ch 18 Flashcards
what is syndrome of inappropriate ADH secretion (SIADH)
high levels of ADH without physiologic stimuli for its release
what must exist in SIADH for diagnosis
normal adrenal and thyroid function
clinical manifestation are related to ____,_____,___ in SIADH
enhanced renal water retention
hypoatremia (low Na+)
hypo-osmolality (solute loss)
what is the most common cause of SIADH
ectopic secretion of ADH by tumor cells
what are the clinical manifestations of SIADH
thirst dyspnea on exertion (SOB) fatigue dulled consciousness progressing to abdominal cramps vomitting confusion seizures
when is SIADH seen
in infectious pulmonary diseases
associated with psychiatric disease after treatment with a variety of drugs
what is diabetes insipidus
insufficiency of ADH leading to polyuria and polydipsia
what are the 3 types of diabetes insipidus
neurogenic
nephrogenic
psychogenic
what is neurogenic of diabetes insipidus
-insufficient amounts of ADH
lesion on hypothalamus or posterior pituitary interferes with ADH synthesis, transport or release
what is nephrogenic of diabetes insipidus
-inadequate amounts of ADH
insensitivity of renal tubule to ADH
what is psychogenic of diabetes insipidus
caused by an extremely large volume of fluid intake which results in a partial resistance to ADH
what are the clinical manifestation related to with diabetes insipidus
water excretion
hypematremia
hyper-osmolality
what are the two diseases of posterior pituitary
SIADH
diabetes insipidus
what are the 3 disease of the anterior pituitary
hypopituitarism
hyperpituitarism
hyper secretion of growth hormone
hyper secretion of prolactin
what is hyperpituitarism caused by
a benign slow growing pituitary adenoma
what are the manifestations of hyperpituitarism
headache and fatigue
visual changes
hypo secretion of neighboring anterior pituitary hormones
what are the 2 types of hyper secretion of GH
acromegaly
gigantism
what is the growth hormone (somatropin)
enhances linear bone growth in children, enhances a.a. transport across membranes, increase protein synthesis, increases F.A mobilization and utilization, decrease glucose uptake and use
a deficiency of GH in children often look like and how to treat
normal intelligence, short stature, obesity with immature facial features, puberty often delayed
treat with GH
what is acromegaly
hyper secretion of GH during adulthood
what is gigantism
hyper secretion of GH in children and adolescents
what is prolactinoma
most common hormonally active pituitary tumors leading to hyperprolactinemia
increased levels of prolactin in females causes
amenorrhea (absence of menstration)
galactorrhea (milky discharge)
hirsutisum (excessive body hair)
osteopenia due to estrogen deficiency (bone loss)
increased levels of prolactin in males cause
**hypogonadism (a failure of testes to function properly)
**erectile dysfunction
impaired libido (sexual dysfunction)
oligospermia (low sperm count)
diminished ejaculate volume
what are alteration of thyroid function
hyperthyroidism
hypothryoidism
what two disease of hyperthyroidism
thryotoxicosis
graves disease
what is thyrotoxicosis
higher than normal levels of TH from any source
what is graves disease
autoimmune
abnormal stimulation of thyroid gland by IgG antibodies
what does graves disease cause
exophthalmos (bulging eyes)
irritability
weight loss
fatigue
what is congenital hypothyroidism
appears normal at birth due to maternal TH
common cause of preventable mental retardation
cretinism- TH essential for normal brain developments and growth
what is acquired hypothyroidism
older children and adults
slowing down of metabolic processes
myxedema- nonpitting mucous edema
what is primary and secondary causes of acquire hypothyroidism
primary cause- destruction of thyroid gland
ex: hashimotos disease -autoimmune
secondary cause- impaired pituitary
what are alterations of the parathyroid function
hyperparathyroidism
hypoparathyroidism
what is primary hyperparathyroidism
excess secretion of PTH from one or more parathyroid glands
what is secondary hyperparathyroidism
increase in PTH secondary to a chronic disease
what are clinical manifestations of hyperparathyroidism
hypercalcemia: too much calcium in bone
hypercalciuria: kidney stones
fatigue
depression
anorexia
what is the most common cause of hypoparathyroidism
damage to PT glands during thyroid surgery
what are clinical manifestations of hypoparathyroidism
hypocalcemia- muscle spasm hyper-reflexia asphyxiation- deprived of oxygen dry skin hair loss cataracts cone deformities
what is hypoparathyroidism
abnormally low PTH levels
what is diabetes mellitus
chronic hyperglycemia along with disturbances of carbohydrates, fat and protein metabolism
what is diagnosis of DM based on
more than one elevated fasting plasma glucose level
elevated BG in response to oral glucose tolerance test
polys X3
glycoslyated hemoglobin (A1C)
what is type 1 diabetes
lack of insulin and relative excess of glucagon
insulin dependent
what is the epidemiology of type 1
most commonly diagnosed in those younger than 18
what is the etiology of type 1
beta cell destroyed due to autoantibodies
what are the clinical manifestations of type 1
polys X3
weight loss
fatigue
ketoacidosis due to increased metabolism of fats and proteins
what is type 2 diabetes
much more common
non insulin dependent
what is the epidemiology of type 2
native americans hispanics blacks most over 40 obesity
what is the etiology go type 2
impaired beta cell function
peripheral insulin resistance
increased hepatic glucose production
what are the clinical manifestations of type 2
pruritus (itching)
recurrent infections
visual changes
paresthesias (burning)
what goes along with diabetes management type 2
dietary- restriction of calories for overnight individual, balance fat, protein, carbs and high fiber
exercise
oral antidiabetic agents
