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What regulates pituitary trophic hormones?
- Regulates most other endocrine glands/organs
- in the sella turcia.
- Connected to the hypothalamus via stalk.
- The hypothalamus regulates pituitary trophic hormones
What are the the cell types and hormones the Anterior Lobe of the Pituitary gland secrete?
- Somatotroph 50% Growth Hormone
- Mammotroph 10-20% Prolactin
- Corticotroph 10-20% Corticotropin (ACTH)
- Gonadotroph 10% Gonadotropins (LH, FSH)
- Thyrotroph 5% thyrotropin (TSH)
What are some hormones that the posterior lobe of the pituitary gland secrete? What is it composed of?
- Composed of unmyelinated nerve fibers:
- Antidiuretic hormone (ADH, aka vasopressin)
Anterior lobe of Pituitary pathology
what is it's main cause/what is it almost always associated with?
How are the symptoms produced? two ways...
- Almost always associated with adenoma
- Symptoms produced via
- 1. Hormone production (over production)
- 2. Mass effect: Gets so big it compresses surrounding structures. Hypertrophy.
What happens during hyperfunction (hyperpituitarism) with Adenomas affecting
- Prolactin 30%: amenorrhea, infertility, galactorrhea, loss of labido
- Growth Hormone: 17%: Gigantism (prepubertal), acromegaly (adults)
- Corticotropin 14%: Cushing's syndrome (hypercortisolism)
- Mixed, Gonadotropin, Thyrotropin = rare
- Nonfunctional 25%: mass effect
Anterior Lobe of the Pituitary Gland
What is it?
- Deficiency of one or multiple hormones
- Nonfunctional pituitary adenoma (mass effect)
- Ischemic necrosis: Need over 75% destruction to cause problems
- Ablation/destruction by surgery, radiation or adjacent tumor.
Manifestations of hypofunction (hypopituitarism)
- GH: Pituitary dwarfim
- Gonadotropin: major sex hormone regulator, deficiency causes Amenorrhea and infertility in women. Decreased libido, impotence and lack of pubic/axillary hair in men.
- Prolactin: No post partum lactation
- TSH: Hypothyroidism
- ACTH: Hypoadrenalism
Posterior Lobe of the Pituitary Gland Pathology
- Oxytocin: involved in brith, no significant clinical abnormalitites
- ADH: Functions in kidneys to promote resorption of free water. If there is a decrease in ADH too much water loss through urine can cause diabetes insipidus.
How does it develop?
- Develops from an invaginationof endoderm which arises at the base of the tongue, migrates caudally to its location anterior to the thyroid cartilage.
- Histology: Follicles filled with colloid. Glassy, icy, smooth, pink looking.
most common causes: (4)
- Graves disease (number 1 cause)
- Ingestion of excessive exogenous thyroid hormone (TH) - this happens when someone has hypothyroidism and take too much TH = overcompensate.
- Hyperfunctional multinodular goiter
- Hyperfunctional thyroid adenoma
Clinical manifestations? (2 main ones)
- Diagnosis: elevated TH and decreased TSH (primary hyperthyroidism)
- Clinical manifestations: Hypermetabolic state and overactivity of the sympathetic nervous system.
How does the thyroid gland regulate the body?
Manifestations of Hyperthyroidism (8)
- Thyroid gland is like the thermostat of the body, regulator of energy, mood and other organ functions.
- Hyperthyroid people = hypermetabolic state, increase sympathetic nerve activity.
- heat intolerance
- weight loss despite increased appetite
- muscle weakness
- congestive heart failure
What is a thyroid Storm
- Abrupt onset of hyperthyroidism
- patients can die of cardiac arrhythmia due to sudden onset of aggressive hyperthyroidism or it goes undiagnosed for a while.
What is it?
- Female predominance, common, 5F:1M
- Autoimmune disease where thyroid is overactive producing excessive amounts of thyroid hormones. Has a significant genetic component
- 1. Hyperthyroidism
- 2. Exophthalamos (40%) buldging of the eye out of the socket, bug eyes
- 3. Skin lesions: pretibial myxedema pink thickening/scaly skin over tibia.
Autoimmune significant genetic component?
enlargement of what?
Hyperplasia or what?
Increase/decrease of serum components?
- Autoimmune disease where autoantibodies attack TSH receptor so it's constantly stimulated secreting TH
- diffuse enlargement of the thyroid on gross examination
- Hyperplasia of follicles with lymphoid infiltrates
- Increase in serum-free TH, decreased serum TSH
Common causes (3)
- Ablation by surgery or radiation therapy (removal of thyroid/damage by radiation)
- Hashimoto thyroiditis: autoimmune disease, inflammation of the thyroid.
