic examination, the follicular epithelial cells in untreated cases are tall, columnar, and more crowded than usual. This crowding often results in the formation of small papillae, which project into the follicular lumen. Such papillae lack fibrovascular cores, in contrast with those of papillary carcinoma. The colloid within the follicular lumen is pale, with scalloped margins. Lymphoid infiltrates, consisting predominantly of T cells, with fewer B cells and mature plasma cells, are present throughout the interstitium; germinal centers are common.

Clinical Features of Graves Disease

The clinical manifestations of Graves disease include, as well as those associated uniquely with Graves disease: diffuse hyperplasia of the thyroid, ophthalmopathy, and dermop- athy. The degree of thyrotoxicosis varies from case to case, and the related changes may sometimes be less conspicu- ous than other manifestations of the disease. Increased flow of blood through the hyperactive gland often produces an audible bruit. Sympathetic overactivity produces a charac- teristic wide, staring gaze and lid lag. The ophthalmopathy of Graves disease results in abnormal protrusion of the eyeball (exophthalmos). The exophthalmos may persist or progress despite successful treatment of the thyrotoxicosis, sometimes resulting in corneal injury. The extraocular muscles often are weak. The infiltrative dermopathy most commonly involves the skin overlying the shins, where it manifests as scaly thickening and induration of the skin (pretibial myxedema). The skin lesions may be slightly pigmented papules or nodules and often have an orange peel texture. Laboratory findings in Graves disease include elevated serum free T4 and T3 and depressed serum TSH. Because of ongoing stimulation of the thyroid follicles by TSIs, radioactive iodine uptake is increased diffusely.

2. FATTY ACID METABOLISM

3. PYLORIC STENOSIS

The term ‘pyloric stenosis’ is normally a misnomer. The stenosis is seldom at the pylorus. Commonly, when the con- dition is due to underlying peptic ulcer disease, the stenosis is found in the first part of the duodenum, the most common site for a peptic ulcer. True pyloric stenosis can occur due to fibrosis around a pyloric channel ulcer. However, in recent years the most common cause of gastric outlet obstruction has been gastric cancer. In this circumstance the metabolic con- sequences may be somewhat different from those of benign pyloric stenosis because of the relative hypochlorhydria found in patients with gastric cancer.

Gastric outlet obstruction
● Gastric outlet obstruction is most commonly associated with longstanding peptic ulcer disease and gastric cancer
● The metabolic abnormality of hypochloraemic alkalosis is usually only seen with peptic ulcer disease and should be treated with isotonic saline with potassium
● Endoscopic biopsy is essential to determine whether the cause of the problem is malignancy
● Aggressive medical therapy for peptic ulcer disease often leads to resolution
● Endoscopic dilatation of the gastric outlet may be effective in less severe cases of benign stenosis
● Operation is frequently required, with a drainage procedure being performed for benign disease and appropriate resectional surgery if malignant

These are most interesting, as the metabolic consequences of benign pyloric stenosis are unique. The vomiting of hydro- chloric acid results in hypochloraemic alkalosis. Initially the sodium and potassium may be relatively normal. However, as dehydration progresses, more profound metabolic abnor- malities arise, partly related to renal dysfunction. Initially, the urine has a low chloride and high bicarbonate content, reflecting the primary metabolic abnormality. This bicarbon- ate is excreted along with sodium, and so with time the patient becomes progressively hyponatraemic and more profoundly dehydrated. Because of the dehydration, a phase of sodium retention follows and potassium and hydrogen are excreted in preference. This results in the urine becoming paradoxically acidic and hypokalaemia ensues. Alkalosis leads to a lowering in the circulating ionised calcium, and tetany can occur.

4. This kind of Organ is known as Endocrine organs. These organ are not mainly the part of alimentary gut but they participate actively in food digestion and its metabolism like Parathyroid hormone secreted by Parathyroid glands helps in regulating the calcium metabolism through our food content as well by salvaging calcium. Similarly Thyroid hormone helps in increasing BMR and then regulate food metabolism and help in providing energy demands of the body.

5. Portal Triad is made up of = Bile duct, Hepatic artery, Portal vein

6. Main part of stomach is = Antrum and Body of Stomach because here mainly all the enzymes of stomach are being made and secreted.