Endo Pathology Flashcards
A 28 year old woman delivers a baby girl at 9 months (full term). There are no major complications at delivery, but the following abnormality is noted in her genital region. What is her potential diagnosis, prognosis and treatment?
Congenital adrenal hyperplasia:
- 90% due to 21-hydroxylase deficiency leading to impaired cortisol production.
- 5% due to 11-beta hydroxylase–> decreased cortisol, virilization, Na retention, HTN due to mineralocorticoid activity of 11-deoxycortisol
- See impaired cortisol production–> excess androgen production–> virilization of females, infertility in males and females. Adrenal hyperplasia (below)
Variants:
- Hypoaldosteronism (salt wasting)–> hyponatremia, hypotension, hyperkalemia, elevated renin (due to low aldosterone secretion)
Prognosis: premature closure of epiphysis (short stature), infertility
Treatment: Glucocorticoids, mineralicorticoids, reconstructive surgery
A 35 year old man comes to your office complaining of fainting spells that are occuring with increasing regularity. He also reports some GI upset with diarrhea and pain. Upon examination you notice that he appears quite tan, and you ask him if he has been traveling in a warmer climate or using tanning beds, which he denies- he says he’s just darker skinned than his relatives. Based on his symptoms and the hisotological sample below, what is his potential diagnosis?
Primary adrenal cortical insufficiency due to Addison Disease:
- Etiology: TB most common cause (worldwide), Autoimmune disorders most common in USA (50% polyglandular autoimmune disorders. Chronic (can take a while for symptoms to arise)
- Histo: adrenal destruction, atrophy, lymphocytic infiltration
Symptoms and Signs:
- weakness, anorexia, skin pigmentation (elevated MSH), hypotension– (failure of adrenals–> increased ACTH–> increased MSH)
- gastrointestinal - vomiting, diarrhea, abdominal pain
personality changes, organic brain syndrome
Labs: serum Na low, potassium elevated, lymphocytosis and elevated eosinophil count
Treatment: glucocorticoids and mineralocorticoids
*Other causes of adrenal insufficiency:
Tumor, amyloidosis, sarcoidosis, hemorrhage, infections
An 18 year old girl arrives in the Emergency Room after her first week at college. She has been living in a dorm and awoke reporting a severe headache, stiffness in her neck and sensitivity to light (photophobia). By the afternoon she developed a fever and her roommate was having trouble rousing her, and called the ambulance. You have diagnosed her with bacterial meningitis and have begun treatment with antibiotics. Within a few hours of seeming to have recovered, her stats suddenly begin to slide (bradycardia, decreased respiration) and she slips out of conciousness. After trying to revive her she utimately succumbs to her illness. Upon autopsy, the following discovery is made. What is her diagnois?
Waterhouse-Friderichsen syndrome: meningiococcal or pseudomonal septicemia with adrenal hemorrhage leading to acute adrenal insufficiency
Acute adrenal insufficiency can also be caused by:
- Abrupt withdrawal of corticosteroid therapy (adrenal glands get “lazy” during therapy, don’t respond quickly enough to withdrawal
- Excessive stress (infection/surgery) on borderline functioning glands (may have had underlying adrenal insufficiency due to Addison’s for example)
Symptoms: hypotension, shock, abdominal/back pain- life threatening
Treatment: Emergent hormone replacement therapy (steroids)
A man comes to the office complaining of frequent episodes of anxiety and hyperventilation. While he states he is not currently having an episode, you measure his BP at 155/100 which is markedly higher than his previous BP measurements. What is his possible diagnosis and treatment based on the histologic sample below?
Pheochromocytoma= tumor of adrenal medulla (below)
Symptoms: episodic or sustained HTN/ malignant HTN (can lead to MI, aortic dissection); encephalopathy, papilledema, paroxysms of anxiety, hyperventilation/ convulsions, heat intolerance, mimics hyperthyroidism.