what are the 3 oral anti diabetic agents for diabetes management in type 2
Sulfonylureas
Meglitinides
Metformin
what is induces risk for gestational diabetes
family history of diabetes high risk ethnic group advanced maternal age prior history of gestational diabetes overweight
what are acute complications of DM
hypoglycemia diabetic ketoacidosis (type 1) hypersmolar hyperglycemia nonketotic syndrome(type 2) somogyi effect dawn phenomenon
what is hypoglycemia
insulin shock
BG 45-60
what are clinical manifestations of hypoglycemia
pallor tremor anxiety palpitations diaphoresis-sweating tachycardia dizziness fatigue confusion seizures coma
what is diabetic ketoacidosis - type 1
complication of insulin deficiency and increase of catecholamines, cortisol glucagon, GH
glucose production increase and usage decrease
fat is mobilized
what is hypersomolar hyperglycemia nonketotic syndrome - type 2 and the treatment
high mortality due to high serum glucose (more than 600) leading to severe dehydration
treatment: manage fluid/electrolytes and glucose control
what is somogyi effect
combination of hypoglycemia followed by rebound hypoglycemia
what is dawn phenomenon
early morning risk in BG with no hypoglycemia during the night due to nocturnal elevations of GH
what are chronic complications of DM
microvascular
marcovscular
diabetic neuropathies
infection
what is microvascular disease
due to capillary basment membrane thickening, ischemia, hypoxia
what are the 2 under microvascular disease
retinopathy
nephropathy
what is retinopathy
due to blood vessel changes and RBC aggregation
more likely to occur in type 2 as a result of long standing hyperglycemia before diagnosis
what is nephropathy
most common cause of end stage renal disease
death from renal failures more common in type 1 as a result of proteinuria
what is marcovascular complication
cause morbidity and mortality especially in type 2
what are the 3 under microvascular complications
CAD
stroke
peripheral vascular disease
what is CAD
most common cause of death in type 2
what is stroke
2 x as common with diabetics
what is peripheral vascular disease
due to occlusion of small vessels which may results in gangrene of the lower extremities
what are the 2 types of neuropathies
somatic
autonomic
what are infections associated with chronic complicatons
increased risk due to senses impairment, hypoxia, proliferation of pathogens, decreased blood supply WBC impairment
what are the disorders of the adrenal cortex
cushings syndrome
congential adrenal hyperplasia
cushing disease
what is cushing syndrome
glucocorticoid hormone excess
excessive anterior pituitary secretion of ATCH
what causes cushing syndrome
excess production of ACTH due to pituitary tumor
benign or malignant adrenal tumor
non pituitary ACTH secreting tumor
what are the manifestation of cushing syndrome
altered fat metabolism -moon face and buffalo hump
muscle weakness due to protein breakdown
deranged glucose metabolism
susceptibility to infection
what is the treatment for cushing syndrom
surgery
irradiation
medication
what is congenital adrenal hyperplasia
deficient production cortisol leads to increased ACTH
what happens with males in CAH
seldom diagnosed at birth unless have enlarged genitals or lose salt
what happens with females with CAH
ambiguous genitalia due to increase in androgens
what is the treatment for CAH
cortisol replacement
recontructive surgery
what is primary for adrenal cortical insuffciency
addison disease
increased ACTH and decreased cortical hormones
lifetime replacement therapy
what are the clinical manifestations of adrenal cortical insufficiency
deficiency mineral- glcocorticoids
hyperpigmentation due to increased ACTH
sparse pubic- axially hair in women
what is secondary adrenal cortical insufficiency
hypopituirarism or due to removal of pituitary gland
more common due to rapid removal of glucocoritcoids and adrenal cortical atrophy
Mr. Metzner has polyuria with a urine volume of 8 L/day. His urine specific gravity is 1.02. His serum sodium (Na+) is 150 mEq/L, and his plasma osmolality is 300 mOsm/kg. He is always asking for more cold liquids to drink. What type of hormonal alteration is Mr. Metzner exhibiting? What are some possible causes of this alteration?
Mr. Jones has diabetes insipidus, which has three forms: neurogenic, nephrogenic, and psychogenic. The neurogenic form is caused by a hypothalamic, infundibular stem, or posterior pituitary problem, that decreases or inhibits antidiuretic hormone (ADH) synthesis, transport, or release. This may be caused by pituitary tumors, brain tumors, infections, immunologic problems, or thrombotic problems.
- The nephrogenic form of diabetes insipidus may be acquired, permanent, or reversible. It is caused by renal tubule insensitivity to ADH. In this form the amounts of ADH are normal but the tubules are no longer able to respond to the hormone. Examples of renal problems that can lead to diabetes insipidus include pyelonephritis, amyloidosis, destructive uropathies, and polycystic kidney disease. It may also be secondary to anesthetic drug use and the use of lithium carbonate.
- The psychogenic form of diabetes insipidus is caused by compulsive water drinking by individuals with psychiatric disorders. In this form the individual has periodic polyuria, high urine volume, and plasma osmolarity of less than 285 mOsm/kg.
Mrs. Johnson is admitted to your unit with tachycardia, fever, agitation, and diarrhea. Her medical history is nonsignificant except for a history of recent pneumonia, and she takes no regular prescription or over-the-counter medication. She also reports that she has been very upset at the recent death of her mother. Her diagnosis is thyrotoxic crisis. She asks you to explain what is happening to her.
John is a 40-year-old recently diagnosed with Addison disease. He asks you to explain what happened to him and explain how he can live a normal life.
