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THE ADRENAL GLAND
Topic Review December 14th, 2022
Presenter: Hamisi Mkindi, M.D,Resident,Internal Medicine
Supervisor:Prof.Samuel E. Kalluvya: Head of
Endocrinology,Diabetes and Infectious
diseases,Bugando Medical Center
THE ADRENAL GLAND
 Under and Over production of hormones
 Clinical Conditions and presentations
 Diagnostic criteria and managementt
AT THE ADRENAL
CORTEX…
ADRENAL
INSUFFICIENCY
 Adrenal insufficiency can be caused
by diseases of the adrenal gland
(primary),
 Interference with corticotropin (ACTH)
secretion by the pituitary gland
(secondary)
 Interference with
corticotropin-releasing hormone (CRH)
secretion by the hypothalamus (tertiary)
ADRENAL
INSUFFICIENCY..
Etiology:
Primary = adrenocortical disease = Addison’s disease
1.Autoimmune: isolated or in assoc w/ APS
2.Infection: TB, CMV, histoplasmosis,
paracoccidioidomycosis,syphillis
3.Vascular: hemorrhage (usually in setting of sepsis
Eg:Warerhouse-Friderichson), adrenal vein thrombosis, HIT, trauma
4.Metastatic disease: (90% of adrenals must be destroyed to
cause insufficiency)
5.Deposition diseases: hemochromatosis, amyloidosis,
sarcoidosis
6.Drugs: azole antifungals, etomidate (even after single dose),
rifampin, anticonvulsants
Nelson syndrome
ADRENAL
INSUFFICIENCY..
Secondary = pituitary failure of ACTH secretion
 But aldosterone intact b/c RAA axis
 Any cause of primary or secondary
hypopituitarism
-Hypophysitis
 Glucocorticoid therapy (can occur after ≤2 wk
of “suppressive doses”; dose effect variable;
even <10 mg of prednisone daily chronically can
be suppressive
 Megestrol (a progestin with some glucocorticoid
activity)
ADRENAL
INSUFFICIENCY
Tertiary causes:
 Refers to causes that relate to
hypothalamic abnormalities that reduce
corticotropin-releasing hormone (CRH)
secretion.
 Abrupt cessation of high-dose glucocorticoid
therapy
 Correction (cure) of hypercortisolism
(Cushing's syndrome)
ADRENAL INSUFFICIENCY-Symptoms
 Primary or secondary: weakness and fatigability
(99%), anorexia (99%), orthostatic hypotension
(90%), nausea (86%), vomiting (75%), hyponatremia
(88%)
 Primary only (extra s/s due to lack of aldosterone
and ↑ ACTH): marked orthostatic hypotension
(because volume depleted), salt craving,
hyperpigmentation (seen in creases, mucous
membranes, pressure areas, nipples), hyperkalemia
 Secondary only: ± other manifestations of
hypopituitarism
ADRENAL INSUFFICIENCY-Diagnostic
studies
 Early a.m. serum cortisol: <3 µg/dL virtually diagnostic; ≥18 µg/dL
generally consistent with intact adrenal function
 Standard (250 µg) cosyntropin stimulation test (testing ability of ACTH
→ ↑ cortisol)
 Normal = 60-min (or 30-min) post-ACTH cortisol ≥18 µg/dL
 Abnormal in primary b/c adrenal gland diseased and unable to give
adequate output
 Abnormal in chronic secondary b/c adrenals atrophied and unable to
respond (very rarely, may be normal in acute pituitary injury b/c
adrenals still able to respond→ use early a.m. cortisol instead)
 All glucocorticoids (incl creams, inh. & drops) affect test. Must know
exposure to interpret.
ADRENAL INSUFFICIENCY-Diagnostic
studies cont..
