Endocrine Flashcards
Hyperosmolar
(Low ADH) = Low water to particle ratio
Hypoosmolar
(High ADH) = High water to particle ratio
SIADH - Syndrome of inappropriate ADH
HIGH Level of ADH
Causes: Tumors - ectopic production of ADH Meds - narcotics, chemo, hypoglycemics, NSAIDs Pulmonary disorders - pneumonia Surgery - unclear reason
SIADH Patho
Enhanced renal water retention (CARDINAL FEATURE)
ADH acts in Renal collecting ducts. More ADH means more water reabsorbed.
Dilutional Hyponatremia - More water vs. same amount of salt
SIADH Manifestations
result from the Hyponatremic state
Thirst, Impaired taste, Anorexia, Dyspnea on exertion, Dulled sensorium, Serum Na levels rapidly decline, GI symptoms, No peripheral edema, extreme drops cause confusion/muscle twitching/convulsions/neurologic damage
DI - Diabetes Insipidus
LOW level of ADH
Causes:
Neurogenic Central DI - Low secretion
Neuro = brain
Nephrogenic DI - inadequate response to ADH by the kidneys
Nephro = kidneys
DI Pathophysiology
Partial/Total inability to concentrate urine (reabsorb water)
Water loss leads to:
Hypernatremia - high salt to water ratio
Hyperosmolality - high particle to water ration
DI Manifestations
Polyuria - excessive production of urine
Nocturia - waking up to piss
Thirst
Long-term DI: larger bladder capacity and hydronephrosis (dilation/distention of kidney)
Hypopituitarism
deficiency of one or more pituitary hormones (TSH, Corticotropin, Substance B, Prolactin)
Hypopituitarism (causes)
Inadequate supply of hormones from the pituitary to hypothalamus
Damage to pituitary gland
Inability of pituitary gland to produce hormones
May result from vascular infarction, aneurysm, or tumor
Hypopituitarism (patho)
Pituitary gland is very vascular and it sella turcica compartment
affected by inflammation and ischemia
Adenomas can compromise hormone output
Hyperpituitarism
hypersecretion of pituitary hormones
Primarily caused by pituitary adenomas
Hyperpituitarism (patho)
Local expansion of adenoma
i.e. Impinge on optic chiasm
Impinge on other nerves
Panhypopituitarism
deficiency of ALL pituitary hormones
ACTH deficiency
(loss of cortisol)
Nausea, vomiting, anorexia, fatigue, decreased urine output, and weakness. Potential death 2 weeks of complete absence of ACTH.
TSH deficiency
Cold intolerance, skin dryness, mild myxedema (swelling of skin/underlying tissue), decreased metabolic rate
FSH and LH deficiency
Females: Amenorrhea (no period), atrophic vagina, uterus, and breast.
Males: testicular atrophy and beard growth is stunted
GH (growth hormone) deficiency
Adults: fatigue, social withdrawal, loss of motivation, osteoporosis, altered body composition
Children: hypopituitary dwarfism
Pituitary adenoma manifestations
Manifestations are related to tumor growth and hormone hyper/hypo secretions.
Acromegaly
result of continuous hypersecretion of GH
*Almost always caused by GH-secreting adenoma
Acromegaly (patho)
GH secretion occurs over time and levels are never lost
If it occurs in children it develops into Gigantism
Connective Tissue proliferation and excess bone growth
High incidence of heart disease, hypertension, atherosclerosis
If untreated, associated with decreased lifespan
Acromegaly (manifestations)
Connective tissue proliferation - Large tongue, interstitial edema, enlarged overactive sweat glands, coarse skin and body hair
Bony proliferation - vertebral growth, enlargement of face, hands, and feet. Protruding forehead and lower jaw.
