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173 Cards in this Set

  • Front
  • Back
when is hyperplasia of the pituitary expected
increased number of lactotrophs during pregnancy or multiparous women
what is located superior and lateral to the pituitary
superior - optic chiasm
lateral - cavernous sinus containing internal carotids and CN III, IV, V, and VI
blood supply of the pituitary
arterial blood goes directly to posterior lobe
venous blood goes mostly to anterior lobe (portal system)
arises from ectoderm of the mouth cavity, Rathke's pouch
adenohypophysis (anterior lobe)
comes for the neuroectoderm of the diencephalon
neurohypophysis (posterior lobe)
cells of the anterior lobe of the pituitary
chromophils - acidophils (40%) and basophils
chromophobes (50%)- poorly staining
hormones associated with acidophils (simple proteins)
GH
prolactin
beta subunit of glycoproteins produced by basophils (FSH, LH, TSH)
portion of molecule that is unique for each hormone
polypeptides that are produced by basophils
ACTH
MSH
this pituitary adenoma can make any hormone
chromophobe adenoma
for storage and release of hormones made in the hypothalamus
posterior lobe
where is ADH and oxytocin manufactured
ADH - supraoptic nucleus of hypothalamus
Oxytocin - paraventricular nucleus
posterior lobe is often absent in this
anencephaly
pituitary aplasia
defective Rathke's pouch formation associated with absent anterior lobe
adrenals and thyroid are hypoplastic
chronic inflammation of the pituitary
granulomatous - TB, sarcoidosis, syphilis
metastatic carcinoma of the pituitary comes from which sites
breast
lung
thyroid
xanthomatosis in the pituitary
neurohypophysis - diabetes insipidus from no ADH release
when does hypopituitarism occur
when destruction of at least 75% of the anterior lobe occurs
Sheehan's syndrome
post partum pituitary necrosis during hypovolemic shock
signs of Sheehan's syndrome
women can't nurse her baby
hypothyroidism
Addison's disease
space-occupying effects of pituitary neoplasm
enlargement of sella tursica
bilateral homonymous hemianopsia
increased ICP
malignant neoplasms of the pituitary
usually metastatic and involve the posterior lobe because of greater blood supply
two cells that adenomas mostly arise from in pituitary
chromophobe (75%)
Acidophil (24%)
*both have increased GH or prolactin
If there is a basophil adenoma, what does it produce - very rare
ACTH
functional adenomas are most commonly which 3 hormones
prolactin
growth hormone
ACTH
calcified suprasellar intracranial mass in young person
craniopharyngioma
basophil adenoma secreting ACTH
cushing's disease
Nelson's syndrome
pituitary adenoma arising in a patient who had a previous bilateral adrenalectomy for Cushing's syndrome
Forbes-Albright syndrome
prolactin-secreting adenoma with galactorrhea and amenorrhea
differentiate gigantism vs. acromegaly
gigatism - chronic excess GH before epiphyses close
acromegaly - chronic excess GH after epiphyses close
Simmond's syndrome
hypopituitarism not related to pregnancy
associated with hyponatremia, cerebral edema and confusion
SIADH
low urine specific gravity, polyuria, polydipsia, no glycosuria
diabetes insipidus
MEN I
1. Pancreatic islet tumors (usually gastrinoma) - peptic ulcerations
2. pituitary adenoma/hyperplasia
3. parathyroid adenoma/hyperplasia
MEN IIa
1. Medullary carcinoma of thryoid - produce calcitonin
2. parathyroid adenoma/hyperplasia
3. adrenal medulla lesion (pheochromocytoma)
MEN IIb
same as MEN IIa with the addition of neuromas or neurofibromas
associated with mutation in the RET proto-oncogene on chormosome 10
MEN II syndromes
associated with inactivation of tumor suppressor protein menin
MEN I syndrome
two relationships with the thryoid gland
recurrent laryngeal nerve
parathyroid gland
differentiate what follicular and parafollicular cells secrete
follicular - T3/T4
parafollicular - calcitonin
when is thyroxine metabolically active
when it is free and not bound to albumin, >99% is bound to albumin normally
cretinism
thyroid agenesis or hypoplasia is young individual that is still growing
Is cretinism reversible
If caught early enough - before late stages develop
symptoms of neonatal cretinism
hypothermia
constipation
