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So yeah, this happened. Name, ID number, and score are obscured for obvious reasons, but yeah, this is from my score report.

#me #usmle #step 2 ck #usmle step 2 #medical licensure #medical school

6/4/2023

Today was a rainy cozy day spent eating waffles, drinking hot beverages, and reading novels instead of as well as studying.

#emgoesmed #studyblr #studyspo #med student #med school #med studyblr #ms4 #usmle step 2 #cozy #coffee #tea #pottery #bookblr #reading #the bear and the nightingale

265....

I don't know how that happened but. wow.

#studyspo #studyblr #med school #medical student #pre-med #medical school #step 2 #usmle step 2

What gets you out of bed in the morning?

Me, it’s the panic. The panic of doing poorly on Step 2. Might not sound healthy but it works. Great motivator.

#med student #medicine #medical school #med school #personal #medical student #studyspo #studyblr #study motivation #panic #step 2 prep #usmle step 2 #step 2ck #mine

Diseases of the thyroid gland

----------------------------------

Chapter 1 : Hyperthyroidism.

-----------------

We're going to discuss:

What is Hyperthyroidism?

Causes of hyperthyroidism?

Clinical manifestation.

Lab works

Other investigations

Treatment

What is a thyroid storm?

----------------------------------------

What is hyperthyroidism?

It is a state where there is ⏫ synthesis of the thyroid hormones : T4 & T3 ➡ ⏫ levels of these hormones in the blood.

-------------------------------

Causes:

Graves' disease (diffuse toxic goiter)

Plummer disease (multinodular toxic goiter)

Toxic thyroid adenoma (single nodule)

Subacute thyroiditis & Hashimoto thyroiditis. (Transient hyperthyroidism)

Fetal thyrotoxicosis

Other rare causes:

- postpartum thyroiditis (transiet)

- Iodine-induced hyperthyroidism.

- Excessive dose of levothyroxine.

------------------

1. Graves' disease:

Autoimmune disorder.

Thyroid-stimulating immunoglobulin TSI (IgG) binds to the TSH receptors on the thyroid cells ➡ triggers the synthesis of excess thyroid hormones.

Younger women >

Goiter : every thyroid cell is hyperfunctioning so it affects ALL parts of the gland >> diffuse. Non tender

2. Plummer disease:

Starts with chronic lack of dietary Iodine ➡ low levels of T4 ➡ triggers high levels of TSH ➡ Thyroid hypertrophy & hyperplasia.

The growth is uneven >> nodules.

These nodules become toxic when a genetic mutation happens and causes TSH recepters to be constantly ON. >> ⏫⏫⏫ T4/T3.

That elevation acts as a negative feed back to the pituitary gland to secrete less TSH >> the rest of the thyroid is not functioning >> atrophy .

3. Adenoma : 2% of all cases.

4. Thyroiditis:

Inflammation of the thyroid gland >> releasing the previously synthesized thyroid hormones ➡ temporary ⏫⏫ in circulating T4/T3.

A hypothyoid phase may follow.

5. Fetal thyrotoxicosis:

Classically in an infant born to a mother with Graves disease. TSI are IgG and can cross the placenta.

--------------------------------------------

Clinical manifestations : Symptoms

Nervousness.

Irritability

Insomnia.

Fine tremor

Hyperactivity

Heat intolerance & excessive sweating.

Weight loss despite increased appetite.

Proximal muscle weakness.

Palpitations.

Signs:

On the thyroid glad:

Graves' : diffusely enlarged. symmetric . Nontender gland. Bruit may be present.

Subacute thyroiditis: exquisitely tender. Diffusely enlarged (viral illness)

Plummer: bump. Irregular . Asymmetric gland.

Toxic adenoma: single nodule with atrophic gland.

Extrathyroidal:

Eyes: - Edema of the extraocular muscles ➡ proptosis (hallmark of Graves') - lid lag - lid retraction

- corneal exposure ➡ excessive tearing.

Cardiovascular effects: ⏫ Blood pressure.

- Arrhythmias : Sinus tachycardia - Atrial fibrillation

Skin: Warm & moist - pretibial myxedema (specific to Graves')

Neurologic: Hyperreflexia - fine tremor.

-----------------------------------

Lab works:

⏬⏬ TSH

⏫⏫ free T4 & FT3

Other investigations:

1. RAIU:

Radioactive iodine uptake scan.

Useful to differentiate the causes of hyperthyroidisim.

If the uptake is ⏫look for the findings (forms):

Diffuse ( homogeneous) ➡ Graves'

Heterogeneous (multiple nodules of ⏫uptake) ➡ plummer

Focal (one area of ⏫ uptake w/suppression of rest of the gland) ➡ adenoma (hot nodule)

No RAIU findings (⏬⏬uptake) we look at serum thyroglobulin:

⏫ ➡ Thyroiditis /iodine exposure / extraglandular production

⏬ ➡ Exogenous thyroid hormone.