Symptoms of diabetes - polyuria and polydipsia
Hypertension is usually asymptomatic until heart failure symptoms develop
Hyperthyroidism
form of thyrotoxicosis in which excess amounts of TH (thyroid hormones) are secreted from the thyroid gland
Hyperthyroidism (causes)
Grave’s disease
Toxic Multinodular Goiter
Solitary toxic adenoma
Hyperthyroidism (patho)
Genetic or environmental factors
Residual effects of puberty, pregnancy, or iodine-deficient states
Hyperthyroidism (mani)
Ophthalmopathy
Higher metabolism
Hypothyroidism
deficient production of TH by the thyroid gland
Hypothyroidism (causes)
Autoimmune thyroiditis: gradual inflammatory destruction of thyroid tissue by lymphocytes
Congenital hypothyroidism: Infants born w/o thyroid tissue or with hereditary defects in TH synthesis
Surgical removal of thyroid
Radiation exposure to head and neck
Hypothyroidism (patho)
Autoimmune disorder
Genetic disorder
Medical trauma
Hypothyroidism (mani)
Lower metabolism:
weight gain
constipation
cold intolerance
Myxedema Coma
related to hypothyroidism
diminished consciousness due to severe hypothyroidism
medical emergency: hypothermia w/o shivering
hypoventilation
hypotension
Older patients at high risk
Graves disease
Autoimmune disease causing of 50-80% of hyperthyroidism
Thyroid is stimulated by antibodies called Thyroid-stimulating immunoglobulins
Thyrotoxic crisis (Thyroid Storm)
rare emergency where patient suffers severe acute manifestations of hyperthyroidism
pts are undiagnosed or partially treated
**Hyperthermia, atrial tachycardia dysrhythmia, heart failure, dehydration, nausea and vomiting
hypothyroidism
Autoimmune thyroiditis: deficient production of TH due to tissue destruction by lymphocytes Puffy face brachycardia Cold intolerance Edema of extremities
Congenital Hypothyroidism
Normal growth is obtained with hormone replacement therapy
symptoms after 4 months: difficulty eating
protruding tongue
hypotonic muscles of abdomen
Constipation
Hypoglycemia
insulin shock or insulin reaction
*type 1 diabetes = at higher risk
Hypoglycemia (symptoms)
pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgement, confusion, visual disturbance, hunger, seizures and coma
Diabetic ketoacidosis (DKA)
serious complication → deficiency of insulin and increase in levels of insulin counterregulatory hormones
DKA serum levels
serum glucose level >250 mg/dl
serum pH
DKA symptoms
Kussmaul respirations, postural dizziness, CNS depression, ketonuria, anorexia, nausea, abdominal pain, thirst, polyuria
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
severe dehydration: loss of electrolytes (potassium) → neurologic changes (stupor)
HHNKS serum levels
serum glucose >600 mg/dl
serum pH >7.30
Somogyi effect
unique combo of hypoglycemia followed by rebound hyperglycemia
rise in blood glucose occurs b/c of counterregulatory hormones which are stimulated by hypoglycemia → produce gluconeogenesis
Dawn phenomenon
early morning rise in blood glucose concentration w/ no hypoglycemia during night
Microvascular: Retinopathy (Nonproliferative)
microaneurysms, capillary dilation, soft and hard exudates, dot and flame hemorrhages, arteriovenous shunts
Microvascular: Retinopathy (Proliferative)
formation of new blood vessels, vitreal hemorrhage, scarring, retinal detachment
loss of visual activity
Microvascular: Retinopathy (Maculopathy)
macular edema
loss of central vision
Microvascular: Retinopathy (Hyperglycemic lens edema)
shunting of glucose to polyol pathway: hyperosmolar fluid in lens
blurred vision
Microvascular: Retinopathy (Cataract formation)
chronic hyperglycemia
decreasing visual acuity
Nephropathy
glomerular basement mbn thickening, mesangial expansion, glomerulosclerosis, focal tubular atrophy; hyperperfusion and hyperfiltration
nerve dysfunction and degeneration
Neuropathy
oxidative stress, poor perfusion and ischemia, loss of nerve growth factor
nerve dysfunction and degeneration
peripheral neuropathy
oxidative stress, poor perfusion and ischemia, loss of nerve growth factor
distal symmetric sensorimotor polyneuropathy w/ glove and stocking loss of sensation; loss of motor nerve function w/ clawed toes and small muscle wasting in hands and flexor muscles; Charcot joints; acute painful neuropathy w/ burning pain in legs and feet
autonomic neuropathy
oxidative stress, poor perfusion and ischemia, loss of nerve growth factor
heart rate variability and postural hypotension; gastroparesis and diarrhea; loss of bladder tone, urinary retention, risk for bladder infection, ED and impotence in men
Neuropathy (skin and foot lesions)
