• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/66

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

66 Cards in this Set

  • Front
  • Back
HORMONES MADE IN THE OUTER CORTEX
CORTISOL, ALDOSTERONE, AND ANDROGENS (DHEA, DHEAS, TESTOSTERONE, ESTROGEN)
HORMONES SECRETED BY THE INNER MEDULLA
EPINEPHRINE AND NOREPINEPHRINE
WHERE IS CORTICOTROPIN RELEASING HORMONE (CRH) PRODUCED?
HYPOTHALAMUS
WHAT DOES CRH DO IN THE PITUITARY?
STIMULATES ACTH SYNTHESIS
WHEN IS SECRETION OF ACTH INCREASED?
STRESSFUL EVENTS
WHAT INHIBITS THE SECRETION OF ACTH?
CORTISOL IN BLOOD (NEGATIVE FEEDBACK0
WHAT HORMONES DO THE ADRENALS SECRETE?
ALDOSTERONE AND CORTISOL
THIS HORMONE IS SECRETED DIURNALLY WITH HIGHEST LEVEL IN EARLY AM
ACTH
INCREASED SECRETION OF CORTISOL OCCURS WHEN?
EXERCISE, TRAUAM, INFECTION---STRESS IN GENERAL
HOW DOES CORTISOL AFFECT CARBOHYDRATE METABOLISM?
INHIBITS INSULIN SECRETION. INHIBITS GLUCOSE UPTAKE (CAUSES ELEVATED BLOOD GLUCOSE), AND INCREASES HEPATIC GLUCONEOGENESIS
HOW DOES CORTISOL EFFECT FAT METABOLISM?
INCREASES LIPOLYSIS AND QUANTITY OF FREE FATTY ACIDS
HOW DOES CORTISOL EFFECT PROTEIN METABOLISM?
INCREASES PROTEIN BREAKDOWN SO THERE ARE MORE AMINO ACIDS AVAILABLE FOR CONVERSION TO GLUCOSE
MAJOR BIOLOGIC EFFECTS OF INCREASED CORTISOL
TRUNCAL OBESITY/WEIGHT GAIN; SUPPRESSION OF INFLAMMATION/IMMUNE SYSTEM; SUPPRESSION OF BONE FORMATION AND DECREASED ABSORPTION OF CALCIUM; EASY BRUISING, ABDOMINAL STRIAE, THIN SKIN, NA/H20 RETENTION, GROWTH FAILRE IN KIDS; ALTERED MOOD/COGNITION
WHAT ARE THE POSSIBLE CAUSES OF EXCESS CORTISOL?
LONG TERM DOSES OF GLUCOCORTICOIDS****(MC); ACTH PRODUCING PITUITARY TUMOR AS IN CUSHING'S DISEASE**; ADRENAL ADENOMA/CARCINOMA; ECTOPIC SECRETION
BILATERAL EDEMA, GAINED 60 LBS IN 3 YRS; EASILY BRUISES, PURPLE STRIAE; FAT PADS, BUFFALO HUMP---THINK WHAT AND RUN WHAT TEST?
THINK HYPERCORTISOLISM (CUSHING'S)----DO 24 HR UFC X 3
WHAT IS THE MOST PROBABLE CAUSE OF WEIGHT GAIN IN CUSHING'S?
SODIUM AND WATER RETENTION
FIRST TEST DONE FOR SCREENING OF CUSHING'S SYNDROME?
OVERNIGHT DEXAMETHASONE SUPPRESSION TEST
WHAT RESULT OF OVERNIGHT DEXAMETHASONE SUPPRESSION TEST RULES OUT CUSHING'S SYNDROME?
CORTISOL LESS THAN 5 MCG/ML
IF OVERNIGHT DEXAMETHASONE SUPPRESSION TEST IS ABNORMAL (ELEVATED), WHAT IS THE NEXT TEST DONE?
24 HR URINARY FREE CORTISOL X 3
WHAT RESULT IN THE 24 HR UFC CONFIRMS HYPERCORTISOLISM?
ELEVATED URINE CORTISOL
WHAT WILL THE ACTH AND CORTISOL LEVEL BE IN AN ACTH-DEPENDENT CAUSE OF HYPERCORTISOLISM?
ELEVATED ACTH AND ELEVATED CORTISOL
WHAT ARE ACTH DEPENDENT CAUSES OF HYPERCORTICOLISM?
CUSHING'S DISEASE (PITUITARY TUMOR) OR ECTOPIC ACTH SECRETION I.E. SMALL CELL LUNG CANCER
LEVELS OF CORTISOL AND ACTH IN ACTH-INDEPENDENT HYPERCORTICOLISM?
ACTH SUPPRESSED AND HIGH CORTISOL
WHAT CONFIRMS PRESENCE OF ACTH SECRETING TUMOR IN CUSHING'S DISEASE?
MRI
WHAT CONFIRMS ADRENAL ADENOMA OR ADRENAL CORTICOCARCINOMA?