2. Radioactive T3 uptake:

Gives information about the status of TBG

We give resin to the patient + radioactive T3.

Radioactive T3 will bind to resin only when there is no space left on TBG.

SO WHEN THERE IS ⏫T4 ➡ no available seats on TBG ➡ more radioactive T3 will bind to resin ➡ ⏫ radioactive uptake.

The importance of this is to know if there is true hyperthyroidism or increased TBG

High TBG production ➡ low radioactive T3 uptake.

3. Free thyroxine index (FTI) :

Proportional for FREE T4 concentration.

Calculated to correct for the changes in the thyroid binding proteins.

FTI : ( Radioactive T3 uptake × serum total T4) /100

FTI : (patient's radioactive T3 uptake / normal radioactive T3 uptake) × total T4

Normal : 4-11

--------------------------------------------

Treatment :

1. Pharmacologic:

🎐Immediate control of adrenergic symptoms:

B-blockers (propanolol)

🎐 Anti-thyroid drugs: Thionamides

Methimazole:

1- Inhibits thyroid peroxidase ➡ stops the oxidation of Iodide into Iodine

2- Inhibits the coupling of DIT and MIT to form T3 & T4.

PTU (propylthiouracil) :

Shares the same mechanism with Methimazole except that PTU works on the peripheral tissue by

- Inhibiting the converting of T4 into T3.

⚠ Watch for side effects⚠

⚠Agranulocytosis

⚠Skin rash

⚠Arthralgias

Specific ⚠ for PTU is:

Hepatotoxicity.

During pregnancy:

Both can cross the placenta but it is preferred to give:

PTU at the first trimester

Methimazole at the 2nd and 3rd trimester.

Sodium ipodate or iopanoic:

Lowers serum T3 & T4 levels and causes rapid improvement of hyperthyroidism.

Appropriate for acute management of severe hyperthyroidism that's not responding to conventional therapy.

2. RAI ; Radioactive iodine:

Causes destruction of thyroid follicular cells.

Uses IODINE 131

Most common for: Graves' disease & multi-nodular goiter.

If the first dose doesn't control the hyperthyroidism within 6 to 12 months then administer another dose.

✔ Selected pations ✔

✔ Elderly patients w/Graves disease.

✔ Solitary toxic nodule

✔ Patients w/graves disease in whom therapy w/antithyroid drugs fails.

⚠ Warning ⚠

⚠ Hypothyroidism over time in the majority patients. ⚠

Note :

Ophthalmopathy can worsen after RAI prevent that by prophylactic therapy w/prednisone in high-risk patients.

3. Surgery:

Very effective

Only 1% of patients are treated by it.

Often reserved w/patients that have large goiters ; more common in toxic multinodular goiter.

⚠ Side Effects ⚠

⚠ permanent hypothyroidism 30%

⚠Recurrent laryngeal nerve palsy 1%

⚠Permanent hypoparathyroidism 1%

⚠ watch for hypocalcemia (due to inflammation/removal of the parathyroid glands)

------------------------------------------

Treatment plan :

Immediate control of adrenergic symptoms (of any cause) ➡ (beta-blocker) propanolol

Non-pregnant patients w/Graves' disease: beta blocker + Methimazole Taper B-blocker after 4-8 weeks (once methimazole takes effect) give methimazole for 1-2 years then measure TSI at 12 months : ✔ Absent ➡ discontinue therapy. ✔ Relapse ➡ Resume methimazole for 1 more year or radioactive therapy.

Pregnant patients w/Graves' disease : Endocrinology consult is indicated before starting treatment.

Toxic multinodular goiter or Toxic adenoma: RAI or surgery Methimazole pretherapy for surgery and before RAI in selected patients.

------------------------------------

What is a thyroid storm?

Rare, life-threatening complication of thyrotoxicosis.

Characterized by an acute exacerbation of the manifestations of hyperthyroidism.

There's usually a precipitating factor: infection, DKA, stress (Surgery, illness, childbirth)

High mortality rate

Clinical manifestations:

✔ Marked fever

✔ Tachycardia

✔ agitation

✔ Confusion

✔ GI symptoms (nausea , vomiting , diarrhea)

Treatment:

Provide supportive therapy : IV fluids , cooling blankets and glucose

Give antithyroid agents (PTU preferred due to its peripheral effects) followed w/iodine.

B-blockers

Dexamethazone (steroids) to impair peripheral generation of T3 from T4 and to provide adrenal support.

-------------------------

Wow that was a long one XD

I tried to include all the important stuff :)

Resources:

First-aid

Kaplan lecture notes 2019

Medscape

Pocket medicine

Step-up to medicine.