later clinical manifestation of cretinism
broad nose, thick tongue, dry skin, retarded growth, sexual infantilism, deafness, mental retardation
signs and symptoms of adult hypothyroidism
lethargy, cold intolerance, slowed mentation, thick tongue, puffiness of face and tibia
struma ovarii
functioning ovarian teratoma that secretes thyroxine
T4 and TSH levels seen in iatrogenic hyperthyroidism
increased T4
decreased TSH
enzymatic defect in synthesis of thyroid hormones with increased TSH and non-toxic goiter
dyshormogenetic goiter
failure of involution of thryoid stalk found in midline neck
thyroglossal duct cyst
two common places for ectopic thyroid
retro-sternal location
laterally within lymphoid tissue
thyroiditis secondary to bacterial or viral infection, associated with interstitial neutrophils, tender thryoid, and fever
acute suppurative thyroiditis
granulomatous thryoiditis due to cytotoxic T-lymphocytes, preceded by an upper respiratory infection
subacute thryoiditis
two common autoimmune antibodies seen in Hashimoto's disease
thryoblobulin
microsomal antigens
Can you develop Hashimoto's from Grave's disease and vice versa
Yes, both associated with HLA-B8
painless goiter with infiltration of lymphocytes and plasma cells (germinal centers) associated with increased risk of papillary thryoid carcinoma or thryoid lymphoma
Hashimoto's disease
represent end-staged Hashimoto's disease with fibrosed thryoid
Reidel's struma
is using I-131 isotope for diagnnostic purposes causing increased risk for developing carcinoma
No
Non-toxic goiter secondary to increased TSH stimulation
diffuse colloid goiter
Causes of diffuse colloid goiter
Iodine deficiency
dyshormogenetic
goitrogens
nodular colloid goiter
end-stage of diffuse colloid goiter presenting with nodules that are either cold or hot
what kind of nodule doesn't uptake I-131 isotope and is associated with increased risk of thryoid carcinoma
cold nodule
long acting thryoid stimulator
IgG antibody that stimulates thryoid follicules to secrete thyroxine, mimicks TSH
cause of exophthalmos in Grave's disease
accumulations of hydrophilic mucopolysaccharides in extraocular muscles and orbital tissues
Are there nodules associated with grave's disease
No, no nodules present
thyroid gland shows increased amounts of diffuse follicular cells, no lymphocytes or nodules present
Grave's disease
what types of adenomas have increased risk of malignancy
cold nodule in female
solitary nodules in males and children
most common thyroid adenoma
follicular adenoma
most common thryoid carcinoma
papillary carcinoma
thyroid carcinoma associated with lymph node metastasis
papillary carcinoma
thyroid disease associated with orphan Annie eye nuclei and psammoma bodies
papillary carcinoma
thyroid carcinoma associated with blood stream metastasis
follicular carcinoma
how can one distinguish an encapsulated follicular carcinoma from a benign adenoma
capsular and/or vascular invasion
medullary carcinoma
tumor of parafollicular cells (C cells)
autosomal dominant carcinoma associated with MEN syndromes
medullary carcinoma
solid cell tumor with dense fibrous stroma and amyloid deposits
medullary carcinoma
rapidly growing, highly invasive thyroid carcinoma
undifferentiated carcinoma of the thyroid
basic functioning cell of the parathyroid gland
Chief cell
what composes the majority of the parathyroid gland
50% occupied by adipocytes
where do the superior and inferior parathyroid glands arise from
superior - 4th branchial pouch
inferior - 3rd branchial pouch
where are the parathyroid glands located
posterolateral to the lower thyroid lobes
what is the blood supply of the parathyroid glands
superior thyroid artery
calcium and phosphate balance seen in parathormone
increased gut calcium absorption
increased phosphate excretion
decreased calcium excretion
increased osteoclastic stimulation
calcium and phosphate balance seen in calcitonin
increased phosphate excretion
increased calcium excretion
inhibits bone resorption of calcium
calcium and phosphate balance seen in Vitamin D
increases gut calcium absorption
stimulates bone resorption of calcium
where is 1,25-OH Vit. D3 activated
biologically activated in the kidney via 1-a-hydroxylase
All parathyroid glands increase in size
