Pathoma material

Question 1

describe pituitary adenoma and most common type

Answer 1

benign, anterior, functioning makes hormone, non-functioning usually presents with mass effect (bitemporal hemanopsia, hypopituitarism, headache)

Most common is prolactinoma presents as galactorrhea and ammenorrhea in females and decreased libido and headache in males

Question 2

How would you treat a prolactinoma

Answer 2

Dopamine agonist (bromocriptine or cabergoline)

or surgery for larger lesions

Question 3

How does growth hormone cell adenoma present differently in children vs adults

Answer 3

Children-increased linear bone growth (epiphysis are not fused)

Adults-Acromegaly (enlarged hands, feet, jaw, visceral organs, and tongue. death from cardiac failure)

Secondary DM is also often present because GH induces liver gluconeogenesis).

Question 4

How is a GH cell adenoma diagnosed?

How is it treated?

Answer 4

elevated GH and IGF-1. Lack of GH suppression by oral glucose.

Octreotide (SS analog to suppress GH release), GH receptor antagonists, or surgery

Question 5

When do symptoms arise from anterior hypopituitarism?

What are common causes?

Answer 5

when >75% of the pituitary parenchyma is lost

Pituitary adenomas (adults), craniopharyngioma (children), Sheehan syndrome (pregnancy related infarction of pit gland due to blood loss)

Question 6

How does Sheehan syndrome present?

Answer 6

poor lactation, loss of pubic hair, and fatigue

Question 7

What is empty sella syndrome?

Answer 7

Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland. gland is “absent” on imaging

Question 8

Cause, clinical features, diagnosis, and treatment of central DI

Answer 8

ADH deficiency due to hypothalamic or posterior pituitary pathology

features: polyuria, polydipsia, risk of life threatening dehydration. Hypernatremia and high serum osmolality. Low urine osmolality and specific gravity.

Water deprivation test fails to increase urine osmolality

treat with desmopressin

Question 9

Cause, clinical features, treatment of SIADH

Answer 9

excessive ADH secretion most often from ectopic production (SCC lung) or CNS trauma, pulmonary infection, or drugs (cyclophosphamide)

features: hyponatremia, low serum osmolality, AMS, seizures

treat by water restriction or demeclocycline (blocks effects of ADH)

Question 10

increased BMR and SNS activity is due to what in hyperthyroidism?

Answer 10

Increased BMR is due to increased synthesis of Na+/K+ ATPase

Increased SNS activity is due to increased expression of B1-adrenergic receptors

Question 11

What are the common clinical features of hyperthyroidism

Answer 11

Weight loss w/ increased appetite

Heat intolerance and sweating

Tachycardia with increased cardiac output

Arrhythmia

Tremor, anxiety, insomnia, and heightened emotions

DIARRHEA

oligomenorrhea

bone resporption with hypercalcemia

decreased muscle mass with weakness

HYPOCHOLESTEROLEMIA AND HYPERGLYCEMIA

Question 12

Causes and clinical features of Grave’s disease?

Answer 12

IgG that mimics TSH and stimulates TSH receptor (type II HS). MOST COMMON CAUSE OF HYPERTHYROID

diffuse goiter, exopthalmos and pretibial myxedema (fibroblasts express TSH receptor)

Question 13

Histology, Lab findings, and treatment of hyperthyroid?

Answer 13

Irregular follicles with scalloped colloid and chronic inflammation.

increased total and free T4, decreased TSH, hypercholesterolemia, hyperglycemia

treat with Beta-blockers, thioamide, and radioiodine ablation.

Question 14

How does thyroid storm present and how do you treat it?

Answer 14

arrhythmia, hyperthermia, vomiting, w/ hypovolemic shock

treat with PTU, Beta-blockers, and steroids

Question 15

Describe Multinodular goiter

Answer 15

enlarged thyroid with nodules due to iodine deficiency. usually non-toxic

Question 16

What is cretinism and what are causes and features?

Answer 16

hypothyroid in neonates and infants

caused by maternal hypothyroid in early pregnancy, thyroid agenesis, dyshormonogenetic goiter, and iodine deficiency.

features include mental retardation, short stature with skeletal abnormalities, coarse facial features, enlarged tongue, and umbilical hernia.

Question 17

What is myxedema? causes and features?