- Iodine deficiency: Was more of a problem before iodine was common in the diet.
Hypothyroidism: Clinical Manifestations
- Cretinism: Children with hypothyroidism, rare, iodine in diet prevents this (it's caused by iodine deficiency). Impaired development of skeleton and CNS (mental problems) coarse facial features.
- Myxedema: Adults, generalized apathy, mental sluggishness, listless, cold-intolerance, obese, coarse facial features, enlargement of tongue, deepening of voice, constipation, late cardiac effects.
- Serum TSH: Increased TSH due to loss of feedback inhibition (thyroid can't detect it). Not increased in cases caused by primary hypothalamic or pituitary disease.
Common cause of what disease?
What is it/how is it caused?
Patients at risk for other autoimmune disease?
- Female predominance, older women, significant genetic component 10-20F:1M
- Common cause of hypothyroidism
- Autoimmune; progressive destruction of gland: initially euthyroid (normally) progress to hypothyroid.
- Patients usually at risk for other autoimmune disease and B-cell Non-Hodgkin lymphomas
- No established risk of development of thyroid neoplasm.
Goiters: what is it?
most common manifestation of what?
Impaired synthesis of what? What is their cause?
Clinical features are due to what effect?
- Goiters are enlargements of the thyroid. They reflect impaired synthesis of thyroid hormone.
- Most often due to iodine dietary deficiency, some idiopathic
- most common manifestation of thyroid disease.
- Most common clinical features are due to mass effect: cosmetic problem, airway obstruction, dysphagia, compression of vessels.
Hyperfunctional, "toxic" goiter
what is it, how is it caused?
- In a minority of patients with goiters, a "toxic" nodule may develop in a long-standing non-toxic goiter.
- Hyperthyroidism causes goiters
benign or malignant?
- Thyroid nodules are common
- Most nodules are non-neoplastic disease
- 1% are carcinomas
- Noducles in males and young patients are more likely to be neoplastic
- Genetic and environmental factors: exposure to radiation in first 2 decades of life.
What are 5 types of thyroid neoplasms?
- Follicular adenoma
- Papillary thyroid carcinoma
- Follicular carcinoma
- Anaplastic thyroid carcinoma
- Medullary thyroid carcinoma
Thyroid Neoplasms: Papillary Thyroid Carcinoma
cause of thyroid cancer?
genetic mutation of what genes?
- most common of thyroid cancers, peak 3-5th decade F>>M
- Some cases related to radiation exposure
- RET proto-oncogene mutation
- Microscopically characterized by papillary projections
- nuclear clearing - orphan annie nuclei
- nuclear grooves
- Indolent lesions, 10 year survival rates >95%
Thyroid Neoplasms: Follicular Thyroid Carcinoma
% of thyroid cancers
- 10-20% of thyroid cancers
- Older age than papillary
- Occurs in areas with dietary iodine deficiency
- May resemble a follicular adenoma
- must see invasion through the capsule or into the blood vessels.
Thyroid Neoplasm: Medullary Thyroid Carcinoma
Derived from what cells?
Sporadic or familial?
Mutation in what genes?
- Uncommon 5% of thyroid cancer
- Derive from the parafollicular (C) cells: which produce calcitonin (acts in opposition to parathyroid hormone)
- May be sporadic or familial: Component of MEN syndromes.
- All have mutation in the RET proto-oncogene
- Increased serum calcitonin
how many glands?
What are the two types of cells and what do they secrete?
- 4 glands located at each pole of the thyroid
- Chief cells: secrete PTH
- Oxyphil cells: unknown function.
What does PTH do?
Patients with hyperparathyroidism develop what?
- PTH activates osteoclasts: breakdown bone and increase serum calcium concentrations.
- Patients with hyperparathyroidism develop skeletal changes. Ground glass appearance, brown tumor.
- Caused by adenoma or hyperplasia causing hypercalcemia: very common
- Clinical features/symptoms:
- more common in women, often clnically silent
- Bones, stones, groans, moans!
- weakness and fatigue
- Metastatic calcifications: deposition of calcium throughout body, including blood vessels.
most common cause: describe mechanism
Symptoms dominated by what?
- Renal failure
- Symptoms dominated by renal disease: decreased phosphate excretion causes hyperphophatemia depresses serum calcium levels stimulates parathyroid glands.
- Normally kidneys would increase vit D synthesis to increase Ca absorption in gut, but they're not working so reduced intestinal absorption of calcium.