* Histo: neurosecretory granules
* Sporadic or as part of MEN2, NF1 (neurofibro), vHL (von Hippel Landau)
Testing:
- 24-hour urine catecholamines (NE, epi, DA) AND their metabolites (metanephrines)
- Catecholamines= 2X upper limit
- Metanephrines= above upper limit - Plasma free metanephrines= newer test, not specific, but sensitive
Diagnosis: MRI or CT; 123-MIBG scan (uptake of epinephrine by tumor)
Treatment:
Surgical
- be careful in prepping patient to avoid hypertensive crises in surgery:
- start with alpha-blocker (phenoxybenzamine) to control BP, paroxysms (2 weeks pre-op)
- If patient becomes tachycardic–> add beta-blockers (propanolol)
*NEVER add beta before alpha (could have unopposed alpha-adrenergic stimulation) - Can also use Metyrosine= inhibits catecholamine synthesis–> better perioperative course
- AEs: sedation, depression, anxiety, urea elevation
- Therefore, used when resection difficult or radiofrequency destruction being used - Two weeks post-op, re-check 24 hour catecholamines, metanephrines (yearly for 5 years)
- 30% may remain hypertensive despite ressection
Neuroblastoma:
General Features:
- originates in adrenal medulla or sympathetic chain
- 10% of all childhood cancer and 15% of cancer deaths
peak incidence in first three years
- May be congenital- child born with tumor, can also be metastatic
- presumably derived from persistent fetal neuroblasts- don’t involute, die off
Genetics: may be associated with NF-1
Poor prognosis=
- HSR on Chom 2, double minutes–> N-myc amplification (30%)
- Presence of TRKB (nerve growth factor receptor)
Good prognosis: TRKA presence
- Age < 1 year, extra-adrenal, stage IV-S (widely disseminated but NO chromosomal changes- eventually they undergo apoptosis)
Histology: edges blurred like neural tissue (vs adrenal), small round ‘blue’ cells, Homer Wright rosettes
A 45-year old woman came to her doctor after noticing increasing fatigue, coldness, and hair loss (her main reason for coming). She said she noticed that there seems to be a lump on her neck and she’s concerned she could have cancer. Upon physical exam, you note a diffuse goiter and areas of alopecia. The labs show elevated TSH and TSH-receptor antibodies and a biopsy of the thyroid reveals the following. What is her diagnosis and treatment?
Hashimoto’s Thyroiditis: both cell mediated (CD8+ cells) and humoral
- circulating antibodies directed against thyroid microsomal
peroxidase, thyroglobulin, TSH receptor (antagonist)
- genetic predisposition
- may be associated other systemic autoimmune disease
Histology
- lymphoplasmacytic infiltrate
- destruction and atrophy of follicles
- Hurthle (Askanazy) cell metaplasia
Treatment: thyroid hormone replacement
A 35 year old woman comes to your clinic with a persistant sore throat and neck after a cold she got a couple of weeks ago. Recently she has had severe pain in the front of her neck (“right over her adam’s apple”) and has felt like her heart is racing and is concerned she might have some sort of infection or cancer. A biopsy of her thyroid reveals the following. What is her diagnosis, prognosis and treatment?
DeQuervain Thyroiditis= subacute thyroiditis
- follows URI, caused by viral infection (influenza, adenovirus,
echo, coxsackie, possibly mumps) - granulomatous inflammation
- transient hyperthyroidism with destruction of follicles
- euthyroid state restored upon recovery
Treatment: treat symptoms (hyperthyroid, pain)- generally recovers euthyroid state within a few months
A 50 year old woman with a 10 year history of lupus comes to the clinic after having issues with swallowing over the past few weeks. She denies any URIs or sore throats. Upon physical exam there is a hard lump noted over her thyroid that does not move when she is asked to swallow. A biopsy is taken- what is the diagnosis, etiology, and prognosis?
Riedel Thyroiditis
- dense fibrosis of thyroid
- associated with extrathyroidal fibrosis including: retroperitoneum, mediastinum
- not related to other thyroiditides
Histology
- dense hyalinized tissue with chronic inflammatory infiltrate
Etiology= history of inflammatory/autoimmune disorder–> inflammation of thyroid with hyaline tissue–> hard thyroid
Prognosis: needs to be surgically removed to relieve issues with swallowing
This thyroid gland was removed from a 65 year old woman at autopsy; the patient had no history of hyper or hypothyroidism. What is the diagnosis?
