Patho - Disorders of Endocrine Disease and Diabetes Mellitus Flashcards
what is GH?
GH is regulated by hypothalamic release of growth hormone-releasing hormone (GHRH) to anterior pituitary gland, liver is the target
-GH increases lean body mass, reduces fat mass, induces liver to
release glucose under conditions of hypoglycemia
what can GH excess lead to?
hyperpituitarism
-gigantism (children)
-acromegaly (adults)
what can GH deficiency lead to?
hypopituitarism
-dwarfism (decreased linear growth)
-adults = decreased muscle mass but also very vague symptoms
gigantism etiology
-primary pituitary adenoma (tumor on gland)
-idiopathic
-radiation
-trauma
gigantism pathogenesis
-begins in childhood before epiphyseal (plates) closed
-excessive GH production causes increased linear growth
-associated with hypogonadism (delay puberty) leading to delayed epiphyseal closure
gigantism CM
-accelerated growth velocity (>95% pediatric growth chart)
-increased stature, height, linear growth
-untreated, may grow to 8ft tall with increased risk of cardiomegaly and heart failure
acromegaly etiology
pituitary tumor (leading to excess GH)
acromegaly pathogenesis
-prolonged excess production of GH
-primarily bone and connective tissue
-slow and progressive (insidious)
acromegaly CM
-large hands and feet*
-protrusion of lower jaw
-coarse facial features
-signs of osteoporosis
-change in hand, shoe, glove size
-HTN
-arthritis (overgrowth of tissue)
-CAD/CHF
-DM
-enlarged adrenal gland
-amenorrhea (absence of meneses)
-HA
-sweating
-weakness
-deep voice*
what is GH deficiency associated with?
-prolonged labor or breech delivery
-chromosomal anomalies
-congenital malformations: midacial abnormalities (cleft lip/palate)
-midline brain tumors
-head trauma
-nystagmus (rapid, uncoordinated eye movement), retinal abnormalities
GH deficiency CM
-hypoglycemia
-growth below 3rd percentile
-dental eruption delayed
-irregular setting of permanent teeth
-thin hair, poor nail growth
-greater fat mass, decreased muscle mass, delayed bone formation
-delayed puberty
GH deficiency pathogenesis
-decreased/defective GH secretion
-defective generation of or impaired response to somatomedin (impaired mediation)
what happens in antidiuretic hormone disorders?
ADH (vasopressin) secreted by posterior pituitary gland in response to changes in blood osmolarity
-ADH acts directly on renal collecting ducts and distal tubules, increasing membrane permeability and reabsorption of water
-ADH regulates that body’s water balance by controlling amount of water reabsorbed by the kidneys
-> disorders = excessive water retention or excessive polyuria
types of diabetes insipidus (hypothalamic, nephrogenic, transient)
hypothalamic: unable to secrete/produce ADH, usually r/t trauma
nephrogenic: renal tubules unresponsive to ADH
transient: r/t pregnancy, produced by the accelerated metabolism of ADH
what is diabetes insipidus?
lack of vasopressin (ADH) action that leads to inability to concentrate urine and H20, leading to large volume of dilute urine
diabetes insipidus etiology
related to insufficiency of ADH – damage to posterior pituitary, head trauma, intracranial tumors, neurosurgery, drugs, pregnancy, idiopathic
diabetes insipidus pathogenesis
lack of ADH, decreased water reabsorption in kidneys – may be permanent or transient
diabetes insipidus CM
-large volume of dilute urine
-thirst
-increased serum of sodium (b/c concentration isnt eliminated)
-neurological symptoms
-dehydration
-nocturia in adults
-bed wetting in children
what is SIADH?