 Other tests : renin, aldosterone, insulin-induced
hypoglycemia (measure serum cortisol response)
 Metyrapone (blocks cortisol synthesis and therefore
stimulates ACTH, measure plasma 11-deoxycortisol and
urinary 17-hydroxycorticosteroid levels)
 ACTH: ↑ in 1°, ↓ or low-normal in 2°
 Imaging studies to consider pituitary MRI to detect
anatomical abnormalities
 Adrenal CT: small, noncalcified adrenals in autoimmune,
enlarged in metastatic disease, hemorrhage, infection or
deposition (although they may be normal-appearing)
ADRENAL INSUFFICIENCY-
Treatment
 Acute insufficiency: volume resusc. w/ normal
saline + hydrocortisone IV
 Chronic insufficiency:
(1) prednisone ~4–5 mg PO qam or
hydrocortisone 15–25 mg PO qd (⅔ a.m., ⅓ early
p.m.)
(2) fludrocortisone (not needed in 2°
adrenal insufficiency) 0.05–0.2 mg PO qam
(3) backup dexamethasone 4-mg IM
prefilled syringe given to Pt for emergency
situations
ADRENAL CRISIS IN ADRENAL
INSUFFICIENCY
 Precipitants: bilateral adrenal hemorrhage or
infarction, pituitary infarction, pre-existing
adrenal insufficiency + serious infection or GI
illness
 Presentation: shock + anorexia, N/V, abd pain,
weakness, fatigue, confusion, coma, fever Lab
findings: hyponatremia, hyperkalemia (1°)
 Rx: hydrocortisone 50–100 mg IV q8 + IVF; do
not delay for dx tests
CUSHING SYNDROME
CUSHING SYNDROME
 Exogenous
 Endogenous
-ACTC dependent/ACTH
independent
HYPERCORTISOLISM-CUSHING
SYNDROME
 Cushing's syndrome may be either
corticotropin (ACTH) dependent or
independent.
 80 percent of endogenous Cushing's
syndrome cases are ACTH dependent,
and approximately 20 percent are
ACTH independent
CUSHING SYNDROME
CONT…
 Cushing’s syndrome = cortisol excess.
 Cushing’s disease = Cushing’s
syndrome 2° to pituitary ACTH
hypersecretion.
Etiologies
 Most commonly iatrogenic caused by
exogenous glucocorticoids
 Cushing’s disease (60–70%): ACTH-secreting
pituitary adenoma (usually microadenoma) or
hyperplasia
 Adrenal tumor (15–25%): adenoma or (rarely)
carcinoma
 Ectopic ACTH (5–10%): SCLC, carcinoid, islet
cell tumors, medullary thyroid cancer,pheo
 Routine Labs:
-Elevated WBC>11,000/mm3
-Hypokalemia/Metabolic alkalosis due
to increased K excretion/Na
retention/Water flux
Clinical manifestations
 Nonspecific: glucose intolerance or DM, HTN, obesity, oligo- or
amenorrhea, osteoporosis
 More specific: central obesity w/ extremity wasting, dorsocervical fat
pads, spont. Bruising
 Most specific: proximal myopathy, rounded facies, facial plethora, wide
purple striae
 Other: depression, insomnia, psychosis, impaired cognition, hypokalemia,
acne, hirsutism,
 hyperpigmentation (if ↑ ACTH), fungal skin infxns, nephrolithiasis,
polyuria
Treatment
 Surgical: resection of pituitary adenoma,
adrenal tumor or ectopic ACTH-secreting
tumor,
-Or bilat surgical adrenalectomy if unable
to control source of ACTH
 Medical: cabergoline, pasireotide, mitotane,
ketoconazole, or metyrapone to ↓ cortisol,
and/or mifepristone to block cortisol action
at glucocorticoid receptor; frequently used
as bridge to surgery or when surgery
contraindicated
Treatment-Cont…
 Radiation: can do pituitary XRT, but not
effective immediately (takes 6 mo to 2 y)
 Glucocorticoid replacement therapy × 6–
36 mo after TSS (lifelong glucocorticoid
+
Mineralocorticoid replacement if
medical or surgical adrenalectomy)
HYPERALDOSTERONISM
 Characterized by excessive secretion of
aldosterone which causes increases in
sodium reabsorption and loss of K ion
and hydrogen ions.
