• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Endocrinology Lect2,3  2003
 

Endocrinology Lect2,3 2003

on

  • 467 views

 

Statistics

Views

Total Views
467
Views on SlideShare
465
Embed Views
2

Actions

Likes
1
Downloads
34
Comments
0

1 Embed 2

http://www.slideshare.net 2

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Endocrinology Lect2,3  2003 Endocrinology Lect2,3 2003 Presentation Transcript

  • ENDOCRINOLOGY THYROID DISORDERS
  • Thyroid Disorders
    • Thyroid secretes thyroxine (T4) and small amount of triiofothyronine (T3).
    • @ 85% of T3 is converted from T4 in the tissues [ liver, muscle, and kidney]
    • The hormones are transported in the plasma almost entirely bound to thyroxine – binding globulin (TGB),pre-albumin, and albumin.
    • Production is stimulated by TSH in response to thyrotrophin – releasing hormone (TRH) and free T4 (FT4) --- has a negative effect on TSH release.
    •  FT4   TSH   TRH  thyroid production of T4 T3
  • Hyperthyroidism
    • Caused by excess circulating T4 or T3
    • It is a common condition with a prevalence of 20/1000
    • Both male and females effected equally
    • 90% of cases are caused by:
      • Graves disease
      • Toxic multinodular goiter
      • Toxic solitary goiter
  • Graves Disease
    • Onset may be insidious
    • Atrial fib is rare in young patient but occur in over 50% of males patient over 60 y/o
    • Results from IgG antibodies against the TSH – receptor
    • These antibodies are termed thyroid – stimulating antibodies (TSAb)
    • May be responsible for thyroid enlargement in this disease
    • The cardinal signs of Graves’ disease are:
      • Diffuse goiter
      • Vascular bruit can be heard over these goiters
      • Pretibial myxoedema
      • Tachycardia with a bounding pulse
      • Exophthalmos
      • Lid lag (usually on downward eye movement)
      • Lid retraction
      • Peri-orbital puffiness
      • Increased lacrimation
      • Conjunctival edema and ulceration
    • In the elderly a ‘masked’ hyperthyroidism may be found. If presentation of a 60 y/o with atrial fib, heart failure and weight loss
    • THINK HYPERTHYROIDISM!!!
    • Diagnosis is made clinically with confirmation by labs:
      • T3 and T4 and undetectable TSH levels
      • if a single nodule is suspected a thyroid scan may provide useful information
  •  
  •  
  •  
  •  
  •  
  •  
  •  
  •  
  • Treatment Options
    • Anti-thyroid drugs:
      • Carbimazole or methimazole followed by propylthiouracil
    • Beta-blocking drugs in the initial stages of management
    • Sub-total thyroidectomy
    • Radioactive iodine therapy
    • THE CHOICE OF THERAPY DEPENDS UPON A NUMBER OF FACTORS, ESPECIALLY THE PATIENTS AGE AND PREVIOUS HISTORY
    • Any questions?
  • Hypothyroidism
    • Also known as Myxoedema results from the reduced secretion of T3 and T4 from the thyroid.
    • Hashimoto’s accounts for over 90% of the cases
    • Secondary hypothyroidism is much less common and is caused by pituitary disease [ absence of TSH leads to atrophy of thyroid gland]
  • Clinical Presentation
    • Affects all the systems of the body, but the wide range of clinical features means that the diagnosis will be missed.
    • Dominant features in children are:
      • Reduction in growth velocity
      • Arrest of pubertal development
    • Clinical presentation in adults may vary greatly
    • Non – pitting edema [most marked on the skin of the eyelids and hands]  often associated with loss of eyebrow and scalp hair
    • Dryness of the skin
    • Reduced body hair
    • Bradycardia
    • Hypothermia
    • Pericardial and pleural effusions [ can occur and is life threatening]
    • Diagnosis is based on
      • Clinical suspicion
      • Prolonged relaxation time of peripheral reflexes
      • A low voltage EKG
      • Biochemical estimation of T4 and TSH
      • Thyroid Antibodies Assays
    • Causes of hypothyroidism
      • Autoimmune (most common Hashimotos)
      • Drugs induced (Lithium carbonate- which like iodide inhibits the release of thyroid hormones  goiter and hypothyroidism
  • Treatment
    • In all cases is thyroxine
    • In older patients that present with or has a history of ischemic heart disease sudden increase in T4 levels has been known to cause M.I.s
    • Therefore, start on low dose (25ug) and increase very slowly[every 4 – 6 weeks] and should intensify management of anti – anginal therapy
  •  
  •  
  •  
  •  
    • Any questions?
  • What Are the Parathyroid Glands?
    • The parathyroid glands are four pea-sized glands located on the thyroid gland in the neck .
    • The parathyroid glands secrete parathyroid hormone (PTH), a substance that helps maintain the correct balance of calcium and phosphorous in the body.
    • PTH regulates release of the calcium from bone, absorption of calcium in the intestine, and excretion of calcium in the urine.
    • When the amount of calcium in the blood falls too low, the parathyroid glands secrete just enough PTH to restore the balance.
  • Hyper-parathyroidism
    • If the glands secrete too much hormone,the balance is disrupted: blood calcium rises.
    • This condition of excessive calcium in the blood, called hypercalcemia