levels of vasopressin (ADH) elevated at times during which physiologic secretion of ADH from posterior pituitary would normally be suppressed
-because the clinical abnormality is a decrease in osmotic pressure of body fluids, the hallmark of SIADH is hypo-osmolality, resulting in hyponatremia. frequently indicator of underlying disease
SIADH etiology
abnormal production of ADH, lung tumors, drugs, head surgery/trauma, anesthetics
SIADH pathogenesis
excessive secretion of ADH leads to excessive H2O retention leading to hyponatremia and H2O intoxication
SIADH CM
-fluid retention
-hyponatremia
-lethargy
-confusion
-cerebral edema
-seizures
-coma
-muscle cramps
-weakness
-decreased urine output
-weight gain
what is hyperthyroidism
increased levels of thyroid hormones = increased metabolism
low TSH, high T3 & T4
what is hypothyroidism
decreased levels of thyroid hormones = decreased metabolism
high TSH, low T3 & T4
hyperthyroidism etiology (primary, secondary)
primary
-autoimmune (Graves disease)
-thyroid tumor/goiter
secondary
-pituitary adenoma
-exogenous thyroid (medications)
hyperthyroidism pathogenesis
-thyroid follicular cell hyper function, excess of T3 and T4 (Graves)
-excess secretion of TSH (secondary)
hyperthyroidism CM
history
-weight loss
-increased appetite
-nervousness
-heat intolerance
-palpitations
-diarrhea
-irritability
-insomnia
physical
-warm, moist skin
-thin, fine hair
-increased BP, HR
-hyperreflexia
-fine tremor
-eyelid, retraction, lag (eye rolls down)
-enlarged thyroid
graves disease etiology
autoimmune or idiopathic
graves disease pathogenesis
IgG autoantibodies bind to and stimulate TSH receptors on thyroid. the result is excess production of T3 and T4 which leads to hypermetabolic state. thyroid hyperplasia (enlargement) and hypersecretion (increased production) result
thyroid storm and CM
-form of life-threatening thyrotoxicosis
-excessive amounts of thyroid hormones acutely released into circulation
-extreme state of hyperthyroidism “hyperthyroidism on steroids”
-presence of excessive thyroid hormone causes rapid increase in metabolic rate
CM
-hyperthermia
-tachycardia
-agitation
-seizures
-exophthalmos (bulging eyes)
-palpitations
-restlessness
-NVD
what is goiter
-enlargement of thyroid gland in attempt to compensate for inadequate thyroid hormone
-may be present in hyperthyroidism or hypothyroidism
-may be so large that cause respiratory complications
-may be benign or malignant
hypothyroidism etiology (primary, secondary)
primary (disfunction/distruction)
-autoimmune (Hashimoto Thyroiditis)
-iatrogenic (surgery, RAIU ablation)
-congenital d/t dysgenesis
-iodine deficiency
secondary (what arises from primary)
-pituitary failure
-anti-thyroid medications
hyperthyroidism pathogenesis
-thyroid follicular cell hyperfuntion (from constant stimulation) and increased T3 and T4 (Hashimoto)
-excess secretion of TSH (secondary pituitary)
hypothyroidism CM (infants)
-dull appearance, thick, tongue and lips
-prolonged neonatal jaundice
-poor muscle tone
-bradycardia, mottled extremities
-umbilical hernia
-hoarse cry
what is Hashimoto’s thyroiditis? pathogenesis?
most common form of hyperthyroidism, more common in females over 50
autoimmune inflammation and destruction if thyroid cells
Hashimoto’s thyroiditis CM
-decreased BMR
-weakness, lethargy, cold intolerance, decreased appetite
-bradycardia, mild/moderate weight gain
-elevated serum cholesterol and triglycerides
-enlarged thyroid, dry skin, constipation
-depression, difficulties with concentration/memory
-menstrual irregularity
what is myxedema?
-severe hypothyroidism.
-accumulation of proteins in interstitial spaces results in increase of interstitial fluids causing edema.
-altered mental state, altered thermoregulation, hx of precipitating event (trauma, infection/sepsis).
-non-pitting edema commonly in pretibial & facial areas.