Nontoxic multinodular goiter= more common form of nontoxic goiter in older women (vs diffuse goiter). No funcitonal, inflammatory, neoplastic alterations
Your patient comes to your office for her annual physical and you note some changes in her appearance since you saw her two years ago. Her eyes show exopthalmos and proptosis, and there is a diffuse goiter on her neck. She reports feeling “just fine” since you saw her last- in fact, she has lost weight and has more energy. How would you diagnose and treat her condition?
Hyperthyroidism caused by Grave’s disease:
Symptoms:
- Diffuse goiter with bruit
- Opthalmopathy (non-specific): grittiness, photophobia, lid lag & retration
- Specific opthalmopathy: proptosis (see upper AND lower sclera), exopthalmos, (diagnose with Moebius sign), ophthalmoplegia
- Dermopathy: acropachy (clubbing)
Testing: Elevated T3, T4, increased radioactive iodide uptake (vs thyroiditis- no changes in uptake, just increased output of thyroid hormone)
Treatment:
- Thionamides= methimazole (MMI) and propylthiouracyl (PTU)- block activity of TPO, block iodotyrosine coupling
- Iodides (potassium iodide solution)= large doses inhibit TH release (TBG proteolysis inhibition)
- Radioactive iodide (kill Thyroid gland- NOT for use in pregnancy)
Sample of thyroid biopsy:
Papillary thyroid carcinoma
- *FIRST AID**:
- Mos common
- Excellent prognsosis
- Empty appearing nuclei “Orphan Annie’s eyes”
- Psammoma bodies
- Nuclear grooves
- Increased risk after childhood radiation
Pathogenesis: mostly sporadic, but is associated with:
- Iodine excess (animal model)
- in regions endemic for goiter, addition of iodine to diet (increases the proportion of papillary to follicular carcinoma)
- Radiation (atomic bomb survivors, Chernobyl)
- Radiolabeled iodine does not increase the risk of PTC (insufficient dose)
*most common variant of thyroid carcinoma
Histology: variable morphology with some papillary areas, pseudonuclear inclusions (clear nuclei), nuclear groove, psammoma bodies (calcospherites)
- Variants: Pure papillary, Follicular variant (still has nuclear features of papillary CA)
*spreads predominately by lymphatics
Genetics:
- Increased risk among first degree relatives: MEN2
- RET oncogene rearrangement (also mutated in MEN2)
Prognosis= excellent, relatively normal life expectancy even with lymph node metastases at the time of initial surgery. Overall > 90% survival
- *Thyroid follicular carcinoma**:
- good prognosis, uniform follicules
- capsular/vascular invasion–> poor prognosis
No papillary carcinoma features
Ressembles follicular adenoma except for capsular invasion.
- HEMATOGENOUS spread
- Minimal invasion (not through capsule)= good prognosis (90% survivorship at 10 years)
- Widely invasive= through capsule/vascular/bone invasion (50% survivorship at 10 years)
Treatment: surgery, radioactive iodine
A patient with high serum calcitonin had the following biopsied from his thyroid gland. What is his diagnosis and prognosis?
- *Thyroid Medullary Carcinoma**
- parafolliular C cells–> calcitonin
- Sheets in amyloid stroma
- associated with Men 2A, Men 2B, familial medullary thyroid carcinoma
- derived from C cells, C cell hyperplasia is precursor lesion
- 20% are familial and associated with MEN 2
- RET oncogene mutations
- composed of solid sheets of polygonal granular cells with amyloid deposition (procalcitonin)–> produces calcitonin
- may also produce ACTH, glucagon, insulin, HCG, VIP, serotonin
*Invasive and metastatic-
60-70% 5 year survival
A 32 year old woman presents to your clinic concerned that she may be pregnant as she has not menstruated in 3 months and has begun to notice some milky discharge from her nipples. She reports using birth control pills and condoms and wonders how this could have happen. You perform a urine beta-hCG test, which is negative. Upon blood testing you notice elevated prolactin levels. A biopsy is taken from her pituitary gland- what is the probable diagnosis?