#studyblr #study motivation #medicine #biology #medicinewithmarie #endocrinewithmarie #hyperthyroidism #notes #usmle #usmle step 2 #medical student #medblr #notes 2020 #thyroid #education #endocrine notes #nedicine

Anatomy of Trachea, Bronchial Tree and Bronchopulmonary Segments

#usmle #fmge #next #next exam #neetpg #pgi #aiims #nclex #comlex #plab #usmle tsep1 #usmle prep #usmle step 2 #krok1 #krok #mci #pg #anatomy.trachea #lungs #bronchial tree #bronchopulmonary segment #ewlm

Our best discount ever - 25% off any subscription - it's a good time to sign up for the Medical School Bundle! drawittoknowit.com

The internal medicine rotation is one of the toughest clinical rotations med students face. These resources will accompany you on your journey and help you excel on Step 2.

This fantastic #USMLE #Step2 / #InternalMedicine resources post is ripe for a comeback! #TBT

#usmle #usmle step 2 #internal medicine #internalmedicine #stepprep #rotations #medstudentlife #medschoolmeded #future doctor #tbt

Diseases of the thyroid gland

----------------------------------

Chapter 1 : Hyperthyroidism.

-----------------

We're going to discuss:

What is Hyperthyroidism?

Causes of hyperthyroidism?

Clinical manifestation.

Lab works

Other investigations

Treatment

What is a thyroid storm?

----------------------------------------

What is hyperthyroidism?

It is a state where there is ⏫ synthesis of the thyroid hormones : T4 & T3 ➡ ⏫ levels of these hormones in the blood.

-------------------------------

Causes:

Graves' disease (diffuse toxic goiter)

Plummer disease (multinodular toxic goiter)

Toxic thyroid adenoma (single nodule)

Subacute thyroiditis & Hashimoto thyroiditis. (Transient hyperthyroidism)

Fetal thyrotoxicosis

Other rare causes:

- postpartum thyroiditis (transiet)

- Iodine-induced hyperthyroidism.

- Excessive dose of levothyroxine.

------------------

1. Graves' disease:

Autoimmune disorder.

Thyroid-stimulating immunoglobulin TSI (IgG) binds to the TSH receptors on the thyroid cells ➡ triggers the synthesis of excess thyroid hormones.

Younger women >

Goiter : every thyroid cell is hyperfunctioning so it affects ALL parts of the gland >> diffuse. Non tender

2. Plummer disease:

Starts with chronic lack of dietary Iodine ➡ low levels of T4 ➡ triggers high levels of TSH ➡ Thyroid hypertrophy & hyperplasia.

The growth is uneven >> nodules.

These nodules become toxic when a genetic mutation happens and causes TSH recepters to be constantly ON. >> ⏫⏫⏫ T4/T3.

That elevation acts as a negative feed back to the pituitary gland to secrete less TSH >> the rest of the thyroid is not functioning >> atrophy .

3. Adenoma : 2% of all cases.

4. Thyroiditis:

Inflammation of the thyroid gland >> releasing the previously synthesized thyroid hormones ➡ temporary ⏫⏫ in circulating T4/T3.

A hypothyoid phase may follow.

5. Fetal thyrotoxicosis:

Classically in an infant born to a mother with Graves disease. TSI are IgG and can cross the placenta.

--------------------------------------------

Clinical manifestations : Symptoms

Nervousness.

Irritability

Insomnia.

Fine tremor

Hyperactivity

Heat intolerance & excessive sweating.

Weight loss despite increased appetite.

Proximal muscle weakness.

Palpitations.

Signs:

On the thyroid glad:

Graves' : diffusely enlarged. symmetric . Nontender gland. Bruit may be present.

Subacute thyroiditis: exquisitely tender. Diffusely enlarged (viral illness)

Plummer: bump. Irregular . Asymmetric gland.

Toxic adenoma: single nodule with atrophic gland.

Extrathyroidal:

Eyes: - Edema of the extraocular muscles ➡ proptosis (hallmark of Graves') - lid lag - lid retraction

- corneal exposure ➡ excessive tearing.

Cardiovascular effects: ⏫ Blood pressure.

- Arrhythmias : Sinus tachycardia - Atrial fibrillation

Skin: Warm & moist - pretibial myxedema (specific to Graves')

Neurologic: Hyperreflexia - fine tremor.

-----------------------------------

Lab works:

⏬⏬ TSH

⏫⏫ free T4 & FT3

Other investigations:

1. RAIU:

Radioactive iodine uptake scan.

Useful to differentiate the causes of hyperthyroidisim.

