Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
79 Cards in this Set
- Front
- Back
The anterior lobe of pituitary is derived from ___ and the posterior lobe is derived from ____
|
Primative oral cavity (Rathke's Pouch); neuroectoderm
|
|
5 Cell types found in the ant. pituitary and the hormones they secrete
|
1) Somatotroph (50%)- GH
2) Mammatroph (10-20%)- Prolactin 3) Corticotroph (15-20%) - ACTH 4) Gonadotroph (10%) - LH & FSH 5) Thyrotroph (5%) - TSH |
|
2 hormones from the posterior pituitary
|
Oxytocin, ADH
- composed of unmyelinated nerve fibers |
|
Hyperpituitarism
|
Almost always associated w/ adenoma. May produce symptoms by hormone production or by local mass effects
|
|
Increased __ hormone has a frequency of __ and causes amenorrhea, infertility, galactorrhea, loss of libido
|
Prolactin, 30%
|
|
Increased amounts of GH cause what?
|
Gigantism (prepubertal) and acromegaly (adults)
- depends on when the epiphyses closes! |
|
Increased amounts of ACTH cause what?
|
Cushing's syndrome
|
|
Adenomas of __&__ hormone are rare
|
Gonadotropin and thyrotropin
|
|
Causes of hypopituitarism
|
1) Nonfunctional pituitary adenoma
2) Ischemic necrosis; Sheehan's syndrome (peripartum infarct) needs 75% destruction to be noticed 3) Destruction by surgery, radiation, or adjacent tumor |
|
Manifestations of hypopituitarism
|
Dwarfism, amenorrhea/infertility/dec. libido, impotence, lack of sex hairs, no postpartum lactation, hypothyroidism & hypoadrenalism
|
|
Posterior lobe pathology
|
1) Oxytocin: no significant clinical abnormalities
2) ADH: promotes resorption of free water; diabetes insipidus |
|
Diabetes insipidus is caused by pathology of what hormone?
|
ADH
|
|
Embryo and histo of the thyroid gland
|
- Develops from an invagination of endoderm that arises at the base of the tongue
- Follicles filled w/ colloid and lined by cuboidal follicular cells; C-cells are scattered in the follicles |
|
Most common causes of hyperthyroidism (4)
|
1) Grave's disease, #1 cause
2) Ingestion of excessive TH 3) Hyperfunctional multinodular goiter 4) Hyperfunctional thyroid adenoma |
|
Clinical manifestations of hyperthyroid
|
Heat intolerance, weight loss + inc. appetite, irritability, muscle weakness, diarrhea, tachycardia, CHF
|
|
In thyroid storm, patients can die from what?
|
Cardiac arrhythmia
|
|
Hyperthyroidism is diagnosed by increased __ and decreased __
|
TH, TSH (primary hyperthyroidism)
|
|
This disease shows diffuse enlargement of the thyroid on gross exam, hyperplasia of follicles w/ lymphoid infiltrates, and increased serum-free TH and decreased serum TSH
|
Grave's Disease
|
|
Manifestations of Grave's disease
|
- Exophthalmos (40%)
- Skin lesions (pretibial myxedema and scaly thickening of skin over shins) - Hyperthyroidism - Autoantibodies of TSH receptor; constantly stimulated - Female predominance 5:1 in 1-2% of women in US |
|
Common causes of hypothyroidism
|
- Destruction by surgery or radiation
- Hashimoto thyroiditis - Iodine deficiency |
|
__ develops in childhood and causes impaired development of skeleton and CNS; rare now due to iodine supplementation
|
Cretinism
|
|
__ develops in adults; mimics depression; listless w/ cold-intolerance and obesity; enlargement of tongue and course face hair, deepening voice, constipation; accumulation of mucopolysaccharide-rich edema
|
Myxedema
|
|
Measure of serum TSH
|
- Increased in primary due to loss of feedback inhibition
- Not increased in cases caused by primary hypothalamic or pituitary disease |
|
Hashimoto Thyroiditis
|
- Female predominance
- Most common cause of hypothyroidism - Some cases preceded by hyperthyroidism - Autoimmune progressive destruction of parenchyma w/ inflammatory infiltrates (starts as euthyroid); CD4+, CD8+, NK cells - Patients usually at risk for other autoimmune diseases like B-cell NH lymphoma - No established risk of development of thyroid neoplasm |
|
Most common manifestation of thyroid disease is?
|
Goiters!