- symptoms as in primary, renal osteodystrophy.
Clinical manifestations (4)
- Causes: surgical removal, congenital absence (DiGeorge's syndrome), autoimmune.
- Clinical manifestations: hypocalcemia, increased neuromuscular excitability, cardiac arrhythmias, increased intracranial pressure and seizures.
What are Islets of Langerhans
Cell types? (4)
Exocrine pancreas makes what enzymes?
- Islets of Langerhans: clusters of endocrine cells interspersed among the acinar groups (that make up the exocrine pancreas.
- Cell types:
- Beta: 70% insulin
- Alpha: 20% glucagon
- Delta: 10% somatostatin
- PP 1-2% pancraetic polypeptide
What is it?
what is it's main pathology/effect?
Leading cause of what disease?
- Group of metabolic disorders resulting in hyperglycemia due to defects in insulin secretion, insulation action or both.
- Vasculopathy: with long-term complications involving the kidneys, eyes, nerves and blood vessels.
- 21 million americans affected
- leading cause of ESRD (endstage renal disease, blindness and amputation.
Classification of Diabetes
- Type 1: aka juvenile, insulin dependent, 10% of cases, severe insulin deficiency.
- Type 2: aka adult onset, non-insulin dependent. Peripheral resistance to insulin action and inadequate response to insulin secretion by Beta cells.
Presenting symptoms of DM Type 1
what is the main/worse symptom.
- usually presents by age 35
- polyphagia with weight loss
- Ketoacidosis: fat is primary energy source, excess ketones produced because of fat metabolism, decreases blood pH can lead to diabetic coma.
Presenting symptoms of DM type 2
- Usually presents after age 40
- Polyuria and polydipsia may occur
- diagnosis made after routine blood tests
- enhanced susceptibility to infection: periodontal disease
Laboratory diagnosis of Diabetes Mellitus:
Normal glucose range
DM indicated if...
Blodd glucose concentration is higher than?
Fasting glucose is greater than?
Blood glucose is greater than ___ with in 2 hours of ingesting 75g of glucose.
- Normal glucose is 70-120mg/dL
- Random blood glucose concentration of 200mg/dL or higher
- Fasting glucose greater than 126mg/dL on more than one occasion.
- Blood glucose greater than 200mg/dL within 2 hours of ingesting 75g of glucose.
Etiology of Type 1 Diabetes Mellitus:
- Absolute lack of insulin secondary to autoimmune destruction of B-cells
- Genetric susceptibility + autoimmune factors + environmental insult.
- abrupt onset
- Patients require insulin from outside sources to survive.
Etiology of Type 2 Diabetes Mellitus:
- Multiple genes play a role: each has its own risk and modified by the environment.
- peripheral tissues cannot respond properly to insulin (insulin resistance)
- B-cell dysfunction: inadequate insulin secretion in the face of insulin resistance and hyperglycemia.
Disposing factors to Type 2 Diabetes Mellitus:
3 main ones
- 1. Obesity: 80% are obese, 60% exhibit glucose intolerance, adipose tissue appears to be antagonistic to insulin.
- 2. Pregnancy
- 3. Stress.
Manifestations of DM
what is the big problem/effect of DM?
what are the affects on the pancreas?
- Vasculopathy: Big thing is vascular disease, occurs because of sugar problems. Responsible for 80% of DM-related deaths. Atherosclerosis, MI, gangrene of lower extremities, thickend basement membrane, especially around small blood vessels (MICROANGIOPATHY)
- Pancreas: destruction of islets of langerhans, heavy inflammatory infiltrate, amyloid.
Manifestations of DM on the Kidneys?
rank of cause of death?
- 2nd leading cause of death behind vaculopathy
- Glomerular lesions
- Diffuse glomerulosclerosis: 90% of diabetics within 10 years, not specific to diabetics, microangiopathy around glomerular capillaries and depsotion of matrix. Proteinuria, total renal failure.
- Nodular glomerulosclerosis: 35% specific to diabetics, ball-like deposition of matrix, total renal failure.
Mainfestations of DM to the eye?
- 4th leading cause of blindness
- Microangiopathy and microaneurysms
- Retinal detachment and vision loss.
Islet Cell Tumors:
What part of the pancreas is affected?
- Most are from the exocrine pancreas.
- May be functional or non-functional
- Insulinoma occurs.
- Gastrinoma: 90-95% of patients with really bad peptic ulcers.
What is Zollinger-Ellison Syndrome?