loss of sensation, poor perfusion, suppressed immunity, increased risk of infection
high risk for pressure ulcers and delayed wound healing; abscess formation; development of necrosis and gangrene, particularly of toes and foot; infection and osteomyelitis
Macrovascular (Cardiovascular)
endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies
hypertension, CAD, cardiomyopathy, heart failure
Macrovascular (cerebrovascular)
endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies
increased risk for ischemic and thrombotic stroke
Macrovascular (Peripheral vascular )
endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies
claudication, nonhealing ulcers, gangrene
Infection
impaired immunity, decreased perfusion, recurrent trauma, delayed wound healing, urinary retention
wound infections, UTI’s, increased risk for sepsis
Cushing syndrome
refers to clinical manifestations resulting from chronic exposure to excess cortisol
cushing disease
refers to excess endogenous secretion of ACTH
ACTH-dependent
overproduction of pituitary ACTH by pituitary adenoma or by ectopic secreting non pituitary tumor (small cell carcinoma of lung)
ACTH-independent
caused by cortisol secretion from rare benign or malignant tumor of one or both adrenal glands
Adrenal Cortex Dysfunction (mani)
weight gain (most common) → results from accumulation of adipose tissue in trunk, facial and cervical areas → “truncal obesity”, “moon face”, “buffalo hump”
Adrenal Cortex Dysfunction (patho)
1) normal diurnal or circadian secretion patterns of ACTH and cortisol are lost; 2) there is no increase in ACTH and cortisol secretion in response to a stressor
hyperaldosteronism
characterized by excessive aldosterone secretion by adrenal glands
primary hyperaldosteronism
promotes: increased renal sodium and water reabsorption w/ corresponding hypervolemia and hypertension; renal excretion of potassium
extracellular fluid volume overload, hypertension and suppression of renin secretion are characteristic of primary disorders
**hypertension and hypokalemia (hallmark manifestations)
secondary hyperaldosteronism
results from extra-adrenal stimulus of aldosterone secretion → most often angiotensin II through renin-dependent mechanism
Patho: effect of increased extracellular volume on renin secretion varies
**hypokalemic alkalosis, changes in myocardial conduction and skeletal muscle alterations may be seen (particularly w/ severe potassium depletion)
Addison disease
low levels of cortisol secretion
either because of inadequate stimulation of the adrenal glands by ACTH or a primary inability of the adrenals to produce and secrete the adrenocortical hormones
Addison disease (patho)
primary adrenal insufficiency
Rare, most common in adults (30-60), more common in women autoimmune mechanisms that destroy adrenal cortical cells Chronic infections (TB) primary cause in underdeveloped countries
inadequate corticosteroid and mineralocorticoid synthesis
elevated serum levels of ACTH (loss of negative feedback)
Addison disease (mani)
mild to moderate hypocorticolism: weakness and easy fatigability
skin changes: hyperpigmentation and vitiligo
anorexia, nausea, vomiting, and diarrhea
development of hypotension that can lead to complete vascular collapse and shock
pheochromocytomas
tumor of the adrenal medulla:
adrenomedullary hyperfunction
chromaffin cell tumors
rare, about 10% malignant
pheochromocytomas (patho)
excessive production of catecholamines because of autonomous secretion of the tumor
pheochromocytomas (mani)
persistent hypertension, headache, pallor, diaphoresis, tachycardia, and palpitations
HTN results from increased peripheral vascular resistance
acute episodes of HTN related to hypersecretion of catecholamine levels in the blood (affects cerebral blood flow)
hypermetabolism and sweating related to chronic activation of sympathetic receptors in adipocytes hepatocytes, and other tissues
glucose tolerance (catecholamine-induced inhibition of insulin release
can be very vascular, rupture, and cause massive and potentially fatal hemorrhage
Hyperparathyroidism
hypersecretion of Parathyroid hormone (PTH) and hypercalcemia (hypophosphatemia)
Muscular problems
Headache, nausea, vomiting
Fatigue, anorexia, depression
Kidney stones (due to hypercalcemia in urine)
Primary Hyperparathyroidism
hypersecretion of Parathyroid gland itself usually due to adenoma
Secondary Hyperparathyroidism
hypersecretion in response to hypocalcemia
Hypoparathyroidism
hyposecretion of PTH and hypocalcemia (hyperphosphatemia)
Dry skin, hair loss
Bone deformities
Low nerve excitement threshold
muscle spasms, seizures, hyperreflexia