- most common clinical features are due to mass effects: cosmetic issues, airway obstruction, dysphagia, compression of vessels |
|
Impairment of __synthesis --> __ in serum TSH--> __&__ of follicular cells --> gross enlargement of gland
|
TH; increase; hypertrophy and hyperplasia
|
|
Hyperfunctional "toxic" goiter
|
In a minority of ppl a "toxic" nodule may develop in a long-standing, non-toxic goiter. Hyperthyroidism
|
|
Thyroid Neoplasms (and how are they caused)
|
- Common
- Most are non-neoplastic; 1% are carcinomas; nods in young and males are more likely to be neoplastic - Exposure to radiation in first 2 decades |
|
Solitary nodules, grossly separated from normal thyroid by a thin & discrete capsule, microscopically composed of follicles w/ varying amounts of colloid
|
Follicular adenoma
|
|
Most common cause of thyroid cancers (3-5th decades F>>M), 60-70% multifocal, many have mutations in the RET proto-oncogene
|
Papillary thyroid carcinoma
|
|
Pathology of papillary thyroid carcinoma
|
- Nuclear clearing, "orphan annie nuclei" !
- papillary projections - nuclear grooves, inclusions, enlargement - Indolent lesions have >95% 10 yr survival; poor prog if extra thyroid extension in elderly |
|
Accounts for 10-20% of thyroid cancers, areas w/ iodine deficiency, may resemble ademona w/ discrete capsule, must see invasion through the capsule or into a BV
|
Follicular carcinoma
|
|
Rare, <5%, typically presents as rapid enlargement in a long standing goiter, extremely poor prognosis
|
Anaplastic thyroid carcinoma
|
|
Uncommon (5%), derived from parafollicular (C) cells, sporadic or familial, always a mutation of RET proto-oncogene, increased serum calcitonin
|
Medullary thyroid carcinoma
|
|
Embryo and histo of the parathyroid gland
|
- Derived from the 3rd and 4th pharyngeal pouches
- 4 glands, one at each pole of thyroid |
|
Chief cells secrete ___& oxyphil cells secrete__
|
PTH and unknown
|
|
Hyperparathyroidism
|
- Primary or secondary
- PTH activates osteoclasts - Skeletal changes ( ground glass appearance, Brown tumor) |
|
This is caused by adenoma or hyperplasia, more common in women and is often silent, painful bones, weakness & fatigue, osteitis fibrous cystica and osteoporosis, metastatic calcifications
|
Primary hyperparathyroidism
|
|
Most commonly caused by renal failure and symptoms are dominated by renal disease, renal osteodystrophy
|
Secondary hyperparathyroidism
|
|
Mechanism of secondary hyperparathyroidism
|
Vitamin D needed for calcium absorption in the gut, vitamin D comes from kidney, when kidney's fail so does production of vitamin D
|
|
Hypoparathyroidism is found in what disease
|
DiGeorge's syndrome
|
|
Clinical manifestations of hypoparathyroidism
|
1) Hypocalcemia
2) Increased neuromuscular excitability 3) Cardiac arrhythmias 4) Increased intracranial pressure and seizures |
|
Causes of hypoparathyroidism
|
Removal, congenital absence, autoimmune
|
|
Embryo and histo of the pancreas
|
- Arises from endoderm of the foregut
-Islets of Langerhan (endocrine) interspersed among the acinar group of cells (exocrine) |
|
Cell types of the pancreas
|
Beta (70%)- Insulin
Alpha (20%) - Glucagon Delta (10%) - Somatostatin PP (1-2%) - Pancreatic polypeptide |
|
Diabetes Mellitus
|
- Group of metabolic disorders resulting in hyperglycemia due to defects in insulin secretion
- Leading cause of end-stage renal disease, blindness, and amputations - Involves kindeys, eyes, nerves, BV |
|
___ is caused by severe insulin deficiency while ___is caused by insulin resistance and inadequate response to insulin by beta cells
|
Type 1, type 2
|
|
Presenting symptoms of type 1 diabetes
|
Polyuria, polydipsia, polyphagia w/ weight loss, ketoacidosis (due to fat usage as energy, excess ketones in blood, decreased pH) which can lead to a diabetic coma
|
|
Presenting symptoms of type 2 diabetes
|
Usually present after 40, polyuria and polydipsia, diagnosis by blood or urine test, enhanced susceptibility of infections
|
|
Type I diabetes
|
- Absolute lack of insulin secondary to autoimmune destruction of beta cells
- Genetic susceptibility + autoimmune factors + environmental factors - Abrupt onset - Requires insulin for survival |
|
Type II diabetes
|
- Collection of multiple genetic defects, each contributing its own predisposing risks modified by environment
- Insulin resistance - Beta cell dysfunction results in inadequate insulin secretion in the face of insulin resistance and hyperglycemia |
|
Disposing factors of type 2 diabetes
|
OBESITY(80%, 60% w/ glucose intolerance,adipose is antagonistic to insulin, obese kids=>obese adults), pregnancy, stress
|
|
Manifestations of DM in pancreas
|
