Endocrine Flashcards
Hyposecretion of hormones
A genesis
Atrophy
Destruction
Hyper-secretion of hormones
Tumor
Hyperplasia
Anterior pituitary Hormones
FLAT PIG
Somatotroph
Growth Hormone
Mammography
Prolactin, essential for lactation
Corticotroph
Corticotropin (ACTH)
Gonadotroph
Gonadotropins (LH, FSH)
Thyrotoph
Thyrotpin (TSH)
Posterior pituitary is composed mostly of
Glial cells and axonal processes
Posterior pituitary stores
Oxytocin
Antidirutetic hormone
Anterior pituitary hyperfunction almost always associated with
adenoma
Adenoma: ACTH
Cushing syndrome
Nelsons syndrome
Adenoma: GH
Gigantism
Acromegaly
Adenoma: Prolactin
Galactorrhea and amenorrhea
Sexual dysfunction, infertility
Adenoma: TSH
Hyperthyroidism
Adenoma: FSH LH POMC
Hypogonadism
Mass effects
Hypopituitarism
Anterior lobe hypofunction causes
Nonfunctional pituitary adenoma
Postpartum ischemic necrosis
Ablation/destruction by surgery radiation or adjacent tumor
Hypofunction: GH
Pituitary dwarfism
Hypofunction: Gonadotropin
Amenorrhea and infertility in women
Decreased libido impotence and lack of pubic auxiliary hair in men
Hypofunction: Prolactin
No postpartum lactation
Hypofunction: TSH
Hypothyroidism
Hypofunction: ACTH
Hypoadrenalism
Gigantism is caused by
An edema in the anterior lobe that secretes GH
Gigantism occurs before
Closure of the peiphyseal plates in the long bones
Clinical features of gigantism
Generalized increase in the size of the body
Arms and legs are disproportionately long
Acromegaly is caused by
Increased GH due to an adenoma AFTER epiphyseal plates close
Acromegaly clinical features
Enlarged bones of the hands feet and face
Prognathism, development of a diastema
Hypertension and congestive heart failure may be seen
Gigantism or acromegaly have a better prognosis
Acromegaly is more guarded- due to complications of hypertension and CHF
Pituitary dwarfism potential causes
Failure of the pituitary gland to produce growth hormones
Lack of response to growth hormone by tissues
Clinical features of pituitary dwarfism
Short stature
Small jaws and teeth
Pituitary dwarfism treatment
Hormone replacement therapy if caused by lack
-prognosis good if replacement works
The thyroid gland produces hormones that regulate
The rate at which the body carries out its necessary functions
Thyroid storm
Sudden onset of severe hyperthyroidism usually triggered by stress. A medical emergency-patients often die of cardiac arrhythmia if untreated
Hyperthyroidism treatment
Depends on cause
Reactive iodine can be used to destroy overactive thyroid tissue
Graves Disease female predominance
7:1
Autoimmune disease with a significant genetic component
Graves Disease manifestations
Hyperthyroidism
Exophthalamos
Skin lesions
Hypothyroidism caused by
Decreased thyroid hormone production
- iodine deficiency
- AI destruction of thyroid
- Ablation surgery or radiation
Cretinism
Hypothyroidism developing in infancy or early childhood
Myxedema
Hypothyroidism developing in older children and adults
Cretinism signs
Impaired development of skeleton and CNS
Short stature
Severe mental retardation
Protruding tongue
Myxedema
Generalized apathy Mental sluggishness-can mimic depression Obesity Cold intolerance Enlarged tongue
Hypothyroidism: Serum TSH
Increased in primary cases due to loss of feedback inhibniotn
Not increased in cases caused by primary hypothalamic or pituitary disease
Hypothyroidism: treatment
Thyroid hormone replacement therapy
Hypothyroidism: prognosis
Good unless treatment delayed
Hashimoto thyroiditis mostly seen in
Older women significant genetic component
Hashimoto thyroiditis is a common cause of
Hypothyroidism
Hashimoto thyroiditis is a ____ Disease
Autoimmune
Progressive destruction of gland
-initially euthyroid progress ot hypothyroidism
Hashimoto thyroiditis patients are usually at risk for