If the uptake is ⏫look for the findings (forms):

Diffuse ( homogeneous) ➡ Graves'

Heterogeneous (multiple nodules of ⏫uptake) ➡ plummer

Focal (one area of ⏫ uptake w/suppression of rest of the gland) ➡ adenoma (hot nodule)

No RAIU findings (⏬⏬uptake) we look at serum thyroglobulin:

⏫ ➡ Thyroiditis /iodine exposure / extraglandular production

⏬ ➡ Exogenous thyroid hormone.

2. Radioactive T3 uptake:

Gives information about the status of TBG

We give resin to the patient + radioactive T3.

Radioactive T3 will bind to resin only when there is no space left on TBG.

SO WHEN THERE IS ⏫T4 ➡ no available seats on TBG ➡ more radioactive T3 will bind to resin ➡ ⏫ radioactive uptake.

The importance of this is to know if there is true hyperthyroidism or increased TBG

High TBG production ➡ low radioactive T3 uptake.

3. Free thyroxine index (FTI) :

Proportional for FREE T4 concentration.

Calculated to correct for the changes in the thyroid binding proteins.

FTI : ( Radioactive T3 uptake × serum total T4) /100

FTI : (patient's radioactive T3 uptake / normal radioactive T3 uptake) × total T4

Normal : 4-11

--------------------------------------------

Treatment :

1. Pharmacologic:

🎐Immediate control of adrenergic symptoms:

B-blockers (propanolol)

🎐 Anti-thyroid drugs: Thionamides

Methimazole:

1- Inhibits thyroid peroxidase ➡ stops the oxidation of Iodide into Iodine

2- Inhibits the coupling of DIT and MIT to form T3 & T4.

PTU (propylthiouracil) :

Shares the same mechanism with Methimazole except that PTU works on the peripheral tissue by

- Inhibiting the converting of T4 into T3.

⚠ Watch for side effects⚠

⚠Agranulocytosis

⚠Skin rash

⚠Arthralgias

Specific ⚠ for PTU is:

Hepatotoxicity.

During pregnancy:

Both can cross the placenta but it is preferred to give:

PTU at the first trimester

Methimazole at the 2nd and 3rd trimester.

Sodium ipodate or iopanoic:

Lowers serum T3 & T4 levels and causes rapid improvement of hyperthyroidism.

Appropriate for acute management of severe hyperthyroidism that's not responding to conventional therapy.

2. RAI ; Radioactive iodine:

Causes destruction of thyroid follicular cells.

Uses IODINE 131

Most common for: Graves' disease & multi-nodular goiter.

If the first dose doesn't control the hyperthyroidism within 6 to 12 months then administer another dose.

✔ Selected pations ✔

✔ Elderly patients w/Graves disease.

✔ Solitary toxic nodule

✔ Patients w/graves disease in whom therapy w/antithyroid drugs fails.

⚠ Warning ⚠

⚠ Hypothyroidism over time in the majority patients. ⚠

Note :

Ophthalmopathy can worsen after RAI prevent that by prophylactic therapy w/prednisone in high-risk patients.

3. Surgery:

Very effective

Only 1% of patients are treated by it.

Often reserved w/patients that have large goiters ; more common in toxic multinodular goiter.

⚠ Side Effects ⚠

⚠ permanent hypothyroidism 30%

⚠Recurrent laryngeal nerve palsy 1%

⚠Permanent hypoparathyroidism 1%

⚠ watch for hypocalcemia (due to inflammation/removal of the parathyroid glands)

------------------------------------------

Treatment plan :

Immediate control of adrenergic symptoms (of any cause) ➡ (beta-blocker) propanolol

Pregnant patients w/Graves' disease : Endocrinology consult is indicated before starting treatment.

Toxic multinodular goiter or Toxic adenoma: RAI or surgery Methimazole pretherapy for surgery and before RAI in selected patients.

------------------------------------

What is a thyroid storm?

Rare, life-threatening complication of thyrotoxicosis.

Characterized by an acute exacerbation of the manifestations of hyperthyroidism.

There's usually a precipitating factor: infection, DKA, stress (Surgery, illness, childbirth)

High mortality rate

Clinical manifestations:

✔ Marked fever

✔ Tachycardia

✔ agitation

✔ Confusion

✔ GI symptoms (nausea , vomiting , diarrhea)

Treatment:

Provide supportive therapy : IV fluids , cooling blankets and glucose

Give antithyroid agents (PTU preferred due to its peripheral effects) followed w/iodine.

B-blockers

Dexamethazone (steroids) to impair peripheral generation of T3 from T4 and to provide adrenal support.

-------------------------

Wow that was a long one XD

I tried to include all the important stuff :)

Resources:

First-aid

Kaplan lecture notes 2019

Medscape

Pocket medicine

Step-up to medicine.

#usmle step 2

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Recently Viewed Tags

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