Sukumbi Review of Endocrine

Sukumbis Review of Endocrine

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Slide 1

Shows 2 pictures of the same lady taken at different times. Her complaint included new onset hypertension, diabetes mellitus & onset of gaps.

Which of the following will you be interested in checking? Basal level of growth hormone, blood glucose level, blood level of insulin, blood level of insulin-like growth factor

Insulin-like growth factor that is produced by the liver. This woman has acromegaly, do not pick growth hormone, b/c this is released in a pulsatile manner, would not indicate properly

The MC cause of death in patients with acromegaly is which of the following? Chronic renal failure, MI, congestive heart failure, stroke, natural death

**congestive heart failure** The MC cause of such a change is in which of the following? Carcinoma of the pituitary gland,

adenoma of prolactin secreting cells, adenoma of somatotrophs, adenoma of corticotrophs Adenoma of somatotrophs, it is usually a benign growth. Acromegaly occurs in patients who

already have fusion of the epiphysis, so bones can get fatter, but not longer Look at the R slide, the face contour if very coarse and the jaw is widened. You might see

some elongation of the jaw, called prognathism. Her fingers are broad & described as sausage-shaped. Also on the inside the woman has organomegaly enlarged organs

Prolactinoma is the MC pituitary growth. Remember that GH is an antagonist to insulin & that it is a metabolic hormone that affects all organ systems. This patient could possibly have hypertension.

Sometimes the location of the tumor rises above the sella turcica & can compress the optic chiasma affecting CN II bitemporal hemianopsia

EXTRA

34 y/o lady with a history of infertility was accompanied to the hospital by her husband. She has amenorrhea, lost libido, & the husband noticed she had a lot of milk in her breasts (shes lactating). She is not on any medication and further tests revealed the fact that she is not pregnant.

Which of the following will be your best approach in managing your patient? Irradiation, surgery, antibiotics, bromocriptin

Bromocriptin, this woman has prolactinoma, a tumor of the pituitary. The MC presentation of this is described in the question.

Note that sometimes, medication can cause this kind of condition. Will have no ovulation, no libido, will be infertile. Patients usually will come to the hospital

before it becomes a macroadenoma (tumor of pituitary that is > 10mm), otherwise it is a microadenoma. You would not use radiation for a microadenoma. Bromocriptin is like dopamine, it is an antagonist, it will inhibit the proliferation of the glands tissues.


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Slide 2

Related to slide above, another picture of acromegaly. Blood glucose, GH, **insulin-like growth factor is elevated** Look at slide thickened supraorbital ridge Slide 3

39 y/o lady shown here before & after treatment for Dx of Cushings disease.

This implies what? She has been taking excess cortisol orally, she has adrenal gland adenoma, she has oat cell carcinoma of the lung that is producing ACTH, has a pituitary adenoma that is producing ACTH

Pituitary hypothalamic problem, the other things listed as answer choices can deal with Cushings SYNDROME, we are talking about Cushings DISEASE.

They will also have DM xs glucose in the blood. This patient would have osteoporosis. Would have a problem climbing stairs b/c it affects the proximal muscles the hamstrings & quadriceps will atrophy proximal myopathy of Cushings

Slide 4

This is Cushings syndrome. Striae breaking down the collagen .: the skin is

breaking down. She has weight gain, **truncal obesity**, proximal

myopathy, features of DM, moonfaced, & you think she has Cushings syndrome.

What is the first thing you do? Ask her about medication, because the MC cause of Cushings is the administration of

exogenous cortisol. She could be taking steroids for asthma, lupus, etc. If no medication 24 hour urine estimation for cortisol & its metabolites. If it is , then there

is xs cortisol & you must do a low-dose dexamethasone administration test. Give this woman a low-dose, after 24 hours get a urine sample again & estimate the cortisol. If the cortisol this woman does NOT have a pituitary adenoma b/c adenomas do not respond to low-dose dexamethasone.

If on the other hand, you do the same thing & there is no change in the urine cortisol urine level do a high-dose dexamethasone if there is a change in the 24 hour cortisol urine level, then the woman has a problem in the pituitary causing excess cortisol.