- *Prolactinoma** (lactotrope adenoma)= most common type of pituitary adenoma. Can see amyloid deposition and psammona bodies
- *Symptoms:**
- amenorrhea, galactorrhea (proliactin), low libido, infertility: increased prolactin–> decreased GnRH
- bitemporal hemianopia (impinge on optic chiasm)
- Treatment: dopamine agonists (bromocriptine, cabergoline)
(spherical, calcified structures seen in tumors throughout body- papillary thyroid cancer, meningiomas, serous ovarian carcinoma). Conversely, can see absence of cell type differentiation (previous image)
Symptoms:
- Females: galactorrhea, infertility, amenorrhea
- males: decreased libido, erectile dysfunction
Normal islet of langerhaans tissue
Below is a histologic sample from the pancreas of an obese 55 year old African American woman. She was reporting increasing thirst and urination over the past several months and her doctor performed a fasting blood sugar which was measured at 150 mg/dL. What is her diagnosis and what is notable in the histologic sample?
Type 2 Diabete Mellitus
Histology: no reduction in islet cell number, but distinct fibrosis and amyloid deposition in islets of Langerhaans. Additionally, there is hyaline arteriosclerosis in pancreatic tissue
A six year old boy was brought to his pediatrician by his mother after she noticed he seemed to be eating more while losing weight over the past two months. Additionally he was always drinking water and on longer car rides they had to stop so he could use the restroom. Based on the hisotologic sample below, what is his diagnosis?
Type 1 DM: see lymphocytic infiltrate leading to destruction of beta cells in islets of Langerhaans
A 65 year old man with poorly controlled diabetes presents to his physician for testing. After measuring high levels of protein in his urine, the physician orders a biopsy of his kidney tissue and the following is note. What is his diagnosis?
Diabetic glomerulosclerosis: consistently elevated glucose (uncontrolled DM) causes glucose spillage in kidneys. Glucose–> cross-linking of proteins–> basement membrane thickening in arterioles. Eventually leads to breakdown of arterioles–> proteinuria (kidney damage)
A 55 year old man presents to his physician complaining of gradually worsening feelings of light-headedness, lethargy, insatiable hunger, and sweating. The physician takes blood panels which are notable for elevated insulin, proinsulin, c-peptide, and decreased beta-OHB. Based on the specimen below, what is the patient’s diagnosis?
Insulinoma: most common endocrine pancreatic tumor. Only 5-10% malignant (vs. highly malignant exocrine pancreatic tumor).
Symptoms= related to hypoglycemia from excess insulin production; sweating, nervousness, hunger, lethargy, coma
Histology__: amyloid deposition, insulin-producing tissue (stain) seen outside of islets of Langerhaans (below)
A 45 year old man presents to the emergency room after vomiting blood. He reports that he’s been taking tums and prilosec for the past few months because of recurrent GERD, but he’s never experienced any bloody vomit before. What is his diagnosis, and based on the histologic sample of his pancreas (below), what could be causing this?
Diagnosis: peptic ulcer disease caused by gastrinoma= ~25% of islet cell tumors, sporadic (some seen in multiple endocrine neoplasia type 1). Gastrin-producing cells are NOT native to endocrine pancreas (normally found in duodenal mucosa)
- 70-90% malignant
- Seen in Zollinger-Ellison syndrome: intractable gastric acid hypersecretion, severe peptic ulcers in duodenum/jejunem, high serum gastrin levels, thickened gastric folds
A man presents to your office with a red rash that he states is recurrent on different parts of his body. The rash appears to be accompanied by some breakdown of skin. Additionally his lab panels reveal anemia. Below is a sample of an islet of langerhaans from his pancreas- what is a possible diagosis?