hyperplasia of parathryoid glands seen in MEN syndromes or kidney disease
associated with secondary hyperparathyroidism
renal disease causes hyperplasia of all parathyroid glands
most common cause of primary hyperparathyroidism
Adenoma - not all glands are hyperplastic
palpable mass with serum calcium of > 15 mg/dL, and is adherent to adjacent tissue
Parathyroid carcinoma
two common causes of primary hyperparathryoidism
single adenoma
MEN syndrome
manifestation of hyperaparathyroidism
polyuria, nephrocalcinosis, nephrolithiasis, metastatic calcification, osteitis fibrosa cystica
Lab findings in hyperparathyroidism
serum - increased calcium, PTH, alkaline phosphate, decreased phosphate
urinary - increased cAMP, hydroxyproline, calcium, phosphate
manifestations of hypoparathyroidism
numbness and tingling, tetany, cataracts, calcification of basal ganglia,
Lab findings in hypoparathyroidism
serum - decreased calcium, PTH, increased phosphate
urinary - decreased phosphate and calcium
associated with QT interval prolongation
hypoparathyroidism
associated with myasthenia gravis
thymus hyperplasia
thymoma
thymic follicles may participate in formation of autoantibodies
myasthenia gravis - autoantibodies against ACh receptors at NMJ
3 neoplasms of thymus gland
thymoma
germ cell neoplasm
lymphoma
most common pineal gland tumor
germinoma - such as seminoma
what are the 4 layers of the adrenal gland from top to bottom and what they each secrete
zona glomerulosa - mineralcorticoids
zona fasiculata - glucocorticoids
zona reticularis - androgens and some estrogen
medulla - catecholamines (mainly epinephrine)
what layer of the medulla is not controlled by ACTH
zona glomerulosa - controlled by serum potassium or RAAS
makes up the bulk of the adrenal gland (80%)
zona fasiculata
what part of the adrenal gland is not essential for life
adrenal medulla
what part of the adrenal gland still function if the pituitary is knocked out
zona glomerulosa
two syndromes caused by functional adenomas
Cushing's syndrome - excess cortisol
Conn's syndrome - excess aldosterone
adrenal tumor with hemorrhage and necrosis
adrenal carcinoma
most common cause of femal pseudohermaphroditism
congenital hyperplasia of adrenal gland
what causes the hyperplasia in congenital hyperplasia of the adrenal gland
decreased cortisol production leads to increased ACTH feedback and hyperplasia
3 congenital hyperplasia deficiencies
21-OH
11-OH
17-OH
most common congenital hyperplasia deficiency
21-OH deficiency
associated with decreased aldosterone and cortisol with increased androgen production - hypotensive male
21-OH deficiency
associated with decreased cortisol with increased deoxy-corticosterone and androgens - hypertensive male
11-OH deficiency
associated with decreased cortisol and androgens with increased aldosterone - hypertension
17-OH deficiency
most common cause of cushing's syndrome
iatrogenic - hospital administered steroids
secondary causes for cushing's syndrome
1. basophil adenoma of pituitary (Cushing's disease)
2. ectopic ACTH tumor (small cell tumor of lung)
3. exogenous excessive cortisol
primary cause for cushing's syndrome
bilateral adrenocortical hyperplasia
functioning adrenal adenoma
most common cause for Conn's syndrome
functioning adrenal adenoma
Are most adrenal adenomas functioning
No - most are non-functional
syndrome associated with hypertension, hypokalemic metabolic alkalosis, tetany and paresthesias
Conn's syndrome
what causes the tetany and paresthesias in Conn's syndrome
the alkalosis leads to increased negative charges on albumin which binds calcium leading to hypocalcemia
Causes for acute adrenal insufficiencies
1. waterhouse-friderichsen syndrome
2. hypovolemic shock
3. abrupt steroid withdrawal (adrenal glands cannot react in time)
effects of acute adrenal insufficiencies
shock, hypoglycemia, hyperkalmia, hyponatremia
what is needed for chronic adrenal insufficiency to occur (Addison's Disease)
loss of at least 90% of the cortex of both adrenals
causes of primary and secondary Addison's disease
primary - autoimmune, TB, AIDS, Metastatic tumors
secondary - destruction lesions of hypothalamus and/or pituitary
compare effects seen in primary vs. secondary Addison's disease