Now what if you give both low-dose & high-doses & there is still no change? Then may have an ectopic source or an adenoma of the adrenal gland itself.


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Now measure the ACTH in the blood & see if there is an ectopic source of this like oat cell carcinoma. Sometimes it is an adenoma of the adrenal gland do imaging to Dx the adrenal gland

Remember that high stress will cause an extensive release of cortisol into the body. Cushing syndrome glucose, water, & Na, BUT prolactin is not in any type of Cushing

syndrome. *They can ask you a question just as simple as: What cancer of the lung does this patient have?

Small cell carcinoma of the lung Upon examination of a Cushings syndrome patient, you find hyperpigmentation of her skin

most likely to be from pituitary b/c high stimulation of pituitary will also release MSH, causing darkened skin. Remember, MSH is synthesized from the same precursor molecule that produces ACTH. They sometimes use the slides from the lab video, picture of 2 hands, 1 normal and 1 pigmented.

If the source in this patient is exogenous cortisol then the adrenal gland will atrophy, b/c its the release of ACTH that keeps the gland level at normal

Slide 5

42 y/o man has just been diagnosed w/ HTN. His blood pressure was 170/105 mm Hg. He was started on thiazide diuretics, and on the 3rd day he became very weak, lethargic & severely constipated. His serum Na was normal, serum K lower than normal, serum renin activity was on the lower side. An image study was done & shown on the slide.

Which does he most likely have? Pheocytochroma, neofibroma, Addisons disease, Conns syndrome, hypertension

Conns/1 hyperaldosteronism overproduction of aldosterone renin b/c the aldosterone suppresses the RAS

HTN, losing hydrogen & K metabolic alkalosis. Must remove the tumor for these patients. Most of the time it is an adenoma of zona glomerulosa.

This picture can also be used with a pheochromocytoma question. Slide 6

Gross specimen of the adrenal gland w/ a well-circumscribed mass in the middle. Cortical part of adrenal gland.

How do you determine if it is benign or malignant? Absence of capsule, it is always benign, presence of metastasis

Metastasis is the best predictor of malignancy Slide 7

Specimen removed from a 42 y/o lady who was diagnosed w/ HTN. In addition, she has palpitations, occasional chest pain, & sweating. This was removed from her abdomen.


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What do you expect to find in the urine of this patient? C-peptide, glucagons, VMA, IGF VMA (Vanillomendallic acid). This is pheochromocytoma overproduction of catecholamines

.: find catecholamines & their metabolites VMA & metanephrines. Know the 10% rule 10% bilateral, 10% malignant (presence of metastasis), 10% Familial, 10% Extra-adrenal. Neural crest cells are the cell of origin for this kind of tumor.

Slide 8

Woman w/ a staring appearance. *Take note of the visible sclera above the iris of the eyes.

What is responsible for her staring look? Accumulation of mucopolysaccharides in the upper eyelids, in the retroorbital space, or excess sympathetic activity

Excess of sympathetic activity keeps their eyelid in an excited state lid lag. If you are talking about exophthalmos, then the problem deposition of GAGs, swelling of extra-ocular muscles, LC infiltration, & edema pushing the eyeball from the back. You have to look from the top or side to check for exophthalmos.

If this patient has Graves, what is true about the thyroid gland? She is likely going to have a hot spot on her radioiodine scanning, a diffusely cold picture, one lobe hot and other lobe cold, have a diffusely hot picture

**it will be diffusely hot** the thyroid follicles are taking up the iodine & functioning. If one side is hot & one side is cold, it is NOT Graves disease. If you get all cold spots, it is NOT Graves. You will find **TSI antibodies** in this patient stimulates the thyroid follicles to convert the colloid into thyroxin thyrotoxicosis d/t hyperthyroidism. It will be a T2HS.

Other symptoms of hyperthyroidism tremors, sweating, flushed warm skin, diarrhea, weight loss, excess eating & heat intolerance

Apart from Graves, what are other causes of hyperthyroidism? People who are trying to lose weight will take thyroxin called factitious hyperthyroidism

Slide 9

Related to slide above. This shows pretibial myxedema, the dermopathy

assoc w/ Graves local accum of GAGs localized thickening & hyperpigmentation of the skin on the anterior feet & lower legs.