-may progress to Myxedema coma (hypothyroid crisis)
-result of severe or prolonged hypothyroidism & may be life-threatening.
what is parathyroid gland
-serum CA+ levels provide feedback for Parathyroid hormone (PTH) secretion
-PTH maintains normal CA+ levels by increasing bone resorption of CA+, and reabsorption from kidneys and intestines.
So….
-decrease in CA+ = PTH release = bone reabsorption
-elevation in CA+ = suppression of PTH secretion
hyperparathyroidism etiology
-chief cell adenomas (most common)
-hyperplasia
-renal failure
-idiopathic
hyperparathyroidism pathogenesis
PTH increases resorption of CA+ and release of phosphorus & CA+ by bones, increases bicarb excretion & decreases acid excretion leading to hypokalemia & metabolic acidosis
hyperparathyroidism CM
-depression
-paresthesias
-impaired vision
-HTN
-nausea
-renal calculi
-bone pain
-abdominal pain
-bone demineralization
-dehydration
-may be asymptomatic
hypoparathyroidism etiology
-removal of parathyroid gland during thyroidectomy
-idiopathic
-autoimmune
hypoparathyroidism pathogenesis
Inability to maintain normal serum CA+ concentrations due to decreased PTH
hypoparathyroidism CM
-dysrhythmias
-abdominal cramps
-irritability/anxiety
-paresthesias
-muscle spasms
-dry scaly skin
-tetany (twitchiness)
-laryngeal stridor
addison disease etiology
destruction/dysfunction of adrenal cortex
addison disease pathogenesis
-destruction of adrenal cortical tissue causes adrenal gland hypofunction -hyposecretion of aldosterone, cortisol & androgens
-decreased aldosterone=loss of Na+ and H20=hypovolemia and hypotension
-K+ retained resulting hyperkalemia
addison disease CM
-depression, fatigue, decreased libido
-hypotension
-EKG changes
-muscle weakness
-skin hyperpigmentation (bronze look)
-ND
-anorexia
-hyperkalemia
-hyponatremia
-hypoglycemia
cushing’s syndrome etiology
-pituitary Adenoma
-adrenal adenoma (benign)
-adrenal carcinoma (malignant)
-abnormal ACTH (CA)
-exogenous steroids (common)
cushing’s syndrome pathogenesis
adrenal cortex hyperfunction results in excess production of cortisol & aldosterone. syndrome caused by chronic exposure to excessive circulating levels of glucocorticoids
cushing’s syndrome CM (hx, physical)
history:
-weight gain
-fatigue
-oligomenorrhea
-weakness
-easy bruising
-peptic ulcers
-poor wound healing
-decreased libido
-hypokalemia
physical
-central obesity
-muscle wasting
-striae
-hyperglycemia
-hypertension
-hirsutism (excessive hair growth)
-buffalo hump
-acne
-glycosuria (high sugar levels in urine)
-moon face
hyperaldosteronism etiology
adrenal tumor or excessive circulating renin
hyperaldosteronism pathogenesis
excessive production & excretion of aldosterone by the adrenal cortex causing Na+ and H20 retention by the kidney
hyperaldosteronism CM
-HTN
-hypokalemia
-renal damage
-cerebral infarcts (brain infarctions, disruption of blood flow)
-fluid retention
-tetany (muscle spasms)
-electrolyte imbalances
-muscle weakness
what is pheochromocytoma? etiology?
tumor of adrenal medulla causes excessive production of secretion of catecholamines
neoplasia syndromes
pheochromocytoma pathogenesis
tumor causes excessive secretion of epinephrine/norepinephrine
pheochromocytoma CM
-HTN
-agitation
-headache
-palpitations
-tachycardia
-NVD
-polyuria
-tremors
diabetes diagnosis criteria
-Random glucose > 200 mg with classic signs and symptoms
-OR: fasting glucose > 126 mg, twice
-OR: HbA1C >6.5
-OR: BG>200 mg/dl 2 hrs after a 75-g oral glucose load
type 1 DM
type 2 DM
Type I DM: Destruction of pancreatic beta cells leads to insulin dependence
-complete insufficiency
-Must have exogenous insulin.
