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PDAT2 > Lec 6 Adrenal Therapy + Cushing + Conn's Syndrome > Flashcards

Lec 6 Adrenal Therapy + Cushing + Conn's Syndrome Flashcards

1
Q

Mineralcorticoid Effects

(Aldosterone)

A

<– REABSORBS Na & Water

Secretes Potassium & Mg –>

comes from Zona Glomerulosa

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2
Q

Glucocorticoid INCREASES / ACTIVATES

Cortisol

​Glucocorticoid Activity

A
  • Carb metabolism
    • increased gluconeogenesis / glycogen storage
    • diminished glucose utilization
  • Lipid metabolism
    • redistribution of fat –> buffalo hump/moonface
    • enhanced lipolysis / more FFA
  • CV effects –> HT
  • CNS excitabolity & mood
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3
Q

Glucocorticoid Decreases / Inhibits

Cortisol

Glucocorticoid Activity

A
  • Growth & Development
    • decreased skeletal growth in pediatrics
  • Anti-Inflammatory
    • ​supresses T lymphocytes / cytokines / inflammatory mediators
    • INCREASE in erythrocytes / platelet conc
  • Imunosuppresant
  • Bone Effects
  • Skeletal Muscle
  • Would Healing
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4
Q

Carbohydrate Metabolism

​Glucocorticoid Activity

A

Increased Gluconeogenesis

Increased Glycogen Synthesis / Storage in LIVER

Diminshed Glucose utilization

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5
Q

Growth & Development

​Glucocorticoid Activity

A
  • Decreased Skeletal Growth in Pediatrics*
  • decrease in bone growth / premature epiphyseal closure*
  • impairment of GH release*
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6
Q

Lipid Metabolism

​Glucocorticoid Activity

A

Redistribution of Body Fat

Moon Face / Buffalo Hump

Enhanced Lipolysis –> increased FFA

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7
Q

Anti-inflammatory Action

​Glucocorticoid Activity

A
  • Supresses T-lymphocyte activation*
  • Supresses production of Cytokines by T-helper cells*
  • Prevents release of Prostaglandins / Histamines / LK’s*

VasoCONSTRICTION &** decrease **Capillary Permeability

INCREASED Erythrocyte / Platelet Conc

RBC / Platelets

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8
Q

Bone Effects

​Glucocorticoid Activity

A

Increased Bone Catabolism

more OsteoCLAST

  • Reduced Bone Formation*
  • less Osteoblast activity*
  • reduced absorption of Calcium*
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9
Q

Cardiovascular Effects

​Glucocorticoid Activity

A

Increased risk for:

Hypertension

Atherosclerosis

Stroke

HT Cardiomyopathy

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10
Q

Skeletal Muscle

​Glucocorticoid Activity

A

EXCESS Steroid -> Muscle Wasting (myopathy)

Steroid Deficit: –> Weakness & Fatigue

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11
Q

Hypothalmic - Pituitary - Adrenal Axis

HPA

A
  • Hypothalmus -> CRF (corticotropin releasing hormone)
    • Anterior pituitary -> ACTH
      • Adrenal Cortex - Secretes:
        • Androgens
        • Corticosteroids
          • -> NEGATIVE FEEDBACK
            • ​to hypothalmus & anterior pituitary
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12
Q

Cortisol Circadian Rhythm

A

Most predictable time = In the morning before meals

Peaks at meals (HIGHEST @ Breakfast)

very difficult to replicate the circadian rhythem with STEROIDS

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13
Q

Cortisol Plasma Protein Binding

A
  • Cortisol is Highly Protein Bound (>95%)
    • ​​so it is hard to get rid of, takes a time rid of cortisol
    • Albumin
    • CBG (Corticosteroid Binding Globulin)
  • Only Free Cortisol is active, can increase or decrease:
    • HIGH STRESS (surgery / major operation)
      • –> up to 4x normal levels​
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14
Q

What INCREASES Cortisol Secretion?