CT OF ADRENAL GLANDS
TWO CONDITIONS IN ACTH-INDEPENDENT HYPERCORTICOLISM?
EXOGENOUS CORTICOSTEROID USE; ADRENAL ADENOMA/CORTICOCARCINOMA
WHAT DOES THE HIGH DOSE DEXAMETHASONE SUPPRESSION TEST DO?
DETERMINES WHETHER HYPERCORTICOLISM IS CAUSED BY ECTOPIC ACTH SECRETION OR CUSHING'S DISEASE
TX OF CUSHING'S SYNDROME
IF EXOGENOUS USE OF DRUGS IS CAUSE---REDUCE DOSE; IF THERE IS A TUMOR----REMOVE
20 Y/0- WEAKNESS, FATIGUE, POOR APPETITE, WEIGHT LOSS, DIARRHEA, AMENORRHEA, LIGHTHEADNESS X SEVERAL MONTHS; LABS SHOW LOW SODIUM, ELEVATED POTASSIUM---BP IS LOW AND UNSTABLE----WHAT SHOULD YOU THINK?
ALDOSTERONE DEFICIENCY
MAIN ETIOLOGY OF ADDISON'S (PRIMARY ADRENAL INSUFFICIENCY)
AUTOIMMUNE ADRENALITIS
PTS WITH ADDISON'S PRESENT WITH THESE SYMPTOMS
WEAKNESS, FATIGUE, HYPERPIGMENTATION, NAUSEA, VOMITING, ANXIETY
IN CHRONIC CASES OF ADDISON'S, WHAT WILL BE THE LEVELS OF CORTISOL AND ALDOSTERONE AND WHAT WILL THOSE ABNORMALS CAUSE?
LOW CORTISOL (SERUM ACTH WILL BE ELEVATED AS A RESULT) AND LOW ALDOSTERONE (SERUM NA IS LOW AND K HIGH AS A RESULT)
ADDISON'S MORE COMMON IN MEN OR WOMEN
WOMEN
ADDISON'S IS OFTEN ASSOCIATED WITH THESE OTHER CONDITIONS
OTHER AUTOIMMUNE ENDOCRINE DISORDERS LIKE VITILIGO, HASHIMOTO'S THYROIDITIS, AND DM
WHAT CAUSES HYPERPIGMENTATION IN ADDISON'S?
ELEVATED ACTH STIMULATES MELANOCYTES TO MAKE MELANIN
WHAT CAUSES HYPONATREMIA AND HYPERKALEMIA IN PRIMARY ADRENAL INSUFFICIENCY?
LOW ALDOSTERONE LEVELS
WHAT IS THE MAJOR ISSUE IN SECONDARY (PITUITARY) ADRENAL INSUFFICIENCY
INADEQUATE SECRETION OF ACTH BY THE PITUITARY GLAND
MOST COMMON CAUSE OF INADEQUATE SECRETION OF ACTH BY THE PITUITARY GLAND
SUDDEN/RAPID WITHDRAWAL OF LONG TERM EXOGENOUS CORTICOSTEROID TX THAT HAS SUPPRESSED ACTH
WHAT ARE OTHER CAUSES OF SECONDARY ADRENAL INSUFFICIENCY (BESIDES DRUG WITHDRAWAL)?
PITUITARY TUMORS, POSTPARTUM PIT. INFARCT
S/S OF SECONDARY ADRENAL INSUFFICIENCY
SAME AS PRIMARY EXCEPT THERE IS PALLOR INSTEAD OF HYPERPIGMENTATION (ACTH IS LOW); ELECTROLYTES ARE USUALLY NORMAL B/C ALDOSTERONE IS NOT AFFECTED
WHAT ARE NORMAL CORTISOL LEVELS AND ACTH LEVELS IN AM WHEN THERE IS PRIMARY ADRENAL INSUFFICIENCY?
LOW AM CORTISOL LEVEL AND ELEVATED PLASMA ACTH (ACTH IS BEING RELEASED BY PITUITARY, BUT ADRENALS ARE NOT RESPONDING TO MAKE CORTISOL)
PRIMARY ADRENAL INSUFFICIENCY PROVEN BY WHAT TEST
SIMPLIFIED COSYNTROPIN (ACTH) STIMULATION TEST
NORMAL RESPONSE TO COSYNTROPIN STIMULATION TEST
INCREASED CORTISOL LEVEL
AN INCREASED CORTISOL LEVEL IN COSYNTROPIN TEST RULES OUT WHAT
ADDISON'S DISEASE
WHAT IS COSYNTROPIN?
SYNTHETIC ACTH
IF SCREENING TEST CONFIRMS PRIMARY ADRENAL INSUFFICIENCY, WHAT DO WE DO TO FIND THE SOURCE?
