Introduction – Hypothyroidism

00:01 In this discussion, we will take a look at hypothyroidism.

00:04 Generally speaking, a patient walking through the door will have decreased basal metabolic rate, tired fatigued, constipated, gaining weight without necessarily consumption of too much food.

00:20 Hypothyroidism defined by insufficient circulating thyroid hormone levels for normal cellular functioning, extremely common especially in women due to Hashimoto, a chronic lymphocytic type of thyroiditis.

00:35 At this juncture, you should be able to integrate your complete picture of Hashimoto to the point where initially you may have in a female is experience-is experiencing Hashitoxicosis.

00:52 Some point in time, with that lymphocytic infiltration may result in hypothyroidism primary type.

01:00 Your patient with hypothyroidism will have puffy face, puffy hands; eye, periorbital region will be puffy.

01:14 Differentiate this from Graves’ disease.

01:17 This is not exophthalmos; mixed edema in all parts of the body.

01:24 There is no pathognomonic sign or symptoms for hypothyroidism.

01:27 Typical patient is lethargic, fatigued, multi… mild constipation, cold intolerance, dry skin, dulled facial expression, puffiness of the face, around the eyes, coarse hair.

01:46 The complexion is going to be yellow because of decreased conversion or decreased metabolism of carotene.

01:56 Do not confuse this with jaundice; this is vitamin A that is not being properly metabolized due-due to decreased T3, T4.

02:07 Loss of lateral eyebrows and that’s an interesting symptom, isn’t it? There will be delayed DTR or delayed relaxation of deep tendon reflexes, growth failure in children because of lack of long bone growth, think of that child; it may have cretinism, yellowing of the skin, why? Because of increased carotene accumulation, short stature, extreme, extremely low IQ, galactorrhea, a decrease in T… a decrease in T3, T4 result in increase in TRH and TSH, thus resulting in hyperprolactinemia and galactorrhea.

02:49 Hypercholesterolemia, especially LDL, type 2 hyperlipidemia, why? Because if you have decreased T3, T4, the LDL receptors aren’t working properly.

03:02 By definition, what is type 2 hyperlipidemia? It is the fact that the LDL receptors aren’t working properly and one that you are also familiar with is the familial type autosomal dominant where the LDL receptors aren’t working or it could the acquired type, right? Your T3, T4 plays a pivotal role in receptor activity.

03:24 Hoarseness, hypoventilation, dyspnea, sleep apnea, pleural effusion all seen with hypothyroidism.

03:34 Everything is slowed down, there is going to be ileus, the tongue is going to be enlarged called macroglossia.

03:38 Once again, think of that cretin who is going to then have an enlarged tongue in that child.

03:44 Myalgias, arthralgias, non pitting edemas, depression, psychosis, carpal tunnel syndrome.

03:50 Bunch, a bunch of symptoms and signs that you can expect with hypothyroidism, cannot miss it.

03:58 With hypothyroidism, there might be amenorrhea, anemia, platelet defects, dry skin, and once again, accumulation of carotene.

04:06 This is not jaundice, delayed puberty might occur.

04:11 Continue discussion of signs and symptoms of hypothyroidism.

04:14 You would expect there to find increased systemic vascular resistance.

04:21 Remember that if you did have thyroid hormones normally then as far as your cardiovascular system is concerned, everything is working in sync and you would have the normal effects of the catecholamines.

04:34 The beta 2 receptors normally located on your blood vessels would then cause dilation.

04:39 However, in hypothyroidism, due to lack of your norepinephrine working upon your beta 2 receptors may result in increased systemic vascular resistance.

04:52 This is then confirmed by diastolic hypertension.

04:58 Because the receptors aren’t working properly, you can expect your beta 1 receptors to be not functioning.

05:03 Therefore, there will be decreased anatropy and decreased cardiac output, therefore you would find there to be decreased systolic function.

05:12 Any time there is decreased systolic function, eventually you will also find decreased diastolic function because you cannot properly fill up your heart and that’s a huge physiologic concept, isn’t it? If the receptors aren’t working properly, beta 1 in the heart, your heart rate here would be decreased, bradycardia, and there is a possibility of accumulating fluid in the pericardial cavity, pericardial effusion.

05:40 Let us now talk about hypothyroidism and the different causes.

05:44 The most common is the one that we should cover initially.

05:49 Chronic lymphocytic infiltration of a thyroid gland known as Hashimoto.

05:53 We have silent thyroiditis, there is quite a bit of overlap that will be taking place between a hyper and hypothyroidism in these topics, especially when dealing with thyroiditis and the reason for that is initially you could find hyperthyroid symptoms, may slowly start dropping the T3, T4 into euthyroid phase and then eventually getting into your hypothyroid phase.

06:28 Some may result in permanent hypothyroid or there is a possibility that if it is a viral or your bacterial that we talked about earlier that there might be a recovery phase.

06:41 Hashimoto permanent hypothyroidism.

06:44 The subacute thyroiditis, the reason that we have the term transient is because with subacute, let’s say that is a granulomatous and the viral infection preceded by an upper respiratory tract infection, initially hyperthyroid, exactly the spectrum that I had walked you through just a few minutes ago.

07:06 Acquired causes of hypothyroidism.

07:10 The patient came in with Graves’ disease, the Graves’ disease was then dealt with by radiation therapy.

07:20 There might have been excess thyroid destruction or excess thyroid removal.

07:29 When there is excess destruction of your thyroid gland, this may then result in acquired hypothyroidism, the patient is now placed on thyroid replacement or thyroid hormone replacements.

07:42 Following head and neck radiation therapy and iodine deficiency, much less seen in developed countries, maybe perhaps a patient coming from a developing country where iodine excess might be limited, therefore resulting in acquired type of hypothyroidism.

08:03 Drugs that may cause hypothyroidism include Lithium, Amiodarone, anti-thyroid drugs such as Propylthiouracil, Methimazole or centrally acting such as Sunitinib and Bexarotene.

08:13 Secondary, tertiary, what does that mean? It means that now you are not looking at a problem within the thyroid gland, you might be looking at problems elsewhere.

08:25 When you say secondary, you are referring to the pituitary for saying or referring to tertiary then you are thinking of the hypothalamus.

08:33 If it is secondary then you do not have enough TSH for whatever reason, why? Or maybe infarction of the pituitary, Sheehan’s, we talked about, pituitary apoplexy, maybe a non functioning type of adenoma or an empty sella, you get the point.

08:49 The pituitary is not present or there is a head injury when the hypothalamus is not releasing TRH secondary and tertiary respectively.

08:59 Central hypothyroidism; central resistant to thyroid hormone, rare, rare, but nonetheless a possibility.

09:07 Congenital, biosynthetic enzyme deficiency, the most famous of them all being peroxidase.

09:13 Congenital absence of thyroid gland known as thyroid aplasia all may result in hypothyroidism.

09:19 At this point, you broaden your differentials for hypothyroidism beyond Hashimoto’s and we are looking at drugs and secondary, tertiary and congenital.

09:27 Let’s continue.