Answer 17

hypothyroidism in older children and adults (dough like tissue due to increased glycosaminoglycans)

caused by iodine deficiency, hashimoto’s, drugs like lithium, and surgical removal or ablation of thyroid.

features include DEEPENING of voice and large tongue, weight gain despite normal appetite, slow mental activity, muscle weakness, cold intolerance with decreased sweating, bradycardia with decreased CO (leads to SOB and fatigue), oligomenorrhea, hypercholesterolemia and CONSTIPATION

Question 18

Cause, features, histology, and associated dz with Hashimoto thyryoiditis

Answer 18

Autoimmune destruction of thyroid gland. HLA-DR5 (HLA-BR8). MOST COMMON CAUSE OF HYPOTHYROID where iodine adequate

initial hyperthyroid from follicle damage then progression to hypo-
Antithyroglobulim and antithyroid peroxidase antibodies

chronic inflammation in the germinal centers and HURTHLE cells (eosinophillic metaplasia of cells lining follicles)

increased risk for Bcell lymphoma

Question 19

Describe subacute granulomatous (De Quervain) thyroiditis

Answer 19

granulomatous thyroiditis following VIRAL infection.

TENDER thyroid with hyperthyroidism. self limited

Question 20

Describe Riedel fibrosing thyroiditis

Answer 20

chronic inflammation with extensive fibrosis of thhyroid

hypothyroidism with “HARD as wood” gland. non tender.

fibrosis may extend into local structures like airway. mimics anaplastic carcinoma but riedel is in young people and malignant cells are absent

Question 21

Describe follicular adenoma

Answer 21

benign follicle proliferation surrounded by capsule

usually non-functional but may secrete thyroid hormone

Question 22

Describe papillary carcinoma

Answer 22

Malignant follicle proliferation surrounded by a capsule however there will be INVASION THROUGH CAPSULE

hematogenous metastisis

Question 23

Describe Medullary carcinoma

Answer 23

malignant proliferation of parafollicular C cells. Secretes CALCITONIN–>hypocalcemia. Calcitonin deposits in tumor as amyloid.

MALIGNANT CELLS IN AMYLOID STROMA

Familial MEN 2A and 2B – RET oncogene

Question 24

Describe Anaplastic carcinoma

Answer 24

undifferentiated malignant thyroid tumor ELDERLY. invasion of local structures resulting in dysphagia or respiratory compromise. poor prognosis.

Question 25

Name the cells that secrete PTH

Answer 25

Chief cells

Question 26

Effects of PTH

Answer 26

increase osteoclast activity which increases calcium and phosphate

increased small bowel absorption of calcium and phosphate (by activating Vit D)

Increase renal calcium absorption (distal tubule) and decrease phosphate “grab calcium dump phosphate”

Question 27

Most common cause of hyperparathyroidism and associated symptoms?

Answer 27

Parathyroid adenoma (benign) usually involving one gland

nephrolithiasis, nephrocalcinosis, CNS disturbances (depression seizure), constipation, PUD, acute pancreatitis, osteitis fibrosa cystica

Question 28

Lab findings associated with hyperparathyroid?

Answer 28

increased PTH, calcium, urinary cAMP, alk phosph (PTH activates osteoblast which lays down bone and produces alk phosph)

decreased phosphate

Question 29

Most common cause of secondary hyperparathyroidism?

Answer 29

Chronic renal failure-less phosph gets dumped so build up binds up calcium leading to activation of PTH (increase alk phosph)

Question 30

Common causes and symptoms of hypoparathyroidism?

Answer 30

Autoimmune damage, surgical excision, DiGeorge syndrome

Numbness and tingling, muscle spasms (trousseau and chvostek signs)

Will result in decreased PTH and serum calcium

Question 31

components of MEN 1

Answer 31

pancreatic neoplasms

parathyroid hyperplasoa

pituitary adenomas

Question 32

Classic presentation of hyperaldosteronism

Answer 32

HTN, hypokalemia, and metabolic acidosis

edema often absent

Question 33

features of hypercortisol =cushing syndrome

Answer 33

moon face, buffalo hump, truncal obesity, abdominal striae, HTN, osteoporosis

Question 34

Name the three enzyme deficiencies and their associated symptoms in congenital adrenal hyperplasia

Answer 34

21 hydroxylase- most common increased androgens. hyponatremia, hypovolemia, hyperkalemia, clitoral enlargement, precosoius puberty

11 hydroxylase looks like 21 but HTN with low renin and aldosterone

17 hydroxylase decreased androgens hypokalemia, decreased renin and aldo

Question 35

Adrenal insufficiency can be associated with gluccocorticoid withdrawl but what is it called when associated with Neisseria infection in children?

Answer 35

Waterhouse-Friderichsen syndrome = hemorrhagic necrosis of adrenal glands –>DIC

Question 36

Chronic adrenal insufficiency is called ??

Answer 36

Addison’s disease

hypotension, hyponatremia, hypovolemia, hyperkalemia, metabolic acidosis, hyperpigmentation.

Question 37

What diseases are associated with pheochromocytoma?

Answer 37

MEN 2A MEN 2B, von Hipel-Lindau, NF1