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79 Cards in this Set

  • Front
  • Back
Hormone inc/decr in Cushing's
Increased cortisol
Hormone inc/decr in Conn's syndrome
Increased aldosterone
Hormone inc/decr in Addison's disease
Deficient aldosterone and cortisol
Hormone inc/decr in Grave's disease
TSH-> increased T4
Cause of Cushing's disease
Primary pituitary adenoma-> increased ACTH-> increased cortisol
Cushing's syndrome etiologies with increased ACTH
Cushing's disease (primary basophilic pituitary adenoma)
Ectopic ACTH production (SCLC)
Cushing's syndrome etiologies with decreased ACTH
Primary adrenal hyperplasia/neoplasia
Iatrogenic (chronic steroids)
MC pit tumor
Prolactinoma w hyperprolacinemia
Staining of Prolactinoma w hyperprolactinemia
chromophobic
Effect of prolactinoma on women
amenorrhea
galactorrhea
Cuases of prolactinoma
hypothal lesions
Meds (methyldopa, reserpine) that interfere w dopamine secretion (inh prolactin)
Estrogen therapy
Second MC pituitary tumor
Somatotropic adenoma w hypersecretion of growth hormone
Staining of somatotropic adenoma
Acidophlic
Liver effects of somatotropic adenoma
Secondary hyperproduction of somatomedins by liver
End organ effects of somatotropic adenoma
End organ effects: caused by growth hormone and somatomedins, esp IGF-1/somatomedin-C
When does gigantism occur in somatotropic adenoma
If adenoma develops begfore epipthyseal closure
When des acromegaly occur in somatotropic adenoma
if adenoma develps after epiphyseal closure
Characteristics of acromegaly
Overgrowth of jaws, face, hands and feet, generalized enlargement of viscera, hyperglycemia, osteoporosis, hypertension
Effects of corticotropic adenoma and hypersecretion of ACTH
Increased production of adrenal cortical hormones (hypercorticism)
AKA Cushing's syndrome
Cuase of cushing's diseases
Basophilic adenoma, a corticotropic adenoma of the pituitary
Cushing syndrome
hypercorticism regardless of cause
Small cell carcinoma of lung: endocrine manifestations?
Cushing syndrome secondary to ectopic ACTH procution
SIADH
Simmond's disease
This is pituitary cachexia or generalized panhypopituitarism
Types of pituitary cachexia
Pituitary tumors
Sheehan syndrome
Sheehan syndrome
Postpartum pituitary necrosis
Cause of Sheehan syndrome
Ischemic necrosis of pituitary gland; associated w/ hemorrhage and shock during childbirth
Loss of gonadotropins, then subsequent loss of thyroid-sti mulating hormone (TSH) and ACTH
MC cause of SIADH
Small cell carcinoma of the lung (ectopic production of ADH)
Clinical features of SIADH
Dilutional hyponatremia due to water retention
Reduced serum osmolality
Inability to dilute urine--> higher than appropriate urine osmolality
Absence of hypokalemia
Absence of hypotension
Presentation of SIADH
Vague, w/ confusion, nausea, irritability, and later seizures followed by coma.
NO EDEMA
Treatment of SIADH
Restriction of fluid intake
Demethylchlortetracycline (if water restriction is poorly tolerated)
Hypertonic saline rarely in severe cases
Frequent measurement of plasma osmolality and body wt
characteristics of Type II DM
Positive family history is MORE common than in type I disease
Begins in middle age usually; more likely to be assoc w obseity
Much more common than type I
Due to increased insulin resistance
Causes of increased insulin resistance
Decreased cell membrane insulin receptors
Post-insulin receptor dysfunction
Impaired processing of proinsulin to insulin
Decreased sensing of glucose by beta cells
Impaired fxn of intracellular carrier proteins
Characteristics of Type II DM
Ketoacidosis is unusual
Plasma insulin levels usually normal or increased; thus insulin is not required usually
Mild carbohydrate intolerance can most often by managed by diet and oral antidiabetic agents
Which pts need insulin?
T1DM pts, eventually T2DM pts
T2DM pts with MI, Infection, Need surgery
Emergency tx of hyperkalemia (along w/ administration of glc)
Emergent tx of hyperkalemia
Insulin plus glucose
Insulin moves potassium from extracellular to intracellular compartment
Glucose keeps blood glc from falling after insulin administration
Mass effects of apituitary adeoma
Can impinge on optic chiasm, leading to bitemporal hemianopia
What is a good treatment of pituitary adenoma bsides surgery
Bromocriptine (dopamine agonist) causes shrinkage
Findings of acromegaly
Large tongue w deep furrows
Deep voice
Large hands and feet
Coarse facial fetaures
Impaired glc tolerance (insulin resistance)
Increased GH in children leading to gigantism
Medical treatment of acromegaly
Octreotide
Normal causes of increase in growth hormone
Stress
Exercise
HYPOGLYCEMIA
Test for increased growth hormone
Oral glucose tolerance test
(if GH still high w high glc, then GH is increased?)