A

Exercise / Physical Stress

Surgery / Major Operation –> 4x normal cortisol

Anxiety / Depression

Anoxeria / Alcoholism

Chronic RENAL Failure

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15
Q

What Decreases Free Cortisol?

A

Increase in CBG –> *Decrease in Free Cortisol*

Estrogen Therapy

Pregnancy

Hypothyrodism / Diabetes

Hematological disorders

Congenital (from birth)

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16
Q

What STIMULATES Aldosterone release?

A

Low BP

Sodium depletion

Beta-adrenergic stimulation

17
Q

What INHIBITS Aldosterone release?

A

HIGH BP

EXCESS Sodium

18
Q

ACTH-Dependent

Cushing’s Syndrome

Etiology

A
  • 80-85% of Cushing Syndrome cases ( HYPERcortisolism )
    • ​80% from Pituitary Adenoma = Cushing’s DISEASE
      • ​tumor is at the pituitary gland
    • 20% from Ectopic ACTH syndrome
      • ​tumor is somewhere else causing more cortisol or ACTH to be secreted
19
Q

ACTH - INdependent

​Cushing’s Syndrome

Etiology

A
  • 20% of all Cushing’s Syndrome cases = HYPERcortisolism
    • 60% - Adrenal Cortical Adenoma
      • ​Benign tumor of the Adrenal Cortex
        • _​_OVERsecreting Cortisol
    • 40% - Adrenal Cortical CARcinoma
      • ​cancerous growth of the adrenal cortex
20
Q

Iatrogenic Cushing Syndrome

Etiology

A

Caused by the TREATMENT:

Prolonged administration of glucocorticoid

in SUPRAphysiological doses

21
Q

Physical Signs/Symptoms

of Cushing’s Syndrome

(HYPERcortisolism)

A
  • Moon Faces / Buffalo Hump / Central obesity
  • Skin Hyperpigmentation
    • ONLY with ACTH-Dependent (cushing;s DISEASE)
      • comes from the EXCESS ACTH
  • ​Thin Skin / Striation / Poor Wind Healing
  • From Excess ANDROGEN Secretion:
    • ​Acne
    • Alopecia (hair loss for men)
    • Hirsutism (hair gain for women)
      • Amenorrhea (no menses)
22
Q

Clinical Symptoms of

Cushing’s Syndrome

(HYPERcortisolism)

A
  • HYPERtension
  • Weakness / Fatigue / Depression
  • Osteopenia (bone loss)
  • Glucose Intolerance
  • Central Obesity
23
Q

Evaluation & Diagnosis

​of ACTH INdependent Cushing’s Syndrome

(HYPERcortisolism)

A
  • Test for Urine Cortisol –> if HIGH
    • Test for ACTH –> if Undetected
      • ​Adrenal Imaging - CT / MRI
        • if abnormal –> ADRENAL TUMOR
          • ​ACTH - Independent
24
Q

Evaluation & Diagnosis

​of ACTH-Dependent Cushing’s Syndrome

(HYPERcortisolism)

A
  • TEST FOR URINE CORTISOL –> if HIGH
    • Test for ACTH –> if Elevated
      • ​Abnormal Pituitary - MRI / DST / CRH
        • CUSHING’S DISEASE
      • Normal Pituitary from MRI
        • No gradient on IPSS / JVS –>
          • Ectopic ACTH Syndrome
        • _​_If gradient is shown –> Cushing Disease
25
Q

Treatment goals

​of Cushing’s Syndrome

(HYPERcortisolism)

A
  • UNTREATED Cushing’s Patients life expectancy is:
    • 4-5 Years
      • due to stroke / heart attack risk
  • Goals:
    • Reduce Mortality
    • Reduce Morbidity / Symptoms
    • Correct lab abnormalities
26
Q

Non-Pharmacologic Therapies

of Cushing’s Syndrome

(HYPERcortisolism)

A
  • 1st line = Surgery
    • recurrance rate is 10-30%
  • 2nd line = Radiation
    • Used for a more mild disease
    • or if they failed surgery
  • ​Bilateral Adrenalectomy
    • removal of BOTH glands
      • –> REQUIRED chronic glucocorticoid / MC replacement
        • very difficult to supplement this
27
Q