 Primary
 Secondary
HYPERALDOSTERENOSI
MS
 Primary (adrenal disorders, renin-independent increase in aldosterone)
Adrenal hyperplasia (60–70%), adenoma (Conn’s syndrome, 30–40%),
glucocorticoid-remediable aldosteronism (GRA; ACTH-dep. rearranged
promoter)
 Secondary (extra-adrenal disorders, ↑ aldosterone is renin-dependent)
-Primary reninism: renin-secreting tumor (rare)
-Secondary reninism: renovascular disease: RAS, malignant
hypertension; edematous states w/ ↓ effective arterial volume: CHF,
cirrhosis, nephrotic syndrome;
hypovolemia, diuretics, T2D, Bartter’s (defective Na/K/2Cl
transporter), Gitelman’s (defective renal Na/Cl transporter)
 Nonaldosterone mineralocorticoid excess mimics hyperaldosteronism
11β-HSD defic. (→ lack of inactivation of cortisol, which binds to
mineralocorticoid recept.)
Exogenous mineralocorticoids
Liddle’s syndrome (constitutively activated/overexpressed distal
tubular renal Na channel)
Clinical Manifestations
 Mild-to-moderate HTN (11% of Pts w/ HTN
refractory to 3 drugs.
 Headache, muscle weakness, polyuria,
polydipsia; no peripheral edema
 Classically hypokalemia (but often normal),
metabolic alkalosis, mild hypernatremia
HYPERALDOSTERENISM-
Diagnosis
 5–10% of Pts w/ HTN; ∴ screen if HTN + hypoK, adrenal mass,
refractory/early onset HTN
 Screening: aldo (>15–20 ng/dL) and plasma aldo:renin ratio
(>20 if 1°) (off spironolactone & eplerenone for 6 wk); Se & Sp
>85%.
 ACEI/ARB, diuretics, CCB can ↑ renin activity → ↓ PAC/PRA ratio
and
βBs may ↑PAC/PRA ratio;∴ avoid.
α-blockers generally best to control HTN during dx testing.
 Confirm with sodium suppression test (fail to suppress aldo after
sodium load) oral salt load (+ KCl) × 3 d, ✔ 24-h urine (⊕ if urinary
aldo >12 μg/d while urinary Na >200 mEq/d) or 2L NS over 4 h,
measure plasma aldo at end of infusion (⊕ if aldo >5 ng/dL)
HYPERALDOSTERONISM-
Treatment
 Adenoma → adrenalectomy vs. medical
Rx w/ spironolactone or eplerenone
 Hyperplasia → spironolactone or
eplerenone; GRA → glucocorticoids ±
spironolactone
 Carcinoma → adrenalectomy
PHAEOCHROMOCYTOMA
PHAEOCHROMOCYTOMA
 Neuroendocrine neoplasm leads to inappropriate and paroxysmal release of
adrenergic agents including epinephrine, norephinephrine, and rarely dopamine
 Pressure (hypertension, paroxysmal in 50%, severe & resistant to Rx, occ
orthostatic)
 Pain (headache, chest pain)
 Palpitations (tachycardia, tremor, wt loss, fever)
 Perspiration (profuse)
 Pallor (vasoconstrictive spell)
 Paroxysms can be triggered by meds (eg, β-blockers) abdominal manipulation
 Associated with MEN2A/2B, von Hippel Lindau
 Up to 40% of pheos/paragangliomas thought to have underlying genetic
etiology; genetic testing frequently recommended
Phaeochromocytoma-Dx
Studies
 24° urinary fractionated metanephrines: 85–97% Se, 69–
95% Sp. Screening test of choice if low-risk (b/c false ⊕ with
severe illness, renal failure, OSA, labetalol due to assay
interference, acetaminophen, TCAs, medications containing
sympathomimetics).
 Plasma-free metanephrines: 89–100% Se, 79–97% Sp
Screening test of choice if high risk, but ↑ rate of false ⊕ in low-
prevalence population. False ⊕ rate lower if patient supine for
30 min (estimated 2.8× ↑ false ⊕ if seated)
 Adrenal CT generally better than MRI; PET for known metastatic
disease or to localize
 Nonadrenal mass but usually easy to find; consider MIBG
scintigraphy if CT/MRI ⊖
 Consider genetic testing if bilateral disease, young Pt, ⊕ FHx,
extra-adrenal
TREATMENT
 Surgical Resection
 Pre operative alpha adrenergic blockade,then beta
adrenergic block.