Symptoms of Sheehan's syndrome
Fatigue
Anorexia
Poor lactation
Loss of pubic and axillary hair
Effects of deficiency of TSH
Secondary hypothyroidism
Effects of deficiency of gonadotropins
Preadolescent kids: retarded sexual maturation
Adults: loss of libido, impotence, loss of muscular mass, decreased facial hair in men, amenorrhea and vaginal atrophy in women
Effects of deficiency of growth hormone
Kids: pituitary dwarfism
Adults:
Increased insulin sensitivity leading to hypoglycemia
Decreased muscle strength
Anemia
Effects of deficiency of ACTH
Secondary adrenal failure
NO hyperpigmentation of skin b/c lack of both ACTH and beta-melanocyte-stimulating hormone
What is waterhouse-freiderichsen syndrome
Acute adrenocortical insufficiency caused by adrenal hemorrhage after meningococcal septicemia
Most common tumor of adrenal medulla in adults
Pheochromocytoma
Where does a pheochromocytoma come from?
Deived from chromaffin cells from the neural crest
Diseases associated w pheochromocytomas
Neurofibromatosis
MEN type II and III
von Hippel-Lindau disease
What do you find in the urine in pheochromocytoma?
VMA (increased urinary excretion of catecholamines and their metabolites--metanephrine, normetanephrine, vanillylmandelic acid)
Most common tumor of adrenal medulla in children
Neuroblastoma
Where can a neuroblastoma occur
MC in adrenal medulla in kids, but can occur anywhere along the sympathetic chain
What do you find in the urine in neuroblastoma?
HVA
How often is a pheochromocytoma benign?
Usually benign (90%)
Uncommon but important cause of surgically correctable hypertension
Pheochromocytoma
Effects of pheochromocytoma
Hyperproduction of catecholamines (epi/NE) by the tumor
Leads to episodic hypertension (may be persistent)
Increased urinary excretion of catecholamines and their metabolites
Is a neuroblastoma malignant or benign?
Highly malignant
What is a highly malignant catecholamine producing tumor that occurs in early childhood?
Neuroblastoma
Presentation of neuroblastoma
large abdominal mass (adrenal medulla mass)
Differentiated form of neuroblastoma
Ganglioneuroma
May also differentiate into benign cells, leading to a marked reduction in n-myc gene amplification
Anatomic lesion in cushing syndrome
Bilateral hyperplasia of adrenal zona fasciculata
Conn's syndrome
Primary hyperaldosteronism
Cause of Conn syndrome
ALDO-secreting tumor
Leads to hyperALDO
Symptoms of Conn syndrome
Hypertension
Sodium and water retention
Hypokalemia
Often hypokalemic alkalosis (metabolic alkalosis)
Mnemonic for alkalosis and potassium
ALKalosis = A Low K+ (hypokalemia)
Renin levels in Conn syndrome
Decreased due to negative feedback of increased BP on renin secretion
Which type of hyperaldosteronism has increased renin
secondary aldosteronism
which type of hyperaldosteronism has decreased renin
primary aldosteronism, or Conn syndrome
Treatment of hyperaldosteronism
Spironolactone
Mechanism of spironolactone used in hyperaldosteronism
It is a K+-sparing diuretic that works by acting as an aldosterone antagonist
Causes of secondary hyperaldosteronism
Renal artery stenosis
Chronic renal failure
CHF
Cirrhosis
Nephrotic syndrome
Pathophysiology of secondary hyperaldosteronism
Kidney perception of low intravascular volume results in overactive renin-angiotensin system
Therefore assoc w high plasma renin
Causes of Addison disease
MC: Idiopathic adrenal atrophy (autoimmune lymphocytic adrenalitis)
Destruction by disease (TB, metatstatic tumor, infxn)
Leads to primary deficiency of aldosterone and cortisol
Sx of Addison disease
Hypotension (hyponatremic volume contraction)
Skin hyperpigmentation
Cause of skin hyperpigmentation in Addison disease
MSH, a by-product of increased ACTH from POMC
Pathology mnemonic for Addison disease
Adrenal Atrophy and Absence of hormone production; involves All three cortical divisions
Increased ACTH
Which kind of hypocorticism (adrenal hypofunction) does NOT lead to skin hyperpigmentation?
Secondary adrenal insufficiency (decreased pituitary ACTH production)
Tumor secretes epinephrine, NE, and dopamine
Urinary VMA levels and plasma catecholamines elevated
Pheochromocytoma