- Reduction of the number and size of islets
- Heavy inflammatory infiltrate - Amyloid deposition |
|
Vascular manifestation of DM
|
- Responsible for 80% DM-related deaths
- Severe and accel. atherosclerosis - MI - Gangrene of lower extremities is 100-fold increased - Thickened membrane in small BV |
|
Kidney's of DM
|
1) Glomerular lesions
- diffuse glomerulosclerosis, 90% of diabetics in 10 yrs (not DM specific) - microangiopathy around glomerular caps and matrix deposition - proteinuria, total renal failure 2) Nodular glomerulosclerosis - 35%; DM specific - ball-like matrix deposition - total renal failure - renal atherosclerosis - pylenonephritis |
|
Eye manifestations of DM
|
- 4th leading cause of blindness
- Microangiopathy and microaneurysms - Retinal detachment and vision loss |
|
T/F patients w/ type 2 diabetes die more often than people w/ type 1
|
False, type 1 die by MI, renal failures, cerebrovascular disease, atherosclerosis, infection
|
|
Insulinoma (Insulin Secreting Islet Cell Tumor)
|
- Beta cell tumor, hyperinsulinism, most are ademonas
- Hypoglycemia quickly occurs from fasting or exercise - Many asymptomatic, 5-10% malignant - Nervousness, confusion, stupor Surgical excision |
|
Gastrinoma
|
- Arise in duodenum, peripancreatic tissues, or pancreas
- Gastric acid hyper secretion - 90-95% of recalcitrant ulcers - Zollinger-Ellison Syndrome |
|
Zollinger-Ellison Syndrome
|
Pancreatic islet cell tumor, hyper secretion of gastric acid and severe peptic ulcers. 60% are malignant and surgery is needed
|
|
Zona __secretes mineralcorticoids (aldosterone), zona ___secretes glucocorticoids (cotisol), and zona ___ secretes sex hormones (estrogen/androgen)
|
Glomerulosa, fasciculata, reticularis
*adrenal cortex |
|
Adrenal medulla (origin, cell type, hormone)
|
Has a neural origin, chromatin cells, source of catecholamines (epinephrine)
|
|
Hypercortisolism (Cushing's disease)
|
- Excessive exogenous glucocorticoids
- Primary adrenal hyperplasia or neoplasm - Primary pituitary source: ACTH oversecretion, Cushing disease, skin pigmentation - Ectopic ACTH secretion by neoplasm, eg lung |
|
Signs and symptoms of Cushing's disease
|
- Hypertension
- Weight gain_ "Moon facies" buffalo bump - Muscle weakness - Osteoporosis - Increased risk for infection - Menstral irregularities, hirsutism, mental disturbances |
|
Characterized by sodium retention and potassium excretion, hypertension and hypokalemia
|
Hyperaldosteronism
|
|
Primary Hyperaldosteronism
|
- Very rare
- Hyperplasia, neoplasm, idiopathic - Decreased levels of plasma renin |
|
Secondary Hyperaldosteronism
|
- Aldosterone release in response to activation of renin-angiotensin system
- Increased levels of plasma renin |
|
Hypoadrenalism
|
- Primary or secondary (decreased stimulation of adrenals from ACTH deficiency)
- Don't appear until at least 90% of adrenal gland has been destroyed - Manifestations: weakness, fatigue, GI disturbances |
|
In patients maintained on exogenous corticosteroids, rapid withdrawal of steroids or failure to increase steroids in response to an acute stress can precipitate an adrenal crisis
|
Acute adrenocortical insufficiency
|
|
Acute adrenocortical insufficiency
|
- Manifestations: vomiting, ab pain, hypotension, coma, death
- Can also be caused by adrenal hemorrhage or stress in a patient w/ existing Addinson's |
|
Causes of Addinson's disease
|
- Autoimmune destruction of steroid- producing cells (most common 60-70%)
- TB - AIDS - Metastatic disease |
|
Addinson's Disease
|
- Progressive destruction of the adrenal cortex
- Serum ACTH may be elevated=> skin & mucosal pigmentation - Destruction of cortex prevents response to ACTH |
|
Potassium retention, sodium loss, hyperkalemia, hypoatremia, volume depletion, and hypotension are seen in what disease?
|
Addinson's disease
|
|
Any disorder of the hypothalamus or pituitary that reduces output of ACTH
|
Secondary chronic adrenocortical insufficiency
- symptoms similar to Addinson's but no skin/mucosal pigmentation |
|
2 types of adrenal neoplasms
|
1- Pheochromocytoma
2- Multiple endocrine neoplasia (MEN) syndrome |
|
Pheochromocytoma
|
- Neoplasm of chromatin cells, F>M, 30-60 yo
- Hypertension, tachycardia, tremor, headache - Large polygonal cells w/ variable pleomorphism |
|
Rule of 10's
|
Bilateral, extra-adrenal, malignant, familial syndromes
|
|
MEN 2B Manifestations
|
- Notable for oral manifestations
- Mucosal neuromas (tongue, labial commisure) - Large, blubbery lips - Marfoid body habitus |
|
Tumors involved in types 1, 2A, 2B MEN syndrome
|
1- Medullary thyroid carcinoma
2- Pheochromocytoma 3- Parathyroid 4- Pituitary 5- Pancreas * RET proto-oncogene |