Other autoimmune disease dn B cell Non Hodgkin
Goiters most common manifestation
Of thyroid disease
Goiters reflect
Impaired synthesis of thyroid hormone
Papillary Thyroid Carcinoma pathology
Microscopically character by papillae projections
Nuclear clearing
Nuclear grooves
Papillary Thyroid Carcinoma ______ mutation
RET proto-oncogene
Follicular thyroid carcinoma May resemble
A follicular adenoma
Follicular thyroid carcinoma must see
Invasion through the capsule or into the blood vessels
Medullary Thyroid Carcinoma derived from
Parafolluclar cells
Medullary Thyroid Carcinoma all have mutations in
RET proto-oncogene
Medullary Thyroid Carcinoma increased
Serum calcium
Parathyroid glans mostly composed of
Chief cells
Parathyroid chief cells secrete
PTH
-important regulator of blood calcium levels
2 cells of parathyroid glands
Chief cells
Oxyphil cells-unknown Function
Does the parathyroid need stimulation from pituitary or hypothalamus
No just needs to detect a decreased level of blood calcium
Actions of PTH
Increase tubular reabsorption of calcium
Increase urinary phosphate excretion
Increase renal conversion of vitamin D into its active from
Increase osteoclast is activity
Net affect of PTH
Increase the level of free calcium which inhibits further PTH secretion
PTH converters Vitamin D
Into its active form which increases the GI calcium absorption
Primary Hyperparathyrodism
An autonomous spontaneous overproduction of PTH
Secondary Hyperparathyroidism
A secondary phenomenon in pts with chronic renal failure
Primary HP is usually a result of
Parathyroid hyperplasia or adenoma
Primary hyperparathyrodism clinical features
Painful bones
Stones
Abdominal Browns
Psychic moans
Painful bones
Fractures associated with osteoporosis
Stones
Kidney stones are frequent in primary hyperpara
Abdominal groans
Constipation peptic ulcers and gallstones are frequent
Psychic Mona’s
Depression lethargy and seizures
Renal insufficiency leads to
Hyperphosphatemia
Hyperphosphatemia
Increased amounts of phosphate in the blood because of decreased excretion
Hyperphosphatemia decreases _______ thereby stimulating_______
Serum calcium
Production of parathyroid hormone—>glands become hyper plastic
Damaged kidneys are unable to produce
Vitamin D
Which leads to reduced absorption of calcium in the intestines
Secondary hyperparathyoirdims calcium blood levels
Are usually near normal
Which hyperparathyroidism is less severe
Secondary
Renal osteodystrophy
Defective bone growth due to renal failure
Causes of hypoparathyroidism
Surgically induced
Congenital absence
AI
Rare
Hypoparathyroidism clinical manifestation
Hypocalcemia
Increased neuromuscular excitability
Cardiac arrhythmias
Increased intracranial pressure and seizures
The endocrine pancreases is composed of
Islets of langerhans
Islet of langerhans cells
Beta cells
Alpha cells
Delta cells
PP cells
Beta cells
Produce insulin
Alpha cells
Produce glucagon
Delta cells produce
Somatostatin
PP cells produce
VIP- a pancreatic polypeptide
Glucagon
Mobilizes carbohydrates stored in the liver into circulation when the body needs them. Promotes glycogenolysis and gluconeogensis in fasting states
Insulin
Major anabolic hormone many synthetic and growth promoting effects-allows glucose to be transported and stored in cells within the body after meals
Somatostatin
Suppresses both insulting and glucagon
VIP
Exerts several GI effects
Normal glucose levels
70-120mg/dL
Diabetic if any one of these criteria
Random glycemic of > 200mg/dL with classical S&S
Fasting glucose levels of >126mg/dL on more than one occasion
Abnormal glucose tolerance test
Insulin and Glucose homeostasis depends on 3 processes:
Gluconeogenesis
Glucose uptake by tissues
Actions of insulin and glucagon
Insulin increases the rebate of
Glucose transport into certain cells of the body
Diabetes Type I
A chronic AI