primary - hyperpigmentation from increased ACTH/MSH, electrolyte disturbances, hyperkalemic metabolic acidosis, hyponatremia, hypotension
secondary - No hyperpigmentation, No ACTH produced from pituitary so only zona glomerulosa is functioning (no electrolyte disturbances)
where is epinephrine and norepinephrine mainly synthesized
epinephrine - adrenal medulla
norepinephrine - sympathetic chain
tumor associated with positive chromaffin reaction with brown reaction with potassium dichromate
pheochromocytoma
two sites where neuroblastomas are found
adrenal medulla - 25%
sympathetic ganglion - mostly
small blue cell tumor with pseudorosettes
neuroblastoma
which site of neuroblastoma has more increased risk of malignancy
paraganglioma
how can you distinguish the site of neuroblastoma
adrenal medulla - secretes epinephrine
paraganglioma - secretes norepinephrine
AD genetic defects of pancreatic B-cell function without B-cell loss
maturity-onset diabetes of the young (MODY)
Gestational diabetes
during pregnancy there is a decrease in ability to use and store carbohydrates
secretes glucagon
alpha cells
secretes insulin
Beta cells
secretes somatostatin
Delta cells in pancreas
*controls how alpha and beta cells make and release glucagon and insulin
autoimmune destruction of pancreatic Beta cells
type I diabetes
diabetes associated with HLA-B8 DR3 and DR4
Type I diabetes
associated with impaired insulin release or defective insulin receptors on target cells
type II diabets
associated with family history of diabetes
type II
associated with severe hyperglycemia
type I
diabetes dependent on insulin
type I
diabetes associated with obesity
type II
which age population is diabetes more associated with
adults - both type I and II
what is the pathogenesis of diabetes
irreversible glycosylation end products (AGE) accumulate in vessel walls and basement membranes
3 classic symptoms of diabetes
polyuria - osmotic diuresis
polydipsia - hyperosmolarity of glucose
polyphagia - catabolism of proteins and fat
normal fasting plasma glucose and post-glucose load levels
< 100 mg/dL
< 140 mg/dL
Diabete fasting plasma glucose level and post-glucose load levels
> 126 mg/dL on two occasions
> 200 mg/dL
two tests to look for diabetes besides fasting glucose levels
glycosylated hemoglobin (HbA1c)
urinary and plasma C-peptide
how would you look for a patient no keeping their blood sugar in check between visits
HbA1c - RBC 120 day life span
normal range for HbA1c
4-7% of RBC
peptide that is removed in the cleavage of proinsulin to form insulin
C-peptide
which type of diabetes will have very low C-peptide
type I diabetes
which has higher concentration of C-peptide, urine or plasma
urine
general manifestations associated with diabetes
retinopathy
cataracts
renal failure
accelerated atherosclerosis
neuropathy
xanthoma formation
ischemic changes
leading cause of blindness in U.S. adults
DM
changes in the eye seen in DM
microaneurysms with hemorrhage
waxy exudates
neovascularizations
retinal detachment
which type of DM is more associated with diabetic nephropathy
type I
How can a physician know when a patient is at risk for diabetic nephropathy
retinal changes occur before renal
cause for diabetic nephropathy
hyperfilatration from dilation of afferent arteriole leading to intra-glomerular hypertension
classic changes seen in diabetic nephropathy
micro-albuminuria
glomerular hypertrophy
thickening of GBM and mesangium
type of glomerular disease associated with DM
nodular glomerulosclerosis
two other kidney disorders associated with DM
necrotizing renal papillitis
pyelonephritis
most common cause of death in DM
MI
cause of diabetic neuropathy
segmental demyelination
type of DM associated with ketoacidosis
type I
type of DM associated with hyperosmolar nonketotic coma
type II
severe dehydration secondary to hyperglycemia diuresis and inadequate water intake
hyperosmolar nonketotic coma
loss of fat at the injection site of insulin
insulin lipoatrophy
what else does TSH-RH stimulate the release of
prolactin
what four things can infiltrate and accumulate in the anterior pituitary
metastatic cancer
amyloid
mucopolysaccharide
iron
causes of primary Addison's disease
1. autoimmune
2. TB
3. AIDS
4. metastasis