Diagnosis: glucagonoma
Symptoms: syndrome of mild diabetes, necrotizing migratory, erythematous rash, anemia, venous thrombosis, severe infections, hypoaminoacidemia
RARE functional islet cell tumor (excess alpha cells)
MOST malignant
A 65 year old man presents to your clinic after having recurrent diarrhea. The stool is greasy and foul smelling. Additionally his fasting glucose demonstrates impaired glucose levels (115). Below is a sample of his pancreas. What are possible diagnoses?
Somatostatinoma= rare, mostly malignant islet tumor.
Symptoms: mild diabetes, gallstones, steatorrhea, hypochlorhydria (decreased gastric acid production)- ALL related to suppression of other hormone producing cells (insulin and glucagon suppressed)
VIPoma= Vasoactive intestinal peptide tumor: rare (<5% of islet cell tumors), mostly malignant
Symptoms: profuse diarrhea, hypokalemia, hypochlorhydria (decreased gastric acid production)
** Functional islet cell tumors may produce other hormones: ACTH, PTH, calcitonin, vasopressin
A 55 year old obese woman came to her doctor for her annual physical. The following was observed with an ophthalmoscope. Additionally, she had an elevated fasting glucose (170 mg/dL), elevated blood pressure (150/90) and elevated LDL cholesterol. What are the changes in her retina and how can they be prevented from progressing?
Non-proliferative retinopathy: microaneurysms, intraretinal hemorrhages, hard exudates (lipid encircling leaking blood vessels)
Prevention: manage blood pressure, manage glucose levels. Screen reina yearly.
A 67 year old man with a 10-year history of type 2 DM has his annual dilated fundoscopic exam and the following changes are observed. What types of changes are shown and what other eye problems is this patient at risk for?
Pre-proliferative retinopathy: development of retinal ischemia appearing as a “cotton wool spot” with venous changes (dilated loops)
Other risks with DM:
- cataracts
- refractory defects due to retinal fluid shifts (temporary blurry vision)
- glaucoma
A 72 year-old woman with a 15 year history of type 2 DM comes to her physician complaining of vision changes over the past few months. Her diabetes has been poorly controlled (HbA1c= 9.1%) and now she is having blurry vision. Based on the fundoscopic exam below, what is her diagnosis and treatment?
Proliferative retinopathy: neovascularization resulting from growth factors responding to retinal ischemia. Friable vessels can hemorrhage, fibrose, and cause retinal detachment and blindness (#1 cause in USA)
Treatment: Laser photocoagulation therapy or intravitreal glucocorticoids, VEGF inhibitors (prevent further vessel growth), vitrectomy (decrease pressure/fluid shifts)
Normal pituitary gland tissue: see acidophil, basophil, and chromophobe tissue
A 54 year old man comes into the office complaining of worsening headaches over the past few months. He has elevated blood pressure and signs of pre-diabetes (fast blood glucose= 115mg/dL). Additionally upon physical exam he mentions that he no longer fits into his wedding ring but he doesn’t feel that he has gained significant weight. Based on the histological sample below, what is his diagnosis and treatment?
Somatotrope (GH) adenoma: histological sample from pituitary gland stained for growth hormone reveals excess GH-producing cells. This patient has acromegaly due to excess GH stimulation.
Treatment:
- surgical ressection of adenoma
- Somatostatin (GH antagonist)
- Radiation (if tumor wrapping around other structures)
Intermediate pituitary lobe: can see squamous rest cells–> can lead to craniopharyngioma formation
Craniopharyngioma: located in sella. On histological specimen, can see calcification and squamoid lining of tumor. Squames can be enlarged and anucleate
Develops from intermeidate pituitary lobe squames
Neurohypophysis: posterior pituitary- produces ADH, oxytocin. Can be mistaken for tumor (and subsequent removal will cause diabetes insipidus). Herring body in the sample will indicate this is not glial tumor (small, pink, rounded structures surrounded by glial cells
Normal thyroid tissue: see colloid with surrounding follicle cells
A 35 year old woman presents to your office complaining of a rash on her legs that has been there for several weeks. Upon physical exam, you notice she has a slight tremor of her hands and tachycardia and she has lost 7 pounds since her last exam. You ask if she has been taking any meds or dieting, which she denies. What is her possible diagnosis based on her symptoms?