Pharmacologic Therapies

of Cushing’s Syndrome

(HYPERcortisolism)

A

Adrenal Enzyme Inhibitors

Useful for AcTH - INdependent Cushing’s Syndrome

  • Most common:
    • Ketaconazole
    • Metyrapone
    • Mitotane
    • Pasireotide for ACTH-Dependent (Cushing’s Disease)
28
Q

Adrenal Enzyme Inhibitors

A

used for AcTH -INdependent Cushing’s Syndrome

  • Inhibits DIFFERENT steps of adrenal hormone productions
    • –> Takes a LONG Time to work (weeks-months)
      • since there is a lot of BOUND CORTISOL in body
  • Dose can increase over time:
    • to compensate for Tumor Growth
      • –> ACTH increases in secretion.
  • HIGH relapse rate
    • using with radiation can lower the rate
29
Q

Ketoconazole

A

Adrenal Enzyme Inhibitor

for –> ACTH-independent Cushing’s

  • INHIBITS Sterol Synthesis:
    • Cortisol
    • ​Aldosterone / Testosterone
      • ​cause side effects
  • Monitor Free Cortisol & Liver Transaminases
    • Many Drug Interactions
30
Q

Metyrapone

A

Adrenal Enzyme Inhibitor

for –> ACTH-independent Cushing’s

  • Inhibits 11B-Hydroxylase
    • ​the FINAL step in cortisol biosynthesis
  • Typically not monotherapy,
    • used with other enzyme inhibitors
31
Q

Mitotane

A

Adrenal Enzyme Inhibitor

for –> ACTH-independent Cushing’s

  • Inhibition of Cortisol / Androgen synthesis
    • in Lower doses
    • ​DOES NOT inhibit Aldosterone**
  • HIGH DOSE –> KILLS the adrenal glond
    • Adrenalectomy
      • but you can KILL BOTH GLANDS (not wanted)
32
Q

Pasireotide

A

ACTH - Secretion INHIBITOR

for Cushing’s DISEASE

(ACTH-Dependent Cushing’s Syndrome)

  • Activates Somatostatin Receptors on Adenomas
    • ​–> INHIBITS ACTH secretion
33
Q

Conn’s Syndrome

Etiology

A

HYPERAldosteronism

Very RARE, 10-20% of resistant HT cases

often discovered when BP does not go down w/ medication

  • Primary: Excess Aldosterone from adrenal source
    • 50% Adenoma 50% Ideopathic
  • Secondary: Extraadrenal hyperaldostonism
    • aldosterone comes from another source (not adrenals)
34
Q

Clinical Presentation / Diagnosis

of Conn’s Syndrome

A

HYPER-Aldosteronism

  • HYPERtension, often RESISTANT
    • patients on 3+ full dose HTN meds
  • HypoKalemia
    • fatigue / muscle weakness / arrythmia
    • High aldosterone retains water/Na ,but K leaves
  • Diagnosed with ARR
    • Aldosterone : Renin Ratio
      • Aldosterone >> Renin
35
Q

Treatment Options

for Conn’s Syndrome

(HYPER-Aldosteronism)

A
  • 1st: Adrenalectomy (surgery)
    • for unilateral disease
  • 2nd: Aldosterone Antagonist medical management
    • preferred in BILATERAL disease
      • Spiranolactone / Epelenone
  • Combination
    • ​often give meds BEFORE surgery
36
Q

Mineralcorticoid Antagonist

Aldosterone

A

​Spiranolactone & Eplerenone

for Conn’s Syndrome = HYPERaldosteronism

  • Mineralcorticoid Aldosterone Receptor blockers
    • at VERY HIGH DOSE vs normal HT dose
  • Inhibits synthesis of Aldosterone and Testosterone
    • ​eplerenone does not block these androgens
    • does not cause gynecomastia / sex issues
37
Q
A

PDAT2 (22 decks)

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