Exam 4: Endocrine Flashcards
Type of disturbance typically seen with tumors/cancer:
Hyperfunction; sometimes mass effect
Types of target cell failure:
↓ in # of receptors Impaired receptor function Presence of antibodies against receptors Antibodies acting as agonists Unusual expression of receptors
Hormones secreted by the hypothalamus:
GnRH (→ FSH/LH) TRH (→ TSH) CRH (→ ACTH) PIF (→ prolactin) GHRH (→ GH)
Hormones secreted by the anterior pituitary:
FLAT PEG
FSH
LH
ACTH
TSH
Prolactin
Growth hormone
Posterior pituitary syndromes:
DI SIADH Oxytocin deficiency Hypopituitarism Null cell adenoma Ischemic necrosis/Sheehan syndrome Ablation
Pituitary adenomas:
Prolactinomas GH adenoma ACTH adenoma Gonadotroph adenoma TSH cell adenoma
Hypothalamus site of hormone synthesis:
Supraoptic and paraventricular nuclei
Requirement for hormones to be transported in blood:
Bound to proteins
Clinical manifestations of SIADH:
Water retention
Hyponatremia
Hypoosmolarity
Cause of neurogenic vs. nephrogenic DI:
Neurogenic: insufficient ADH produced
Nephrogenic: inadequate response to ADH
S/s of DI:
Polyuria
Polydipsia
Unconcentrated urine
Sheehan syndrome is:
Ischemic necrosis of pituitary due to heavy blood loss during delivery
Panhypopituitarism usually from:
Cell destroying/null cell tumors
Non-neoplastic causes of panhypopituitarism:
Head trauma, infection, etc
Most common cause of hyperpituitarism:
Slow-growing benign pituitary adenoma
S/s of pituitary adenoma:
Headache/fatigue
Visual changes
Hyposecretion of neighboring ant.pit. hormones
Cause of acromegaly:
↑ GH during adulthood
Cause of gigantism:
↑ GH during childhood/adolescence
S/s of acromegaly:
Overgrowth in nose, face, scalp, forehead
Anesthesia implications of acromegaly:
Can be difficult to intubate/manage airway
S/s of gigantism:
Proportional growth beyond typical sizes
Cause of dwarfism:
↓ GH in childhood
S/s of dwarfism:
Proportionally stunted growth; 1/3rd are able to go through puberty/reproduce
Three major effects of panhypopituitarism:
Hypothyroidism
Depressed cortisol production
Suppressed sex hormone production
Three major effects of panhypopituitarism:
Hypothyroidism
Depressed cortisol production
Suppressed sex hormone production
Causes of hyperthyroidism:
Graves disease
Hyperfunctioning adenoma
TSH cell adenoma
Iatrogenic
Causes of hypothyroidism:
Hashimoto’s
Iodine deficiency
Ablation
Idiopathic
Carcinomas of the thyroid:
Papillary
Anaplastic
Medullary
Follicular
Part of anterior pituitary that secretes TSH:
Pars distalis
Short feedback loop goes between thyroid and:
Anterior pituitary gland/pars distalis
Long feedback loop goes between thyroid and:
Hypothalamuc
Conditions that cause ↑ TSH and ↑ T3/T4:
Pituitary adenoma secreting TSH
Ectopic TSH production (small cell carcinoma in lung)
Conditions that cause ↑ TSH, ↓ T3/T4:
Hashimoto’s thyroiditis
Iodine deficiency
Conditions that cause ↓ TSH, ↑ T3/T4:
Graves’ disease
Toxic goiter
Thyroxine-secreting thyroid cancer
Conditions that cause ↓ TSH, ↓ T3/T4:
Panhypopituitarism
Null cell adenoma
Sheehan’s syndrome
Pathogenesis of Grave’s disease:
Antibodies called TSIs (thyroid stimulating globulins) act like TSH and cause constant T3/T4 production via ↑ cAMP
Half-time of TSH and TSIs:
TSH: 1 hr
TSIs: 12 hrs
S/s of hyperthyroidism:
Anxiety Irritability Insomnia Rapid/irregular heartbeat Tremors Diaphoresis Heat-sensitivity Weight loss Brittle hair Goiter Light menstrual periods Diarrhea Exophthalmos
Tx for hyperthyroidism:
β blockers
Anti-thyroid meds
Radioactive iodine
Surgery
Pathogenesis of Hashimoto’s thyroiditis:
Autoimmune destruction of receptors and gland, causing inflammation
S/s of hypothyroidism:
Cold sensitivity Constipation Pale, dry skin Puffy face Goiter/hoarse voice Elevated cholesterol Weight gain Muscle aches/tenderness/stiffness Heavy menstrual periods Depression
Tx of hypothyroidism:
Levothyroxine
Iodine if deficient
Role of immune system in Hashimoto’s:
Thyroid-specific helper T cells (CD4) stimulate cytotoxic T cells (CD8) and B cells (humoral)
CD8 cells responsible for parenchymal destruction
B cells secrete antibodies against TSH receptors et al.
