Week 10: Endocrine Flashcards
failure of feedback systems
may fail to funciton properly, may respond to inappropriate signals
dysfunction of an endocrine gland
Inability to produce or obtain an adequate quantity of required hormone precursors
Inability to convert precursors to the active hormone
Excessive or inadequate hormone production
target cell dysfunction
failure of target cell to respond to its hormone
thyroid synthesizes and releases
calcitonin, thyroxine, and triiodothyronine
hyperthyroidism clinical manifestations
increased metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by the sympathetic nervous system, enlargement of thyroid gland
hyperthyroidism tx
methimazole or propylthiouracil
radioactive iodine therapy
surgery
causes of hyperthyroidism
graves disease toxic multinodular goiter toxic adenoma follicular thyroid carcinoma TSH secreting pituitary adenomas
hyperthyroidism endocrine effects
goiter, bruit, diminished sensitivity to endogenous insulin
hyperthyroidism reproductive effects
oligomenorrhea, erectile dysfunction
hyperthyroidism GI effects
weight loss, anorexia, increased peristalsis, changes in vitamin metabolism
hyperthyroidism integumentary effects
excessive sweating, flushing, heat intolerance, hair and nail changes
hyperthyroidism cardiovascular effects
increased cardio output, decreased peripheral resistance, tachycardia at rest
hyperthyroidism pulmonary effects
dyspnea & reduced vital capacity
what is found in 95% of grave’s pts
thyroid antibodies, IgG
clinical s&s of thyrotoxic crisis
Hyperthermia; tachycardia, especially atrial tachydysrhythmias; high-output heart failure; agitation or delirium; and nausea, vomiting, or diarrhea
primary hypothyroidism types
Iodine deficiency Autoimmune thyroiditis (Hashimoto disease) Subacute thyroiditis Painless thyroiditis Iatrogenic thyroiditis Postpartum thyroiditis
hypothyroidism clinical manifestations
Low basal metabolic rate, cold intolerance, lethargy, tiredness, and slightly lowered basal body temperature; also possible diastolic hypertension
Myxedema
all hormones released from the adrenal cortex are synthesized by
cholesterol
disorders of the adrenal cortex
cushings disease
virilization
hyperaldosteronism
addison disease
addisons disease marked by
hyperpigmentation, weight loss, fatigue, low blood pressure, poor appetite
thyrotoxicosis
condition caused by excessive TH
grave’s disease
the most common form of hyperthyroidism; caused by an autoimmune defect that creates antibodies (95% of pt) that stimulate the overproduction of TH, causing TSH and TrH suppression
grave’s clinical manifestation
exophthalmos (dt ^ hyaluronic acid)
orbital fat accumulation
diplopia
pretibial myxedema (swelling
grave’s tx
rad I-
sx
doesn’t remove leg edema or eye conditions
1º hypothyroidism
I- deficiency hashimoto's disease (autoimmune) subacute thyroiditis (nonbacterial inflammation) painless thyroiditis Iatrogenic thyroiditis postpartum thyroiditis
congenital hypothyroidism
TH deficiency at birth, can cause cretinism if not tx
neonatal screening
T4 for tx
thyroid carcinoma
most common thyroid malignancy from rad
∆ in voice and swallowing
dyspnea dt tumor growth
may have normal T3/T4 lvls
myxedema
non-pitting, boggy edema of the skin in hypothyroidism, esp around eyes, hands, feet, tongue
adrenal hyperfunction cm
dt hypercortisolism wt gain glucose intolerance muscle wasting/weakness v bone density easily damaged skin vasoconstriction/HTN i.s suppression neuro ∆
adrenal hyperfunction dx
urinary free cortisol < 100 ug/day
pit MRI
inf petrosal sinus sample