 Alpha adrenergic blockade
10-14 days before surery
Phenoxybenzamine
Daily BP monitoring
High Na diet(>5g/day)-2nd/3rd day ofalpha blockade
Long term alpha adrenerg block.Eg…Zosin
IV Phentolamne-Perioperative
Beta Blockade
Propanolol(1st day),switch to long acting
Catecholamine synsthesis inhibitors ex.Metyrosine
THE END
“In learning you will teach and in
teaching you will learn”-Phill Collins

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Cushing syndrome and Addison disease-Dr.Hamisi Mkindi

  • 1. THE ADRENAL GLAND Topic Review December 14th, 2022 Presenter: Hamisi Mkindi, M.D,Resident,Internal Medicine Supervisor:Prof.Samuel E. Kalluvya: Head of Endocrinology,Diabetes and Infectious diseases,Bugando Medical Center
  • 2. THE ADRENAL GLAND  Under and Over production of hormones  Clinical Conditions and presentations  Diagnostic criteria and managementt
  • 3.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9. ADRENAL INSUFFICIENCY  Adrenal insufficiency can be caused by diseases of the adrenal gland (primary),  Interference with corticotropin (ACTH) secretion by the pituitary gland (secondary)  Interference with corticotropin-releasing hormone (CRH) secretion by the hypothalamus (tertiary)
  • 10. ADRENAL INSUFFICIENCY.. Etiology: Primary = adrenocortical disease = Addison’s disease 1.Autoimmune: isolated or in assoc w/ APS 2.Infection: TB, CMV, histoplasmosis, paracoccidioidomycosis,syphillis 3.Vascular: hemorrhage (usually in setting of sepsis Eg:Warerhouse-Friderichson), adrenal vein thrombosis, HIT, trauma 4.Metastatic disease: (90% of adrenals must be destroyed to cause insufficiency) 5.Deposition diseases: hemochromatosis, amyloidosis, sarcoidosis 6.Drugs: azole antifungals, etomidate (even after single dose), rifampin, anticonvulsants Nelson syndrome
  • 11. ADRENAL INSUFFICIENCY.. Secondary = pituitary failure of ACTH secretion  But aldosterone intact b/c RAA axis  Any cause of primary or secondary hypopituitarism -Hypophysitis  Glucocorticoid therapy (can occur after ≤2 wk of “suppressive doses”; dose effect variable; even <10 mg of prednisone daily chronically can be suppressive  Megestrol (a progestin with some glucocorticoid activity)
  • 12. ADRENAL INSUFFICIENCY Tertiary causes:  Refers to causes that relate to hypothalamic abnormalities that reduce corticotropin-releasing hormone (CRH) secretion.  Abrupt cessation of high-dose glucocorticoid therapy  Correction (cure) of hypercortisolism (Cushing's syndrome)
  • 13. ADRENAL INSUFFICIENCY-Symptoms  Primary or secondary: weakness and fatigability (99%), anorexia (99%), orthostatic hypotension (90%), nausea (86%), vomiting (75%), hyponatremia (88%)  Primary only (extra s/s due to lack of aldosterone and ↑ ACTH): marked orthostatic hypotension (because volume depleted), salt craving, hyperpigmentation (seen in creases, mucous membranes, pressure areas, nipples), hyperkalemia  Secondary only: ± other manifestations of hypopituitarism
  • 14. ADRENAL INSUFFICIENCY-Diagnostic studies  Early a.m. serum cortisol: <3 µg/dL virtually diagnostic; ≥18 µg/dL generally consistent with intact adrenal function  Standard (250 µg) cosyntropin stimulation test (testing ability of ACTH → ↑ cortisol)  Normal = 60-min (or 30-min) post-ACTH cortisol ≥18 µg/dL  Abnormal in primary b/c adrenal gland diseased and unable to give adequate output  Abnormal in chronic secondary b/c adrenals atrophied and unable to respond (very rarely, may be normal in acute pituitary injury b/c adrenals still able to respond→ use early a.m. cortisol instead)  All glucocorticoids (incl creams, inh. & drops) affect test. Must know exposure to interpret.
