Module 5: Endocrine: DI, SIADH, Graves and Hyperparathyroidism, Thyroid Adenoma Flashcards Preview

Pathology Post Midterm > Module 5: Endocrine: DI, SIADH, Graves and Hyperparathyroidism, Thyroid Adenoma > Flashcards

Flashcards in Module 5: Endocrine: DI, SIADH, Graves and Hyperparathyroidism, Thyroid Adenoma Deck (36):

First lets start off with Diabetes Insipidus, what is the etiology?

Deficiency or resistance to the action of ADH


There are two different types of Diabetes Insipidus, the first is central DI, what are some features?

Central DI: absolute deficiency of ADH
---genetic, idiopathic or hypothalamic/pituitary stalk disease


The second type of DI is nephrogenic DI, what are some features?

Nephrogenic DI: resistance to ADH action
--genetic, metabolic (hypokalemia, hypercalcemia) or lithium
--hypercalcemia causes aquaporin in CD to be insensitive to ADH -- decreased urine osmolality --- polydipsia and polyuria


What is the function of ADH?

Response to decreased blood volume and increased plasma osmolality (water is absorbed by osmosis into the blood in response to hypovolemia)
--increased permeability in DCT and CT --- water retention and decreased urine volume
--small volume of urine that is concentrated because all your H20 is being absorbed in the DCT and CT into the blood stream due to dehydration or any state of hypovolemia


What investigations are done for DI?

Water deprivation test:
Central DI: less than 300mosmol/kg and after vasopressin greater than 600mosmol/kg (now water is being reabsorbed so urine can finally concentrate, instead of being super dilute )
Nephrogenic DI: less than 300mosmol/kg and after vasopressin less than 300mosmol/kg (defect is in the kidneys so no matter how much ADH you inject, the urine concentration is not going to change)


Along the same lines as SIADH, what is SIADH?

ADH secretion which continues despite lack of physiological stimuli ---- water retention and hyponatremia
--hyponatremia is due to the dilation of sodium by H20 flooding the bloodstream


What is the etiology for SIADH?

Post op
Intra-cranial disease: encephalitis, meningitis, head injury
Neoplasms: small cell carcinoma of the lung
Pulmonary disease: pneumonia and TB


What are the lab values for SIADH?

High urine osmolality (urine is super concentrated because all the water is being absorbed into the blood stream)
Low plasma osmolality (plasma is super dilute because H20 is constantly flooding the bloodstream due to ADH action and the insertion of aquaporins)


Moving onto Hyperthyroidism, what is the most common cause?

Grave's Disease
--more common in females b/c its an autoimmune condition --- type II HSR
--HLA association
--Type I DM and Addison's alot of the times coincide because of the Type II HSR


What is the etiology for Graves disease?

T cells induce B cells to produce IgG antibodies against the TSH receptor (stimulating Abs)


What is the pathogenesis for Grave's Disease?

Thyroid Stimulating Ig (TSI): IgG that binds to TSH receptor and mimics action of TSH ---- Increased T3/T4
--T4 is peripherally converted to T3 (Active form)
--TSI does not respond to negative feedback


What is seen on gross and histology for grave's disease?

Gross: Very vascular beefy red thyroid and diffusely enlarged (bruit heard on exam because of increased turbulence when you listen)
Histology: Lumen in lined by columnar epithelium (instead of normal cuboidal due to hyperstimulation) and the colloid within the follicular lumen is pale, with scalloped margins (Due to active resorption of the collid)
Hyperactivity of thyroid follicle ---- papillary projections into lumen (without fibrovascular core/psamomma bodies)


What investigations are done for Graves Disease?

Radioactive iodine uptake= HOT NODULE (secretes thyroid hormone)
Most accurate test: measure TSI (very high)
--T3 and T4 will be very high
--TRH and TSH will be very low


What is the treatment for Grave's Disease?

Radioactive iodine ablation --- hypothyroidism (give thyroxine treatments b/c hypothyroidism is easy to treat)


In Grave's Disease there is a triad of symptoms, each card will go through a point in the triad

1. Thyrotoxicosis (hyperthyroidism --- diffuse goiter --- hear bruit) pic 3b
--thyrotoxicosis is toxicity caused by excess thyroid hormones which may be due to hyperactive thyroid gland or exogenous thyroid hormones
--weight loss despite increased appetite, fine tremor, diarrhea, sweating and palpitations


What is the second symptom in the Triad for Grave's Disease?

2. Opthalmopathy: pic 3a to left
--Exophthalmos: TSI stimulates fibroblasts to lay down GAGs in the back of the eye
---Lip lag Lid Retraction (sympathetic overstimulation)


What is the third symptom in the Triad for Grave's Disease?

Pretibial Myxedema (pic 3a to right)
--most consistent feature of Grave's (least likely to see though)
--TSI stimulate fibroblasts to lay down GAG's
--Non-pitting edema


What are the complications of Grave's Disease?