Type II DM: Decrease in beta cell wt or #, or insulin resistance.
-Insulin receptors in target tissues become insensitive or resistant to insulin.
-May be controlled with diet & exercise or oral agents.
DM type 1 etiology
-Damaged pancreatic B cells by genetic, environment, or immunologic factors
-May be autoimmune
-Absolute insulin deficiency d/t B-cell failure
DM type 1 risk factors
-Generally in younger, thinner, “acute” onset
-Genetic predisposition
-May effect any age group, 20% develop DM after age 30
-Heredity
DM type 1 pathogenesis
-Autoimmune destruction of pancreatic B cells causes Insulin deficiency.
-This leads to uncontrolled glucose production by liver & hyperglycemia.
-Glucose spills into urine causing osmotic diuresis & excessive amounts of urine(polyuria).
-Loss of fluids leads to excessive thirst (polydipsia).
Without insulin, body cannot use carbs so uses proteins & fats for energy leading to weight loss.
-Breakdown of nutritional stores leads to excessive hunger (polyphagia).
-Lipolysis (breakdown of fat) produces ketone bodies that lead to acidosis.
-DKA—severe metabolic, fluid, and electrolyte disturbances.
DM type 1 CM
-Onset may be associated with ketoacidosis.
-Polyuria: d/t osmotic diuresis
-Polydipsia: d/t fluid loss.
-Polyphagia: d/t gluconeogenesis (Breakdown of stored glycogen)
-Wt. loss: Impaired metabolism
-Glycosuria: glucose urine (kidney cannot reabsorb glucose)
what is diabetic ketoacidosis?
-occurs primarily in type 1 diabetes
-fat metabolism produces ketones leading to acidosis
-results in severe metabolic, fluid, and electrolyte disturbances
-may be life threatening
diabetic ketoacidosis precipitating factors
-non-compliance
-stress
-infection
-trauma
-pregnancy
-thyroid storm
diabetic ketoacidosis CM
-abdominal pain
-nausea
-vomiting
-metabolic acidosis
-fruit breath odor
-Kussmaul’s respirations (deep, rapid, regular)
-altered LOC
-coma
-death if untreated
DM type 2 etiology
-Etiology unknown but obesity is single most important risk factor.
-Decreased tissue sensitivity & responsiveness.
-Genetic predisposition
DM type 2 risk factors
-Obesity (% body fat)
-H/o gestational DM, HTN, dyslipidemia, high triglycerides
-Sex (female), age, family hx & ethnicity all factors in determining risk
-Sedentary lifestyle
DM type 2 pathogenesis
Three abnormalities:
1. Resistance of insulin in peripheral tissues, mostly muscle & fat but also liver
-Decreased tissue sensitivity & responsiveness to insulin.
-Decrease in # of insulin receptors
2. Defective insulin secretion in response to glucose stimulus
-Deficiency of insulin related to Beta cell dysfunction
3. Increased glucose production by liver
DM type 2 CM
-Polyuria
-Polydipsia (excessive thrist)
-Blurred vision
-Weight gain
what is nonketotic hyperglycemic hyperosmolar coma?
-Extreme hyperglycemia
-Polyuria (excessive urination) in attempt to decrease glucose concentration
-Polyuria leads to profound dehydration and hyperosmotic state
-Neurological manifestations related to hypernatremia
hypoglycemia etiology
-Insufficient food intake
-Unplanned activity
-Inappropriate insulin or sulfonylurea dose
hypoglycemia symptoms
-Pallor
-Tremor
-Diaphoresis
-Palpitations & anxiety
-Hunger
-Visual disturbance
-Weakness
-Paresthesias
-Confusion
-Agitation
-Coma
-Death