-beta cells of the pancreas get destroyed by self reactive T cells and autoAbs
Type I diabetes results in
Absolute deficiency in insulin production
Clinical Type I
Before 20 in normal weight
Character by decreased blood insulin
AutoAbs are detectable in the blood
AKA: Juvenile diabetes
Diabetes Type I symptoms
Polydipsia
Polyuria
Polyphagia
Ketoacidosis
Polydipsia
Increased intake of fluids
Polyuria
Increase in the frequency and amount of urination
Polyphagia
Increased food intake excessive hunger
Ketoacidosis
Accumulation of ketoacidosis in the blood resulting from excessive breakdown of fats
Diabetes II result of
Insulin resistance
Decreased insulin secretion
Adult onset
Type 2 diabetes clinical features
> 40
Obesity
Insulin levels in blood may be normal or increased
Same symptoms as type I
Who is most likely to die from diabetes
Type I
Type I The pancreas
Where as in type 2
the pancreas fails to produce insulin
The pancreas makes insulin but the receptors fail to respond
Diffuse glomerulosclerosis
90% of diabetics
Microangiopathy around glomerular capillaries and deposition of matrix
Proteinuria, total renal failure
Nodular glomeruloscerlosis
15-30% of person with long term diabetes; specific to diabetes
Ball like deposition of matrix at the periphery of the glomerulus
Total renal failure
Zollinger-Ellison Syndrome
Pancreatic islet cell tumor, hypersecretion of gastric acid, peptic ulcers
Hormones produced by the adrenal cortex
Cortisol
Aldosterone
Estrogen
Progesterone
Catecholamines produced by the adrenal medulla
Epinephrine
Norepinephrine
Dopamine
2 Types of Hyperadrenalism
Hypercortisolism
Hyperaldosteronism
Cushing’s syndrome (hypercortisolism) causes
Excess administration of exogenous glucocorticoids
Primary adrenal hyperplasia or neoplasm
Pituitary source
Ectopic ACTH secretion by neoplasm
Primary pituitary source known as cushings
ACTH oversecretion by pituitary microadenoma
Cushing short term clinical features
Weight gain and hypertension
Moon faces
Buffalo hump
Long term cushings clinical features
Decreased muscle mass, weakness
Diabetes
Osteoporosis
Cutaneous striae hirsutism
Mental disturbances: mood swings, depression, psychosis
Menstrual irregularities
Hyperaldosteronism characterized by chronic excess aldosterone secretion results in
Sodium retention, potassium excretion
Hypertension and hypokalemia
Primary hyperaldosteronism
Very rare
Hyperplasia neoplasm idiopathic
Decreased levels of plasma renin
Secondary hyperaldosteronism
Aldosterone released in response to activation of renin angiotensin system
Increased levels of plasma renin
Hypoadrenalism
Primary or secondary
Secondary decreased stimulation of adrenals from deficiency of ACTH
Hypoadrenalism symptoms
Weakness
Fatigue
GI disturbances
Acute Adrenocortical insufficiency
In patients on exogenous steroids
—>rapid withdrawal ——>adrenal crisis
Vomiting Abdominal pain Hypotension Coma Death
Primary Chronic Adrenocortical insufficiency (Addison’s Disease)
Progressive destruction of the adrenal cortex
- ACTH serum elevated
- Destruction of cortex prevents response to ACTH
Primary Chronic Adrenocortical insufficiency (Addison’s Disease) destruction is caused by
AI process
Infection (TB AIDs)
Metastatic Disease
Primary Chronic Adrenocortical insufficiency (Addison’s Disease) Symptoms
Easily fatigued
GI disturbances
Hyperpigmentation
Craving salt
Secondary Adrenocortical insufficiency is any disorder of
Of the hypothalamus or pituitary that reduces output of ACTH
Secondary Adrenocortical insufficiency is similar to Addisons (primary) except t
No skin/mucosa pigmentation
Pheochromocytoma a neoplasm of
Chromaffin cells
chromaffin cells make
Epinephrine
Pheochromocytoma
F>M 30-60
Hypertension
Tachycardia
Tremor
Headache
Pheochryomcytoma rules of 10s
10%
Bilateral
Extra adrenal
Malignant
Familial syndromes