Caused by stimulation of Ab. Generalized myxedema is seen in hypothyroidism & is an accum of MPS face of this patient will be edematous.

Slide 10

Remember that a patient who is diabetic, the MC cause of fainting & going into coma is hypoglycemia. .: put sugar under the patients tongue

If a patient is breathing very deeply/hyperventilating, has a very ketoacidic smell DKA w/ Kussmaul breathing

Hyperglycemic hyperosmolarity can cause a coma


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MC cause of death in DM patients? MI after many years, followed by chronic renal failure

43 y/o lady w/ DM who has not been compliant w/ her medication. Each time she comes to the hospital her blood sugar has been in the normal range.

What will you use to test? Fasting blood sugar, random blood sugar, urinary glucose, glycated hemoglobin test

Glycated hemoglobin test(HbA1c) tells how much sugar flowing in the body for the last 3 months, normal value should be


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glucose, C-peptide, insulin glucose, insulin secretion b/c insulin secretion is stimulated by glucose; b/c it is exogenous insulin, C-peptide levels b/c endogenous insulin production

**You must know that C-peptide rises w/ the bodys insulin production for exam & Step 1**

**Know about AGEs, or advanced glycosylation end products d/t non-enzymatic glycosylation of proteins

AGE on collagen causes cross-links between polypeptides, which can trap plasma & other interstitial proteins can trap LDLs in the blood vessels deposition of cholesterol accelerated atherosclerosis that is seen in DM patients

AGE can also affect the structure of capillaries in the kidney can develop leaky basement membranes

Slide 14

Shows the face of a middle-aged woman who has been diagnosed w/ depression & in addition she has cold intolerance, gaining weight, constipated, sleeps most of the time, has menorrhagia and her tongue is getting big. Her children also noticed that her voice is becoming like a frogs sound.

No thyroxin everything concerning metabolism will be slower. Mucopolysaccharides are accumulating in their vocal cords leading to a croak voice.

What test do you do first? TSH if TSH, problem is w/ thyroid gland 1 hypothyroidism.

Next, estimate the amount of thyroxin in the blood, T3 & T4 should be .

What tells you she might have Hashimotos? Anti-microsomal Ab would be found, destroys the follicles no production of thyroxin.

29 y/o lady has just recovered from a viral URT infection when she developed pain & tenderness of her thyroid gland. In addition, she had sweatiness, palpitations. A Bx from the neck reveals granulomas, WBC count & ESR.

What is your Dx? Postpartum thyroiditis, Hashimotos, Graves, de Quervain thyroiditis de Quervain thyroiditis subacute or granulomatous thyroiditis **this is often associated

with a URT infection, maybe be viral** If a story is given about a woman who has just given birth to a baby, then think of postpartum

thyroiditis something happens with the thyroid gland & that can lead to hypothyroidism lymphocytic infiltration & hyperplastic germinal centers w/in thyroid parenchyma.

Slide 15

Bx specimen from the neck of a 57 y/o lady who had a goiter affecting her thyroid gland. Histology showed normal looking follicles with no stromal invasion & no pleomorphism.


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Follicular adenoma, it is a well circumscribed finding. Papillary carcinoma is the MC of the thyroid gland. It shows Psammoma bodies. Papillary

carcinoma also has the best prognosis, spreads through local LN, not through the blood stream.

Follicular carcinoma spreads through the blood & can spread to the lungs & other organs. The prognosis is poor & have stromal invasion.

Medullary carcinoma affects C-cells which produce calcitonin. Can use calcitonin to monitor this type of cancer. C-cells are from neural crest cells.

Anaplastic cancer carries the worst prognosis. It metastasizes very early, in elderly. Patients who has been exposed to excessive radiation or genetic mutations are at risk for

these kinds of cancers. Plummer syndrome develop cancer from one of the nodules in a multinodular goiter

combo of hyperparathyroidism & goiter, NO exophthalmos Slide 16

Related to above slides. Shows the thyroid gland & tumor on one side.

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Sukumbi Review of Endocrine