1. Arrhythmias: most common cause of death: following a thyroid storm (life threatening complication)
2. HTN
3. Corneal Ulcers (eyes are constantly open ---- dry cornea
4. Hypothyroidism following treatment
5. Heat intolerance and sweating
6. Hypocholesterolemia and hyperglycemia
7. Hyperreflexia


Now Grave's is the most common Hyperthyroid condition, but there are other conditions, each card will go through one. First is De Quervian's, what are some features?

2nd most common cause
Subacute granulomatous Thyroiditis (Self limiting)
--only form of hyperthyroidism that causes a painful thyroid following a viral infection
--present with pain, tenderness and fever
--low TSH b.c free T3 downregulates TRH receptors in anterior pituitary to decrease TSH release ---- thyroid atrophy


The next hyperthyroid condition is Functional Stuma Ovarii, what are some features?

Specialized teratoma of the ovary
--decreased TSH b.c free T3 downregulates TRH receptors in the anterior pituitary to decreased TSH release ---thyroid atrophy


The 3rd hyperthyroid condition is Exogenous Thyroid Supplements, what are some features?

Exogenous Thyroid Supplements
--decreased TSH b.c free T3 downregulates TRH receptors in anterior pituitary to decrease TSH release -- thyroid atrophy


The 4th hyperthyroid condition is anterior pituitary adenoma making TSH (men-1), what are some features?

Only cause of hyperthyroidism with increased TSH


Now moving onto Hypothyroidism, what is the most common cause?

Hashimoto's Thyroiditis
--most common cause of hypothyroidism
--type 2 and type 4 HSR: CD4 T cells, B lymphocytes, and antibodies destroying thyroid follicles
--autoimmune so more common in women


In Hashimoto's Disease, patients have transient thyrotoxicosis, what does this mean?

Hyperthyroidism: release of pre formed thyroid hormones called Hashitoxicosis
Becomes hypothyroid after a few hours


What is the histological appearance of Hashimoto's Disease?

Chronic inflammation with Germinal Center (containing B lymphocytes) and Hurthle cell metaplasia (Atrophic thyroid follicles filled with eosinophilic granular cytoplasm-benign)
--also seen in follicular adenoma and follicular carcinoma of the thyroid


What investigations are done for Hashimoto's Disease?

Antithyrogobulin antibodies
Antimicrosomal antibodies (thyroid peroxidase antibodies)
T3 and T4 low
TSH and TRH elevated (due to lack of negative feedback from T3 and T4)
Increased TRH --- stimulates increased prolactin ---hyperprolactinemia --- decreased GnRH
-females: amenorrhea, galactorrhea, infertility (b/c no LH surge)
--males: gynecomastia, galactorrhea, decreased libido and infertility.


What are complications for Grave's Disease?

1. Dementia: slowed cognitive function
2. Depression
3. Non-Hodgkin's Lymphoma (in the thyroid due to germinal centers, similar to MALToma in the stomach due to H.pylori)
4. Hyperprolactinemia: due to elevated TRH --stimulates prolactin release from the anterior pituitary
5. Atherosclerosis: weight gain and slowed metabolic rate and MI
6. Carpal tunnel: compression of median nerve by generalized myxedema.
7. Cretinism in children: protruding tongue, coarse and dry skin, pot belly, lack of hair and teeth and mental deficiency


Moving onto thyroid (follicular) Adenoma. What is the etiology?

KRAS mutation
--thyroid nodule
--Anaplastic is the most aggressive non malignant and then follicular adenoma


Thyroid nodules can be hot or cold, explain what this means

Hot: secretes thyroid hormone therefore increased radioactive iodine uptake: Increased T3 and T4 and decreased TSH (thyroid atrophies) = toxic adenoma ---- thyrotoxicosis (again benign condition): majority of time follicular adenoma is hot
Cold: does not secrete thyroid hormone therefore decreased radioactive uptake: Normal T3, T4, TSH and TRH: no biopsy needed: always non functional


What is the cell of origin for thyroid adenoma?

Thyroid follicle epithelial cells


What is the main difference in thyroid adenoma and thyroid carcinoma?

Capsule Intact: Thyroid Adenoma
Capsule Invaded: Follicular carcinoma


What is the histology for thyroid follicular adenoma?

Well differentiated thyroid follicles
Intact capsule (on top)
Hurthle Cell Metaplasia: atrophic thyroid follicles filled with eosinophilic granular cytoplasm
--tumor glands on bottom of slide


What is the gross image of thyroid follicular adenoma?

Well encapsulated with very regular margins
---no hemorrhage or necrosis


What investigations are done for thyroid follicular adenoma?

Radioactive iodine uptake = hot or cold
FNAC: does not help with differentiation b/w adenoma and carcinoma b.c cannot check for capsular invasion
Excisional Biopsy: necessary for all cold nodules (best investigation)


What are complications of thyroid follicular adenoma?

1. Become malignant: adenoma to carcinoma via invasion of the capsule if a cold nodule
2. Mass Effect
--Dyspnea: trachea
--Dysphagia: esophagus
--Hoarseness: recurrent laryngeal nerve
3. Hyperthyroidism if it's a hot nodule


Hot or toxic follicular adenoma has what complication?

Can kill you from arrhythmias but not from cancer (becomes thyrotoxicosis)
Cold becomes cancer

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