cushing’s disease
excessive ACTH secretion
most common in 30-50 women
most have pit microadenoma w hypercortisolism
addison’s disease cm
hypocortisolism, hypoaldosteronism weakness, fatigue hyperpigmentation wt loss, poor appetite hypoTN
2º hypocortisolism
addisonian crisis
prolonged admin of exogenous glucocorticoids (pred) inhibits ACTH secretion
CM: similar to Addison’s, no hyperpigmentation
DM
dysfunction of endocrine pancreas
affects metabolism
characterized by hyperglycemia
DM dx
1+ NFG > 7 mmol/L
2hrPG > 11.1 mmol/L, confirmed next day
3 Ps (polydipsia/phagia/uria)
HgBA1C
hyperglycemia
high blood sugar, 80-90% of B-cells must be lost before it occurs, alongside abnormal glucagon
type 1 DM
IDDM
unknown cause, rt genetic and environment
can be immune/non-immune
non-immune T1DM
occurs 2º to other diseases (ex pancreatitis)
immune t1dm
cell-mediated destruction of B-cells, w antibodies found in 85-90%
HLA-DR4 strongly associated
4 characteristics of t1dm
genetic susceptibility
long preclinical period
immunologically mediated destruction of B-cells
hyperglycemia
t1dm clinical manifestations
3 Ps
wt loss
fatigue
dradual insulin deficiency and hyperglycemia
t1dm tx
insulin meal planning exercise self-monitoring transplant (temporary)
ketoacidosis
excessive production of ketones, making the blood acid, body compensates by blowing off acetone, giving breath a fruity scent
diabetic coma may be 1st manifestation
t2dm
more common than T1
genetic and environmental interaction, obesity and sedentary
major factor is insulin resist
t2dm patho
gradual ^ in insulin resist dt lifestyle factors, many years of hyperinsulinemia, eventually B-cell responsiveness drops, hypoglycemia occurs
t2dm cm
often nonspecific, over 30
oft overwt, dyslipidemic, hyperinsulinemic, HTN
PCOS x7 risk
onset 7+ yrs before dx
t2dm tx
restoration of euglycemia
wt loss, exercise
insulin, antihyperglycemics
hypoglycemia
low blood sugar (<3.5 mmol/L)
oft when tx w insulin (insulin shock)
dt hypothalamus sensing low glucose
hypoglycemia cm
tachycardia, palpitations
diaphoresis, pallor
tremors, anxiety
coma, death
hypoglycemia tx
glucagon/glucose
dka
absolute deficiency of insulin and ^ in insulin counterregulatory H
common fx incl: illness, interruption of insulin tx
most common in IDDM
dka patho
increased production of glucose ketones for fuel
hyperketonemia dt peripheral ketone impairment
cir of strong acids w/out bicarb buffer
metabolic acidosis
dka cm
kussmaul resp postural hypoTN CNS depression Anorexia Nausea, abd pain polyuria, thirst glucosuria, ketonuria
dka dx
serum glucose > 250 mg/dL
serum bicarb < 18 mg/dL
pH < 7.3
anion gap
dka tx
serum glucose > 250 mg/dL
serum bicarb < 18 mg/dL
pH < 7.3
anion gap
HHNS
hyperosmolar hyperglycemic nonketotic syndrome
life threatening, in NIDDM
dt infection, rx, nonadherence, coexisting disease
hhns patho
far more fluid deficiency in HHNS
higher glucose and glucose in HHNS
hhns cm
Glycosuria, polyuria dehydration neuro ∆ glucose > 600 mg/dL absent/low urine ketones
diabetic neuropathy
nerve damage that occurs because of the metabolic derangements associated with DM
diabetic retinopathy
retinal ischemia dt bv ∆ and RBC aggregation
diabetic nephropathy
Most common cause of ESRD
damage to glomeruli dt ^ P and glucose lvls
diabetic cad and pvd
Most common cause of ESRD
damage to glomeruli dt ^ P and glucose lvls
diabetic infection risk
impaired senses hypoxemia/low bld supply suppressed i.s and delayed healing rapid pathogen replication dt ^ glucose hypoxia glycosylated HgB impaires O2 release