  • 15.
  • 16. ADRENAL INSUFFICIENCY-Diagnostic studies cont..  Other tests : renin, aldosterone, insulin-induced hypoglycemia (measure serum cortisol response)  Metyrapone (blocks cortisol synthesis and therefore stimulates ACTH, measure plasma 11-deoxycortisol and urinary 17-hydroxycorticosteroid levels)  ACTH: ↑ in 1°, ↓ or low-normal in 2°  Imaging studies to consider pituitary MRI to detect anatomical abnormalities  Adrenal CT: small, noncalcified adrenals in autoimmune, enlarged in metastatic disease, hemorrhage, infection or deposition (although they may be normal-appearing)
  • 17. ADRENAL INSUFFICIENCY- Treatment  Acute insufficiency: volume resusc. w/ normal saline + hydrocortisone IV  Chronic insufficiency: (1) prednisone ~4–5 mg PO qam or hydrocortisone 15–25 mg PO qd (⅔ a.m., ⅓ early p.m.) (2) fludrocortisone (not needed in 2° adrenal insufficiency) 0.05–0.2 mg PO qam (3) backup dexamethasone 4-mg IM prefilled syringe given to Pt for emergency situations
  • 18. ADRENAL CRISIS IN ADRENAL INSUFFICIENCY  Precipitants: bilateral adrenal hemorrhage or infarction, pituitary infarction, pre-existing adrenal insufficiency + serious infection or GI illness  Presentation: shock + anorexia, N/V, abd pain, weakness, fatigue, confusion, coma, fever Lab findings: hyponatremia, hyperkalemia (1°)  Rx: hydrocortisone 50–100 mg IV q8 + IVF; do not delay for dx tests
  • 20. CUSHING SYNDROME  Exogenous  Endogenous -ACTC dependent/ACTH independent
  • 21. HYPERCORTISOLISM-CUSHING SYNDROME  Cushing's syndrome may be either corticotropin (ACTH) dependent or independent.  80 percent of endogenous Cushing's syndrome cases are ACTH dependent, and approximately 20 percent are ACTH independent
  • 22. CUSHING SYNDROME CONT…  Cushing’s syndrome = cortisol excess.  Cushing’s disease = Cushing’s syndrome 2° to pituitary ACTH hypersecretion.
  • 23. Etiologies  Most commonly iatrogenic caused by exogenous glucocorticoids  Cushing’s disease (60–70%): ACTH-secreting pituitary adenoma (usually microadenoma) or hyperplasia  Adrenal tumor (15–25%): adenoma or (rarely) carcinoma  Ectopic ACTH (5–10%): SCLC, carcinoid, islet cell tumors, medullary thyroid cancer,pheo
  • 24.  Routine Labs: -Elevated WBC>11,000/mm3 -Hypokalemia/Metabolic alkalosis due to increased K excretion/Na retention/Water flux
  • 25. Clinical manifestations  Nonspecific: glucose intolerance or DM, HTN, obesity, oligo- or amenorrhea, osteoporosis  More specific: central obesity w/ extremity wasting, dorsocervical fat pads, spont. Bruising  Most specific: proximal myopathy, rounded facies, facial plethora, wide purple striae  Other: depression, insomnia, psychosis, impaired cognition, hypokalemia, acne, hirsutism,  hyperpigmentation (if ↑ ACTH), fungal skin infxns, nephrolithiasis, polyuria
  • 26.
  • 27. Treatment  Surgical: resection of pituitary adenoma, adrenal tumor or ectopic ACTH-secreting tumor, -Or bilat surgical adrenalectomy if unable to control source of ACTH  Medical: cabergoline, pasireotide, mitotane, ketoconazole, or metyrapone to ↓ cortisol, and/or mifepristone to block cortisol action at glucocorticoid receptor; frequently used as bridge to surgery or when surgery contraindicated
  • 28.