Hyperthyroidism: pretibial myxedema.
Further testing:
1: Elevated TSH and T4
2: 24 hour Iodide uptake and scan
- Thyroiditis= NO uptake
- Grave’s disease= high levels of uptake
An older woman comes to your clinic complaining of recent weight gain and fatigue. She reports feeling cold all the time. Upon physical exam you note that there is a slow relaxation phase of ankle relfexes. Additionally there is swelling around her eyes (noted below). What is her possible diagnosis and how would you treat her?
Hypothyroidism: could be caused by:
- Endemic goiter (iodide deficiency)
- Defective synthesis of TH with compensatory goiter
- Inadequate function due to decreased gland mass from:
- “burned out” Hashimoto’s
- Thyroidectomy (mantle radiation–> xerostomia= kill thyroid gland tissue)
- Inadequate TSH, TRH
Treatment:
- Synthetic thyroid horome (levothyroxine= T4, liothyroxine= T3, liothrix= T4+T3)
Based on the histologic sample of thyroid below, what is your diagnosis? How would this be treated?
Grave’s disease.
Treatment: anti-thyroid meds:
- MMI, PTU (thionamides= inhibit TPO)
- Iodides (inhibit TBG proteolysis)
- Iodinated contrast media
- Radioactive iodine
- Surgical removal
Below: treated Grave’s thyroiditis
A palpable mass is imaged with doppler flow and is “cold” and solitary. Upon surgical removal the following specimen is recovered. What is the likely diagnosis of this benign neoplam?
Follicular Adenoma
- benign neoplasm with follicular differentiation
“cold” solitary circumscribed nodule
When multiple, often a component of multinodular goiter = dominant or hyperplastic nodules
- numerous histologic variants (including embryonal, fetal, simple, colloid, Hurthle adenomas)
The following thyroid tissue was found within bone. What type of carcinoma is it and what is the prognosis?
Bone metastasis of Thyroid follicular carcinoma: prognosis worsens once it has completely permeated the capsule and metastasized to other tissues
- HEMATOGENOUS spread
Prognosis: 50% survivorship (vs 90% for non-metastatic) at 10 years
Below= vascular invasion
The following tissue biopsy was obtained from a goiter of a woman who had low-grade thyroid neoplastic biopsies in the past. What is her prognosis?
Anaplastic Carcinoma
- rapidly fatal
- 50% of patients have a history of longstanding goiter
- many had prior lower grade thyroid neoplasms
- RET activation not observed
Parathyroid gland: normal histology:
- Abundant fat cells (30-50%)- hypercellular glands are sign of pathology, so there should be adequate fat spacing
- Gland responsive to Mg, Ca–> secreates PTH from chief cells in response to low levels of calcium
Parathyroid adenoma: hypercellular area within gland
Patient presents to your office complaining of kidney stones and increasing acid reflux. Upon physical exam you note some peripheral muscle weakness and an elevated blood pressure (150/95). You draw labs and see an elevated PTH and serum calcium. The following specimen is removed from the patient’s neck. What is the diagnosis?
Parathyroid hyperplasia:
- 1/3 Associated with MEN1 and 2A
- 1/3 monoclonal
- Lack of cellular pleiomorphism
Histology: Lacking normal cellular spacing, adipose tissue: gland is 100% cellular
- *Symptoms**: Similar to hypercalcemia:
- increased serum Ca, decreased phosphate
- Nephrocalcinosis, renal stones
- Osteitis fibrosa cystica: bone pain, cysts, fractures (bone turnover–> decreased bone mass)
- Polyuria (secondary to hypercalciuria)
- Mental status changes
- Muscle weakness (peripheral neuropathy)
- Peptic ulcer (increased calcium)
- Chronic pancreatitis (increased calcium)
- Hypertension
A 72- year old woman presents to her orthopedist with complaints of pain in her left shoulder. She cannot remember any specific incident when the pain started, but it has gotten progressively worse over the past few months. Additionally, she reports a recent bout of kidney stones which she passed a few weeks ago. What is her diagnosis and treatment?