Role of antithyroglobulin and antithyroid peroxidase antibodies in Hashimoto’s:
Not pathogenic, but useful serologic markers of disease
Pathogenesis of myxedema:
↑ chondroitin and hyaluronic acid cause interstitial fluid ↑ and edema
Pathogenesis of cretinism:
Hypothyroidism (extreme) in fetal life, infancy, or childhood
S/s of cretinism:
Skeletal growth stunted more than soft tissue; obesity, large tongue, etc
Dwarfism Unique facial features Absent/scant secondary hair Poorly developed breasts Potbelly Umbilical hernia
Role of PTH glands:
Regulator of serum Ca++
Antagonizes calcitonin
Excretes PO4-
Role of PTH glands:
Regulator of serum Ca++
Antagonizes calcitonin
Excretes PO4-
S/s of hyperparathyroidism:
Hypercalcemia Hypercalcuria Kidney stones PUD Pancreatitis N/V/anorexia Osteoporosis Confusion/poor memory Muscle weakness/fatigue
Tx of hyperparathyroidism:
Surgery
Anesthetic considerations for hyperparathyroidism surgery:
Positioning - weak bones, muscles
Avoid benzos and muscle relaxants
S/s of hypoparathyroidism:
Hypocalcemia
Tetany, esp. in smaller muscles
Hypocalcemic tetany in the hand is called:
Carpopedal spasm
Tx for hypoparathyroidism:
PTH
Vitamin D
Mineralocorticoid hormones produced in:
Zona glomerulosa of adrenal cortex
Activity of mineralocorticoid hormones:
↑ activity of epithelial Na+ pump
Na+ retention, K+/H+ loss
Most potent naturally occuring mineralocorticoid hormone:
Aldosterone
Glucocorticoid hormones produced in:
Zona fasciculata of adrenal cortex
Glucocorticoid hormone release stimulated by:
ACTH
Activity of glucocorticoid hormones:
Hyperglycemia
Anti-inflammatory
Growth suppression
Sleep/awareness
Most potent naturally occuring glucocorticoid hormone:
Cortisol
Adrenal estrogens and androgens produced in:
Zona reticularis of adrenal cortex
Adrenal estrogens and androgens produced in:
Zona reticularis of adrenal cortex
Production of strong androgens like testosterone:
Weak androgens (DHEA, androstenedione) produced in adrenal cortex and converted to stronger androgens in periphery
Catecholamines produced in:
Chromaffin cells/pheochromocytes in adrenal medulla
Endogenous causes of hypercortisolism/Cushing’s:
Pituitary tumor
Adrenal tumor
Ectopic secreting tumor
Iatrogenic
Causes of hyperaldosteronism/Conn’s:
Overrelease of aldosterone
Overrelease of renin
Most common cause of Cushing’s:
Excess ACTH
S/s of Cushing’s:
Hyperglycemia Hypertension Fat redistribution to trunk/face Fatigue Muscle weakness Moon face Stretch marks Thin skin, easy bruising Slow healing Depression, anxiety, anger Acne Thicker hair Absent menstrual periods ED
Tx for Cushing’s:
↓ steroid use if iatrogenic
Surgery
Radiation
Medical/drugs
Cause of Conn’s disease:
Tumors in zona glomerulosa
S/s of Conn’s:
Hypokalemia Metabolic alkalosis ↑ ECF/blood volume ↑ Na+/H2O retention HTN
S/s of adrenogenital syndrome:
Virilization
Tx of adrenogenital syndrome:
Cortisol
S/s of Addison’s:
Muscle weakness/fatigue Weight loss Anorexia Hyperpigmentation Hypotension/syncope Hypoglycemia Hyponatremia/salt craving N/V/D Irritability Depression
Tx of Addison’s:
HRT
Salt tabs
S/s of pheochromocytoma:
Tachycardia Arrhythmias Sweating Chest pain Upper abdominal pain Headaches Tremors Anxiety/fright Pale skin Hypertension
Tx of pheochromocytoma:
α blockers
β blockers
Tx of pheochromocytoma:
α blockers
β blockers
Reticular activating system response to acute stress:
Activates so we won’t sleep
Amygdala response to acute stress:
Behavioral changes
Arcuate nucleus response to acute stress:
Release of NE from the locus coeruleus
Release of neuropeptide Y (NPY)
Drives BP/HR up
Hypothalamus response to acute stress:
Secretes CRH to stimulate ACTH release from ant pit
Cortisol role in acute stress:
Negative feedback to pituitary and hypothalamus to bring levels back down to normal when appropriate
Effect of chronic stress on stress pathway:
Dampens the negative feedback of cortisol so that you have perpetually ↑ levels of CRH, ACTH, cortisol
Effect of chronic stress on anesthesia:
Labile BPs d/t catecholamine depletion
Hyperglycemia