Pancreatic islet cell tumor, hypersecretion of gastric acid causing severe peptic ulcers. 60% malignant.
Islet Cell Tumors:
What is Insulinoma?
- Insulinoma (Insulin secreting Islet Cell tumor)
- Insulinoma: B-cell tumor, hyperinsulinism, most are adenomas. Hypoglycemia quickly occurs from fasting or exercise. Many are asymptomatic, 5-10% malignant. Nervousness, confusion, stupor. Tx: Surgical excision.
Adrenal Cortex: 3 zones, what they secrete
Adnreal Medulla: what it secretes
- Adrenal Cortex
- zona glomerulosa: mineralcorticoids (aldosterone)
- zona fasciculata: glucocorticoids (cortisol)
- zona reticularis: sex hormones (estrogen/androgen)
- Adrenal Medulla: neural origin, chromaffin, source of catecholamines (epinephrine).
- (cushing syndrome)
- 1. Excess administration of exogenous glucocorticoids (most common): taking stroids, adrenal cortex atrophy.
- 2. Primary adrenal hyperplasia or neoplasm (adrenal adenoma).
- 3. Primary pituitary source (cushing disease): ACTH over-secretion, tumor in pituitary, skin pigmentation.
- 4. Ectopic ACTH secretion by neoplasm, eg lung.
Signs and Symptoms:
Speed of onset?
blood pressure? weight? weakness? bone? infection?
- Usually gradual onset.
- hypertension, weight gain (moon faces, buffalo hump), muscle weakness, osteoporosis, increased risk of infection, menstrual irregularities, hirsutism, mental disturbances.
- caused by sodium retention, potassium excretion: producing hypertension and hypokalemia.
- Primar: very rare, hyperplasia of adrenal gland, neoplasm, idiopathic, decreased levels of plasma renin.
- Secondary: Aldosterone release in response to activation of renin-angiotensin system. Increased levels of plasma renin leading to aldosterone release.
decrease in what? because of deficiency of what hormone?
what % of gland needs to be destroyed for affect?
- Can be primary or secondary: Secondary-decreased stimulation of adrenals from deficiency of ACTH. Need 90% of gland to be destroyed before you see symptoms.
- Manifestations: weakness, fatigue, GI disturbances, anorexia, nausea, vomiting, weight loss, diarrhea.
Acute Adrenocortical Insufficiency:
How is it caused?
- In patients maintained on exogenous steroids... rapid withdrawal of steroids or failure to increase steroids in response to an acute stress can precipitate an adrenal crisis.
- Also caused by adrenal hemorrhage or stress in a patient with existing Addison's disease.
- Symptoms: Vomiting, abdominal pain, hypotension, coma, death.
Primary Chronic Adrenocortical Insufficiency (Addison's Disease).
What is it?
Serum hormone level of what?
- An autoimmune disease usually which causes the progressive destruction of the adrenal cortex.
- Serum ACTH may be elevated causing skin and mucosal pigmentation.
- Destruction of cortex prevents response to ACTH.
Causes of Addison's disease
- 1. Autoimmune destruction of steroid-producing cells: most common 60-70% of cases.
- Also caused by
- 2. AIDS
- 3. TB
- 4. Metastatic disease
Secondary Adrenocortical Insufficiency:
What is it?
What is the big difference in symptoms vs Addison's disease?
- Any disorder of the hypothalamus or pituitary that reduces output of ACTH.
- Symptoms similar to Addison's disease.
- BUT NO skin/mucosa pigmentation because of decreased ACTH.
What is Pheochromocytoma?
neoplasm of what cells?
Main symptom, other symptoms?
Rule of 10's?
- Pheochromocytoma: neoplasm of chromaffin cells which make way too much epinepherine therefore causing HYPERTENSION.
- F>M, 30-60 years old.
- Symptoms: Hypertension! tachycardia, tremor, headache.
- Rule of 10's. 10% bilateral, 10% extra-adrenal 10% malignant, 10% familial syndroms. (KNOW THIS)
Multiple Endocrine Neoplasia (MEN) syndrom.
What is it?
- Types MEN 1, 2A, 2B
- Tumors of Multiple Endocrine Organs: Medullary thyroid carcinoma, parathyroid, pheochromocytoma, pancreas, pituitary.
- Caused by: RET proto-oncogene: germ line mutation causes these tumors.
Multiple Endocrine Neoplasia Syndrome:
Where are the neuromas?
What are the symptoms?
Whats the persons body look like?
- Mucosal neuromas (tongue, labial commisure, eyelids)
- Large blubbery lips.
- Marfanoid body habitus.
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