  • 29. Treatment-Cont…  Radiation: can do pituitary XRT, but not effective immediately (takes 6 mo to 2 y)  Glucocorticoid replacement therapy × 6– 36 mo after TSS (lifelong glucocorticoid + Mineralocorticoid replacement if medical or surgical adrenalectomy)
  • 30. HYPERALDOSTERONISM  Characterized by excessive secretion of aldosterone which causes increases in sodium reabsorption and loss of K ion and hydrogen ions.  Primary  Secondary
  • 31. HYPERALDOSTERENOSI MS  Primary (adrenal disorders, renin-independent increase in aldosterone) Adrenal hyperplasia (60–70%), adenoma (Conn’s syndrome, 30–40%), glucocorticoid-remediable aldosteronism (GRA; ACTH-dep. rearranged promoter)  Secondary (extra-adrenal disorders, ↑ aldosterone is renin-dependent) -Primary reninism: renin-secreting tumor (rare) -Secondary reninism: renovascular disease: RAS, malignant hypertension; edematous states w/ ↓ effective arterial volume: CHF, cirrhosis, nephrotic syndrome; hypovolemia, diuretics, T2D, Bartter’s (defective Na/K/2Cl transporter), Gitelman’s (defective renal Na/Cl transporter)  Nonaldosterone mineralocorticoid excess mimics hyperaldosteronism 11β-HSD defic. (→ lack of inactivation of cortisol, which binds to mineralocorticoid recept.) Exogenous mineralocorticoids Liddle’s syndrome (constitutively activated/overexpressed distal tubular renal Na channel)
  • 32. Clinical Manifestations  Mild-to-moderate HTN (11% of Pts w/ HTN refractory to 3 drugs.  Headache, muscle weakness, polyuria, polydipsia; no peripheral edema  Classically hypokalemia (but often normal), metabolic alkalosis, mild hypernatremia
  • 33. HYPERALDOSTERENISM- Diagnosis  5–10% of Pts w/ HTN; ∴ screen if HTN + hypoK, adrenal mass, refractory/early onset HTN  Screening: aldo (>15–20 ng/dL) and plasma aldo:renin ratio (>20 if 1°) (off spironolactone & eplerenone for 6 wk); Se & Sp >85%.  ACEI/ARB, diuretics, CCB can ↑ renin activity → ↓ PAC/PRA ratio and βBs may ↑PAC/PRA ratio;∴ avoid. α-blockers generally best to control HTN during dx testing.  Confirm with sodium suppression test (fail to suppress aldo after sodium load) oral salt load (+ KCl) × 3 d, ✔ 24-h urine (⊕ if urinary aldo >12 μg/d while urinary Na >200 mEq/d) or 2L NS over 4 h, measure plasma aldo at end of infusion (⊕ if aldo >5 ng/dL)
  • 34.
  • 35. HYPERALDOSTERONISM- Treatment  Adenoma → adrenalectomy vs. medical Rx w/ spironolactone or eplerenone  Hyperplasia → spironolactone or eplerenone; GRA → glucocorticoids ± spironolactone  Carcinoma → adrenalectomy
  • 37. PHAEOCHROMOCYTOMA  Neuroendocrine neoplasm leads to inappropriate and paroxysmal release of adrenergic agents including epinephrine, norephinephrine, and rarely dopamine  Pressure (hypertension, paroxysmal in 50%, severe & resistant to Rx, occ orthostatic)  Pain (headache, chest pain)  Palpitations (tachycardia, tremor, wt loss, fever)  Perspiration (profuse)  Pallor (vasoconstrictive spell)  Paroxysms can be triggered by meds (eg, β-blockers) abdominal manipulation  Associated with MEN2A/2B, von Hippel Lindau  Up to 40% of pheos/paragangliomas thought to have underlying genetic etiology; genetic testing frequently recommended
  • 38. Phaeochromocytoma-Dx Studies  24° urinary fractionated metanephrines: 85–97% Se, 69– 95% Sp. Screening test of choice if low-risk (b/c false ⊕ with severe illness, renal failure, OSA, labetalol due to assay interference, acetaminophen, TCAs, medications containing sympathomimetics).  Plasma-free metanephrines: 89–100% Se, 79–97% Sp Screening test of choice if high risk, but ↑ rate of false ⊕ in low- prevalence population. False ⊕ rate lower if patient supine for 30 min (estimated 2.8× ↑ false ⊕ if seated)  Adrenal CT generally better than MRI; PET for known metastatic disease or to localize  Nonadrenal mass but usually easy to find; consider MIBG scintigraphy if CT/MRI ⊖  Consider genetic testing if bilateral disease, young Pt, ⊕ FHx, extra-adrenal
  • 39. TREATMENT  Surgical Resection  Pre operative alpha adrenergic blockade,then beta adrenergic block.  Alpha adrenergic blockade 10-14 days before surery Phenoxybenzamine Daily BP monitoring High Na diet(>5g/day)-2nd/3rd day ofalpha blockade Long term alpha adrenerg block.Eg…Zosin IV Phentolamne-Perioperative Beta Blockade Propanolol(1st day),switch to long acting Catecholamine synsthesis inhibitors ex.Metyrosine
  • 40.