Osteitis Fibrosa Cystica: degeneration of bone due to hyperparathyroidism (excess PTH stimulates osteoclast activity–> bone turnover–> wears away at bone surface.
Below: histologic slide of broken-down bone tissue- see numerous multinucleated osteoclasts resorbing bone
Treatment: treat underlying hyperparathyroidism (surgical removal of parathyroid glands); eventual treatment for osteoporosis
Normal adrenal gland: gross specimen
Below: Cortex: glomerulosa–> fasciculata–> reticularis–> medulla
Adrenal Cortex: derived from coelomic mesenchymal cells
Zona Glomerulosa
- *- site of aldosterone secretion
- stimulated by angiotensin and potassium
- inhibited by atrial natriuretic peptide and somatostatin**
Zona Fasciculata and Reticularis
- *- glucocorticoids and dehydroepiandosterone**
- Stimulated by ACTH
Adrenal Medulla
- Produces catecholamines
neuroectodermal derivation
Adrenal tissue: Cortical fasciculata to zona reticularis to medulla
Fasciculata= produces glucocorticoids, stimulated by ACTH
Reticularis= produces DHEA-S (androgens)
A patient exhibited signs of excess cortisol (Cushing’s) and had a dexamethasone suppression test which was negative (cortisol levels were unchanged by dexamethasone). Additionally, there were low levels of serum ACTH, thus indicating it was not a pituitary tumor causing the condition. Upon a CT scan of the adrenals, the following was noted. What is the patient’s diagnosis and prognosis?
Adrenal Tumors
- no evidence that hyperplasia leads to adenoma
- most adenomas are hormonally active
- 80% of adrenal cortical carcinomas are functional
- poor prognosis
A 35 year old man presents to his physician with new-onset hypertension and increasing thirst and urination. Lab tests revealed elevated fasting glucose, hyponatremia and hyperkalemia. What is his diagnosis and treatment?
Conn Syndrome= Adrenal carcinoma: can see marked nuclear pleomorphism
- Poor prognosis
Etiology
- aldosteronomas (90%) or hyperplastic adrenals
Symptoms and Signs
- hypokalemia and HTN (secondary to hypernatremia and increased peripheral vascular resistance)
- muscle weakness (secondary to hypokalemia), polyuria, polydipsia, decreased renin (in secondary forms, renin is high)
Treatment: surgery, Na dietary restriction, and aldosterone antagonist (spironolactone)
Pineal gland tissue= epiphysis
- Secretory product= melatonin: sleep aid/inducer, regulates sleep in lower order mammals/ reptiles, releasing factor for arginine vasotocin (anti-gonadotrophic); also secretes serotonin
Pineocytoma=
- Can be associated with precocious puberty (males), obstructive hydrocephalus (cerebral aqueduct proximity)
- Histo: see “rosettes”
Pineoblastoma: no distinct features, may see “photoreceptor differentiation”- generally sheet of blue cells
- High mitotic rate, very aggressive
Normal thymus tissue:
Medulla= pink
Cortex= blue
below: Hassall’s corpuscles
Thymic hyperplasia:
- Lymphoid follicles in thymus
- Associated with myasthenia gravis (2/3): thymus contains nicotinic Ach receptors on epithelial/myoid cells–> autoimmunity to Ach Receptor stimulates thymus?
- Seen with other autoimmune disorders: Graves, Addison’s, SLE, scleroderma, RA
Thymoma= neoplasm of epithelial cells (from Hassall’s corpuscles) with neoplastic lymphocytes
- Seen in 10% of myasthena gravis pts
- Associated with: hypogammaglobulinemia, erythoid hypoplasia myocarditis, dermatomyositis, SLE, scleroderma, RA, Sjogren’s, T-cell leukemia, multiple myeloma
Pineal germinoma= most common adenoma of pineal gland
Histologically similar to seminomas of testis or dysgerminoma of ovary
