ENDOCRINE 1 PHYS. Flashcards
WHAT ARE THE 3 WAYS (FUNCTIONS) IN WHICH A HORMONE CAN ACT?
- ENDOCRINE: HORMONE IN BLOODSTREAM TO TARGET CELL
- PARACRINE: HORMONE ACTS ON NEIGHBOR CELL OF DIFFERENT TYPE
- AUTOCRINE: HORMONE ACTS ON ITS OWN PRODUCER CELL OR NEIGHBORING IDENTICAL CELLS.
HOW MANY GLANDS ARE IN THE ENDOCRINE SYSTEM AND WHAT DOES THE ENDOCRINE SYSTEM DO?
8 GLANDS. 1 SYSTEM WITH SIMILAR FUNCTION/MECHANISM.
REGULATES METABOLISM, MAINTAINES FLUID BALANCE, CALCIUM CONCENTRATION, MAINTAINS BP, CONTROLS GROWTH AND MATURITY.
WHAT HORMONES ACT FASTER AND WHY?
PEPTIDES AND PROTEIN (INSULIN, GH, ADH, ANGIOTENSIN, CALCITONIN, ACTH, OXYTOCIN, GLUCAGON), AND CATACHOLAMINES (E, NE, DA)
THEY ARE NOT BOUND TO PROTEIN IN BLOOD STREAM AND ACT BY BINDING TO CELL MEMBRANE RECEPTORS. GENERATE HORMONAL EFFECT IN SECONDS TO MINUTES.
THYROID AND STEROID HORMONES ARE PROTEIN BOUND AND BIND TO INTRACELLULAR RECEPTORS THAT ACTIVATE THE TRANSCRIPTION OF GENES. TAKES DAYS TO HAVE A RESPONSE.
HOW DOES PROTEIN BINDING OF HORMONES EFFECT METABOLISM?
IT PROTECTS THEM FROM METABOLISM AND RENAL CLEARANCE SO HALF LIFE WILL BE LONGER. PROTEIN BOUND ARE STEROIDS AND THYROID.
HOW IS CONCENTRATION OF HORMONE RELATED TO THE NUMBER OF RECEPTORS?
INVERSELY. MORE HORMONE CIRCULATING….FEWER RECEPTORS.
WHAT ARE THE 3 WAYS IN WHICH SYNTHESIS AND SECRETION OF HORMONES ARE REGULATED?
- NEURAL CONTROLS
- BIORHYTHMS
- FEEDBACK MECHANISMS (POS OR NEG. ) ONLY POS. IS GROWTH HORMONE RELEASE.
WHAT ARE THE 2 PARTS OF THE PITUITARY GLAND AND WHAT ARE THEY CONTROLLED BY?
ANTERIOR LOBE (ADENOHYPOPHYSIS) CONTROLLED BY HYPOTHALMUS POSTERIOR LOBE (NEUROHYPOPHYSIS) CONTROLLED BY NERVE STIMULATION.
WHERE IS ADH (VASOPRESSIN) SECRETED FROM AND WHAT DOES IT DO?
SECRETED FROM POSTERIOR PITUITARY.
ADH CONSTRICTS VASCULAR SMOOTH MUSCLE, INCREASES WATER REABSORPTION FROM KIDNEY.
WITH ADH RELEASE WHAT WILL YOU SEE IN PATIENT?
VASOCONSTRICTION
INCREASE IN URINE OSMOLARITY (HIGH NA)
DECREASE IN SERUM OSMOLARITY
HEMOSTASIS PROMOTION BY INCREASING VON WILLEBRAND FACTOR AND FACTOR 8.
WHAT WILL STIMULATE ADH SECRETION?
INCREASE IN SERUM OSMOLARITY (INCREASE IN PLASMA NA)
DECREASED BLOOD VOLUME
DECREASED BP
POS PRESSURE VENTILATION (PEEP) BECAUSE IT REDUCES CENTRAL BLOOD VOLUME
HOW IS ADH SECRETION REGULATED?
A NEGATIVE FEEDBACK LOOP. WATER DEPRIVATION CAUSING INCREASED PLASMA OSMOLARITY (OR DECR. CIRCULATORY VOL)—ADH RELEASE—–RENAL TUBLULE WATER REABSORPTION—-NORMALIZE SERUM OSMOLARITY. SEE GRAPH.
WHAT WILL BLOOD AND URINE BE LIKE IF YOU HAVE NO ADH?
URINE …HYPOOSMOLAR. LOTS OF DILUTE URINE.
BLOOD….INCREASED SERUM OSMOLARITY. DEHYDRATED.
WHAT IS DI? WHAT WILL YOU SEE IN PT? HOW DO YOU TREAT?
WHAT: LACK OF ADH OR INABILITY OF RENAL TUBULE TO RESPOND TO ADH.
SEE: HALLMARK IS POLYURIA WITHOUT GLUCOSURIA RESULTING IN DEHYDRATION AND HYPERNATREMIA IN BLOOD. THIS HIGH NA CAUSES HYPERREFLEXIA, LETHERGY, SEIZURE, THIRST. URINE OSMO WILL BE 50-200.
TREAT SURG PT WITH NO ADH: CONT INFUSION VASOPRESSIN .1-.2 U/HR INTRAOP. WATCH LYTES/URINE.
ISOTONIC IVF IF PLASMA OSMO < 290
HYPOTONIC IVF IF PLASMA OSMO > 290
WHAT IS SIADH? WHAT DO YOU SEE IN PT? HOW TO TREAT?
POST PIT SECRETES TOO MUCH ADH.
SEE: WATER INTOXICATION, DILUTIONAL HYPONATREMIA IN BLOOD—BRAIN EDEMA. SO YOU GET HA, N/V, LETHARGY, CONFUSION, SEIZURE. EDEMA, HTN.
TX: WATER RESTRICTION. HYPERTONIC SALINE.
ANESTHESIA: USE ISOTONIC FLUIDS….USE SPARINGLY. TREAT N/V.
WHAT IS HPOPHYSECTOMY? WHAT IS ANESTH. CARE FOR THIS PROCEDURE?
REMOVE PITUITARY D/T TUMOR. TRANSSPHENOIDAL APPROACH MOST COMMON.
PREOP: LABS IMPORTANT. PT MAY NEED THYROID HORMONE REPLACEMENT/STEROID COVERAGE.
SIMISITTING…THINK VAE. INCREASED ICP NOT USUALLY A PROBLEM. ARMS TUCKED TABLE 180. LOCAL WITH EPI USED. NASAL PACKING POSTOP. WANT SMOOTH EXTUBATION WITH EARLY NEURO ASSESSMENT. MAY REQUIRE DDAVP REPLACEMENT.
THESE PTS ARE AT RISK FOR DI POSTOP REQUIRING VASOPRESSIN TREATMENT.