  • 41. THE END “In learning you will teach and in teaching you will learn”-Phill Collins

Editor's Notes

  1. Pituitrary hormones from anterior-TSH/ACTH/Gonads-LH-FSH/and growth hormone+prolactin…posterior is ADH/Oxytocin(stored only)made by the hypthalamus. CRH made by the paraventricular necleus of hypothalamus and released at the median eminence from neurosecretory terminals into primary plexus-portal system carries to anterior lobe of pituitary gland and stimulates conrticotropes to release PRO-OPIOMELANOCORTIN which is a precursor for ACTH and alpha msh
  2. Based on receptors we have group1-intracellular and 2 hirmones-cell surface receptors. ACTH acts by binding to specific surface receptors,the melanocortin 2 receptor.MC2R,ACTH upregulated expression of these receptors therefore increasong further response to steroids.Failure of MC2R to activate causes familial glucocorticoid deficiency-rare autosomal disorder xzed by increased ACTH and normalmineral corticoid levels
  3. CYP p450 enzymes involved in biosynthesis of cortcosteroids.Of note are 2 mitochondrial enzymes CYP11B1 and CYP11B2 involved in terminal steps for ortisol and aldosterone symthesis.Restriction of CYP11B2 in(aldosterenone synthase)expression to the ZG is very important physiologically because expression of this enzyme in ZF would render aldostereone production subject to ACTH control.Mutations can occur and this enzyme be expressed in ZF resulting to familial hyperaldosteronims
  4. Binds to specific DNA sequences-glucocorticoid response elements and acts as a transcription factor
  5. Adrenal insufficiency can be caused by diseases of the adrenal gland (primary), interference with corticotropin (ACTH) secretion by the pituitary gland (secondary), or interference with corticotropin-releasing hormone (CRH) secretion by the hypothalamus (tertiary) When Thomas Addison described the disease that now bears his name , bilateral adrenal destruction by tuberculosis was its most common cause. Now tuberculosis accounts for only 7 to 20 percent of cases; autoimmune disease is responsible for 70 to 90 percent, with the remainder being caused by other infectious diseases, replacement by metastatic cancer or lymphoma, adrenal hemorrhage or infarction, or drugs.