AN ABDOMINAL CT (ADRENALS)
THERE IS LOW OR INAPPROPRAITELY NORMAL ACTH AND INCREASED CORTISOL W/ ACTH STIMULATION (SCREENING TEST) IN THIS TYPE OF ADRENAL INSUFFICIENCY
SECONDARY ADRENAL INSUFFICIENCY
THERE IS LOW CORTISOL LEVEL WITH ACTH STIMULATION (SCREENING TEST) IN THIS TYPE OF ADRENAL INSUFFICIENCY
PRIMARY ADRENAL INSUFFICIENCY
HOW DO YOU LOCALIZE A CAUSE OF PRIMARY ADRENAL INSUFFICIENCY
ABDOMINAL CT; CHEST XRAY OF OTHER THEN ADDISON'S IS SUSPECTED
HOW DO YOU LOCALIZE A CAUSE OF SECONDARY ADRENAL INSUFFICIENCY?
EXAMINE DRUGS BEING TAKEN; PITUITARY MRI
WITH EITHER TYPE OF HYPOCORTICOLISM, WHAT MUST BE DONE?
REPLACEMENT THERAPY- HYDROCORTISONE AND PREDINOSINE IN SPLIT DOSES (AM/PM 2/3) AND REPLACEMENT OF ALDOSTERONE BY FLUDROCORTISONE
WHAT ARE SICK DAY RULES?
IN PATIENTS WITH ADDISON'S, DOUBLE THE GLUCOCORTICOID DOSE DURING STRESS, ILLNESS, SURGERY, ETC.
BESIDES REPLACEMENT, WHAT SHOULD ALL HYPOCORTICOLISM PATIENTS HAVE (2 ITEMS)?
EMERGENCY STEROID KIT WITH IM INJECTION OF HYDROCORTISONE AND A MEDICAL ALERT TAG
TX OF SECONDARY ADRENAL INSUFFICIENCY?
CORTISOL REPLAACEMENT, REMOVE/SHRINK TUMOR, SAME AS PRIMARY W/ EMERGENCY KIT, BRACELET, AND SICK DAYS
WHEN DOES ADRENAL CRISIS OCCUR?
DURING INSUFFICIENT GLUCOCORTICOID TX OR IN UNDIAGNOSED ADRENAL INSUFFICIENCY
WHAT ARE PRECIPITATING SITUATIONS FOR ADRENAL CRISIS?
STRESS, SUDDEN WITHDRAW OF GLUCOCORTICOID THERAPY, BILATERAL ADRENALECTOMY, ADRENAL TRAUMA, OR PITUITARY NECROSIS
SYMPTOMS OF ADRENAL CRISIS
NAUSEA, VOMITING, AND HA; ALSO WEAKNESS, DEHYDRATION, HYPOTENSION, FEVER, HYPOGLYCEMIA, CONFUSION, COMA
DIAGNOSIS FOR ADRENAL CRISIS
DRAW BLOOD SAMPLE FOR ASAP CORTISOL ASSAY TO DIFFERENTIATE F/ OTHER CAUSES OF SHOCK; THEN AMDMINISTER SIMPLIFIED COSYNTROPIN STIMULATION TEST
IF THERE IS ACUTE ADRENAL INSUFFICIENCY, WHAT WILL HAPPEN WHEN THE SIMPLIFIED COSYNTROPIN STIMULATION TEST IS DONE
THE SYNTHETIC ACTH WILL BE UNABLE TO STIMULATE A NORMAL INCREASES IN SERUM CORTISOL IN ADRENAL CRISIS, SO CORTISOL WILL REMAIN LOW
TX FOR ADRENAL CRISIS
HIGH DOSE GLUCOCORTICOID VIA IV IMMEDIATELY, TAPER OFF SLOWLY TO ORAL MEDS OVER WEEKS, ALSO TREAT THE UNDERLYING STRESS AND ADMINISTER BROAD SPECTRUM ANTIBIOTICS FOR BACTERIAL INFECTIONS THAT ACTED AS TRIGGERS FOR CRISIS
WHAT SECRETES ALDOSTERONE?
ADRENAL CORTEX
ALDOSTERONE STIMULATED BY WHAT THREE PROCESSES
INCREASED PLASMA K; LOW RENAL PERFUSION PRESSURE; INCREASED SYMP. NERVOUS SYSTEM ACTIVITY
PRIMARY ETIOLOGY OF HYPERALDOSTERONISM
EXCESS ALDOSTERONE PRODUCTION FROM ADRENAL GLANDS
SECONDARY ETIOLOGIES OF HYPERALDOSTERONISM
EXCESS RENIN PRODUCTION BY THE KIDNEYS (MOST COMMON B/C OF RENAL ARTERY STENOSIS)
SYMPTOM OF ALDOSTERONISM
MODERATE HYPERTENSION
DIAGNOSIS OF HYPERALDOSTERONISM
HYPOKALEMIA IN THE ABSENCE OF DIURETIC USE; ELEVATED ALDOSTERONE IN 24 HR ALDOSTERONE LEVEL