    • hypercalcemia is what usually signals the doctor that something may be wrong with the parathyroid glands
    • In 85 percent of people with this disorder, a benign tumor (adenoma) has formed on one of the parathyroid glands, causing it to become overactive.
    • In most other cases, the excess hormone comes from two or more enlarged parathyroid glands, a condition called hyperplasia.
    • Very rarely, hyperparathyroidism is caused by cancer of a parathyroid gland.
    • This excess PTH triggers the release of too much calcium into the bloodstream.
    • The bones may lose calcium, and too much calcium may be absorbed from food.
    • The levels of calcium may increase in the urine, causing kidney stones.
    • PTH also acts to lower blood phosphorous levels by increasing excretion of phosphorus in the urine
    • HPT is most often suspected when a high level of calcium is found in your blood on a routine blood test.
    • measuring the amount of PTH in your blood proves the diagnosis
  • What Are the Symptoms of Hyperparathyroidism?
    • patients have severe symptoms, subtle ones, or none at all
    • When symptoms do appear, they are often mild and nonspecific, such as:
      • a feeling of weakness and fatigue,
      • depression,
      • or aches and pains
    • With more severe disease, a person may have:
      • a loss of appetite,
      • nausea, vomiting,
      • constipation,
      • confusion or impaired thinking and memory,
      • and increased thirst and urination
  • How is HPT treated
    • Surgery to remove the growth in your neck almost always solves the problem.
    • The growth doesn't usually come back
    • Most of your symptoms will stop in the first month after surgery
    • For a short time after surgery, your blood calcium level may be too low
    • This problem is easily treated with medicine.
    • Although surgery is usually recommended for people with HPT (unless they have no symptoms), sometimes other medical problems make surgery too risky
    • If you don't have surgery, tests are needed from time to time to see if the disease is hurting your kidneys, bones or other body systems
    • Women who take estrogen after menopause are partly protected from the effects of HPT.
  • Any questions?
  • Hypoparathyroidism
    • is the clinical condition caused by a lack of parathyroid hormone
    • . Calcium levels in the blood fall, and phosphorus levels rise
    • The most common cause of hypoparathyroidism is injury to the parathyroid glands during head and neck surgery.
    • Rarely, hypoparathyroidism is a side effect of radioactive iodine treatment for hyperthyroidism
    • PTH secretion may be impaired when blood levels of the element magnesium are low or when blood pH is too high, a condition called metabolic alkalosis.
    • DiGeorge syndrome is a childhood disease in which hypoparathyroidism occurs due to congenital absence of the parathyroid glands
    • The incidence is about 4 out of 100,000 people.
    • Symptoms  
      • tingling of lips, hands and feet
      • muscle cramps
      • pain in face , legs and feet
      • abdominal pain
      • dry hair
      • brittle nails
      • dry, scaly skin
      • cataracts
      • weakened tooth enamel in children
      • muscle spasms called tetany
      • tetany can lead to spasms of the larynx with breathing difficulties
      • convulsions or seizures
    • Additional symptoms that may be associated with this disease:
    • menstruation, painful
    • hand or foot spasms
    • consciousness, decreased
    • teeth - delayed or absent formation
  • Signs and tests    
    • low serum calcium level
    • elevated serum phosphorus
    • decreased serum parathyroid hormone level
    • decreased serum magnesium level (possible)
    • occasionally abnormal heart rhythms on ECG
  • Treatment
    • The goal of treatment is to restore the calcium and associated mineral balance within the body
    • Oral calcium carbonate and Vitamin D supplements are usually life-long therapy
    • Blood levels require periodic monitoring to ensure proper dosage
    • . A high-calcium, low-phosphorous diet is recommended
    • Supportive care is necessary for an acute life-threatening attack or hypoparathyroid tetany (prolonged muscle contractions ).
    • Calcium is administered by intravenous infusion
    • Precautions are taken to prevent seizures or larynx spasms
    • Heart monitoring for abnormal rhythms is continued until the person is stabilized
    • When the life-threatening attack has been controlled, treatment continues with oral preparations.
  • Complications
    • acute tetany, which can lead to respiratory obstruction requiring a tracheostomy
    • growth retardation, malformation of the teeth, and retarded mental development, which can occur if hypoparathyroidism develops in childhood
    • over treatment with Vitamin D and calcium, which can cause hypercalcemia (high blood calcium) and sometimes impaired kidney function
    • increased risk of pernicious anemia , Addison's disease , cataract development, and Parkinson's disease
  • Prognosis
    • The probable outcome is good if the diagnosis is made early
    • Dental changes, cataracts , and brain calcifications are irreversible changes.
  •  
  •  
  •  
  •  
  •