  6. Antibodies that react with several steroidogenic enzymes (most often 21-hydroxylase) and all three zones of the adrenal cortex are present in the serum of up to 86 percent of patients with autoimmune primary adrenal insufficiency Autoimmune Polyglandular syndrome. Sex differences — Patients with autoimmune adrenal insufficiency as part of one of the polyglandular autoimmune syndromes are predominantly female (70 percent). In contrast, patients with isolated autoimmune adrenal insufficiency are predominantly male (71 percent) Type I (child onset) :Mucocutaneous candidiasis, hypoparathyroidism, adrenal insufficiency Type II (adult onset) :Adrenal insufficiency, autoimmune thyroid disease, diabetes mellitus type 1 Waterhouse-Friderichson:meningococcemia Before CT/MRI dx of hemorhage was made by autopsies:Hypotension or shock (>90 percent of patients); abdominal, back, flank, or lower chest pain (86 percent); fever (66 percent); anorexia, nausea, or vomiting (47 percent); confusion or disorientation (42 percent); and abdominal rigidity or rebound (22 percent). AIVAMEDED low incidence of clinical adrenal insufficiency in patients with malignant disease is due to the fact that most of the adrenal cortex must be destroyed before hypofunction becomes evident. Other drugs accelerate the metabolism of cortisol and most synthetic glucocorticoids by inducing hepatic mixed-function oxygenase enzymes. They barbiturates and rifampin — Subnormal corticosteroid production during critical illness in the absence of structural defects in the hypothalamic-pituitary-adrenal axis has been termed "functional adrenal insufficiency" or "relative adrenal insufficiency." Large ACTH secreting pituitary tumor-Occurs in pt with Cusing disease who undergo bilaterladrenelectomy without pititary iradiation-localy invasive and difficult to cure and rx by proton therapy
  7. 1-Surgery,Radiation(4-5yr),tumors (primary or metastatic), infection, infiltration (sarcoid, hemochromatosis), autoimmune, ischemia (including Sheehan’s syndrome caused by pituitary infarction intrapartum), carotid aneurysms, cavernous sinus thrombosis, trauma, medications (eg, ipilimumab), apoplexy. 2-(hypothalamic dysfunction or stalk interruption): Tumors (including craniopharyngioma), infection, infiltration, radiation, surgery, trauma
  8. waonavoh
  9. We agree with the Endocrine Society's 2016 Clinical Practice Guidelines and suggest the 250 mcg standard high-dose test
  10. Among all patients presenting with Cushing's syndrome, the most common cause is iatrogenic Cushing's due to exogenous administration of glucocorticoids. The second most common form overall is Cushing's disease (pituitary hypersecretion of ACTH)
  11. Epidemiologically,With active cushing,standardized mortality rate is 1.7-4.7fold greater than general population due to infections,cvd and thrombosis
  12. 1.>2COLLECTIONS DUE TOFALSE –VE,>4X UPPER NORMAL SUGGESTS CS,1-4 INCOCLUSIVE. 2.DST O/N-Plasma Cortisol(At 8-9am) after 1mg at 11 pm <1.8mcg/dl(<50nm/l) no CS 3.Salivary free cortisol-Midnight salivary cortisol>5nmol/l Once you have biomedicaly confirmed that is CS,NEXT STEP ACT dependent(ACTH 15-20) and ACTHindependent(ACTH<5ng/l) by using ACTH AND CORTSOL MENASUREMENT
  13. Principal regulators of aldosteone synthesis are and secretion are RAS and K ion concentration and minor regulators are ACTH,ANP
  14. 11 beta hydroxysteroid dehydrogenase.Named after JW Conn,1st described in 1955 in a pt who had htn with aldosterone producing adenoma. Con syndrome triad:HTN/Hypokalemia/Metabolic alkalosis
  15. Plasma aldosterone concentration,Plasma renin activity
  16. Catecholamine secreting tumor formed by chromaffin cells within the adrenalmedulla.Etiology idiopathic,but ca have a genetic component.Some of the genetic conditions like MENIIA/IIB,Von Hippel Lindau.Classic triad-Episodic pounding headache,Palpitations and tacycardia,diaphoresis.
  17. If >2x ULN +ve
  18. Surgical resection-often curative. Once achieved alpha adrenergic blockade now move to beta blockade Phenoxybenzamine-alpha blockade
  19. 4% of Pts undergoing abdominal CT scan have incidentally discovered adrenal mass; prevalence ↑ with age Differential diagnosis Nonfunctioning mass: adenoma, cysts, abscesses, granuloma, hemorrhage, lipoma,myelolipoma, primary or metastatic malignancy Functioning mass: pheochromocytoma, adenoma (cortisol, aldosterone, sex hormones),nonclassical CAH, other endocrine tumor, carcinoma
  20. From phil collins song-Son of a Man