ENDOCRINE 2 PARATHYROID

Question 0

DO CHANGES IN PROTEIN (ALBUMIN ) AFFECT IONIZED CALCIUM?

HOW DOES PH AFFECT IONIZED CA?

Answer 0

NO, ONLY CHANGES IN PH AFFECT IONIZED CA.
ACIDOSIS INCREASES FREE IONIZED CA
ALKALOSIS DECREASES FREE IONIZED CA

Question 1

WHAT TYPE OF CALCIUM EXERTS PHYSIOLOGIC EFFECTS? AND WHAT DOES CALCIUM DO?

Answer 1

IONIZED CALCIUM.
TOTAL BLOOD CALCIUM DOESNT ALWAYS REFLECT THE IONIZED CALCIUM.
IT CONTROLS HEMOSTASIS, MUSCLE CONTRACTION, NEURAL TRANSMISSION, CELL DIVISION, AND BONE FORMATION.

Question 2

WHAT HORMONES REGULATE PLASMA CA? (AND HOW?)

Answer 2

VITAMIN D. ACTIVE VIT D INCREASES PLASMA CA (AND PHOS) BY PROMOTING ABSORPTION.

• PTH. INCREASES EXTRACELLULAR CA (DECREASES PHOS)
• CALCITONIN. REDUCES SERUM CA. (“WEAK OPPOSITE OF PTH”)

Question 3

PTH IS THE MAJOR HORMONAL REGULATOR OF CALCIUM AND PHOSPHATE. HOW DOES IT GET RELEASED? HOW DOES IT INCREASE CA?

Answer 3

PTH SECRETED FROM CHIEF CELLS OF PARATHYROID WHEN LOW ION. CA, HIGH PHOS., OR ACUTE LOW MAG.
PTH CONTROLS CA VIA NEG FEEDBACK MECHANISM.
INCREASES CA BY: BONE EROSION AND ABSORPTION OF ITS CA. INCREASES CA REABSORPTION BY KIDNEY DCT. PTH STIMULATES CONVERSION OF VIT D TO ACT. VIT D FOR CA ABSORPTION.

Question 4

HOW DOES CALCITONIN REDUCE SERUM CALCIUM?

Answer 4

BY INHIBITING BONE OSTEOCLASTS—–SO BONE IS MAINTAINED/FORMED—-NO CA RELEASED INTO BLOOD.

Question 5

WHAT ARE THE CLINICAL FEATURES OF HYPOPARATHYROIDISM AND WHY?

Answer 5

HYPOPARATHYROIDISM = LOW CA. CATIONS DROP, CELL MEMBRANE THRESHOLD MORE NEGATIVE (CLOSER TO THRESHOLD FIRE) AND ARE MORE EXCITABLE (MORE AP).
SEE: LOW CA, HIGH PHOS.
-CV: PROLONGED QT, LOW BP, DECREASED CARDIAC CONTRACTILITY.
-NM: NM EXCITABILITY
-NEURO: TENTANY, SIEZURES, NUMBNESS, TINGLING.
NO GI/RENAL EFFECTS.

Question 6

WHAT ARE ACUTE VS CHRONIC S/S OF HYPOPARATHYROIDISM?

Answer 6

ACUTE: CARDINAL SIGNS: NM EXCITABILITY (SPASMS) AND HYPOCALCEMIC TETANY.
YOULL SEE….LARYNGEAL MUSCLE SPASM, MUSCLE CRAMPS, NUMBNESS, TINGLING, HYPERACTIVE DEEP TENDON REFLEX.
CHVOSTEK SIGN (IPSILATERAL FACIAL M. TWITCH)
TROUSSEAUS SIGN (FLEX OF WRIST AND THUMB EXTENSION OF FINGERS RESPONSE TO BP CUFF)
CHRONIC: FATIGUE, CRAMPS, LETHARGY, CATARACTS, CALCIFICATION OF SUB Q TISSUE, THICK SKULL.

Question 7

ANESTH CONSIDERATIONS FOR HYPOPARATHYROIDISM?

Answer 7

REMEMBER INCREASES IN BICARB, PHOS, AND CITRATE (ANIONS) WILL LOWER (NEUTRALIZE) CALCIUM EVEN FURTHER!
BE CAREFUL WITH CITRATED BLOOD.
DIURESIS CAUSES FURTHER CA LOSS.
ALKALOSIS DECREASES CA FURTHER.
EXAGERATED RESPONSE TO MR.
TREAT ACUTE EPISODE: BOLUS 100-200 MG CA OVER 10 MIN.
FOLLOW WITH MAIN INFUSION 1-2MG/KG PER HR CA.
MONITOR CA MG PHOS K AND DREATININE.

Question 8

WHAT IS NORMAL SERUM CA?

Answer 8

8.5-10

Question 9

WHAT ARE THE CLINICAL FEATURES OF HYPERPARATHYROIDISM?

Answer 9

CV: HYPERTENSION, SHORTENED QT INTERVAL
MS: BONE PAIN, FRACTURES, WEAKNESS, ATROPHY
NEURO: SOMNOLENCE , DEPRESSION, HYPOTONIA
GI: N/V
RENAL: KIDNEY STONES, POLYURIA

Question 10

ANESTHESIA FOR HYPERPARATHYROIDISM?

Answer 10

CALCIUM LEVELS > 14 NEED IMMEDIATE TX.
CORRECT VOLUME/LYTES. PT WILL BE DEHYDRATED AND HAVE N/V.
AVOID SEDATION!…HIGH CA DEPRESSES CNS
CAREFUL POSITIONING….PRONE TO FRACTURES!
HYDRATE WITH NON CA CONTAINING SOLUTIONS (.9NS) NOT LR. MAINTAIN IV VOL…THEYRE DEHYDRATED.
AVOID HYPOVENTILATION (ACIDOSIS INCREASES ION CA)
UNPREDICTABLE RESPONSE TO MR. SENSITIVE TO NMDR. MONITOR EKG FOR DYSRHYTHMIAS TREAT WITH CA CHANNEL BLOCKER (VERAPAMIL 5-10 MG)