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Internal Medicine pt.1 > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What are the layers that secrete the adrenal hormones?

A
  • Zona Glomerulosa -> mineralcorticoids -> aldosterone
  • Zona Fasiculata -> glucocorticoids -> Cortisol
  • Zona Reticularis -> androgens -> sex hormones (dihydrotestosterone & estradiol)
  • Medulla -> epinephrine & norepinephrine
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2
Q

Which enzyme is responsible for the formation of the sex hormones & cortisol?

A

17a -> for both

21 & 11B -> cortisol only

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3
Q

Which enzymes are responsible for the formation of aldosterone?

A

21 & 11B

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4
Q

if there is a deficiency in enzyme 17a, what will be affected?

A
  • NO cortisol & NO sex hormones

- aldosterone will increases -> Conn’s disease

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5
Q

if there is a deficiency in enzyme 21, what will be affected?

A
  • NO aldosterone & NO cortisol

- increase in sex hormones -> adrenogenital syndrome

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6
Q

if there is a deficiency in enzyme 11B, what will be affected?

A
  • NO aldosterone & NO cortisol but their precursors are present
  • so there is an increase in sex hormones but no syndrome
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7
Q

What will occur in case of any adrenal hormone deficiency?

A
  • positive feedback to the pituitary gland to secrete more ACTH -> which will cause hyperplasia in the adrenal gland -> leading to an increase in the only normal pathway while the rest are still deficient
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8
Q

What is the function of aldosterone?

A
  • Na & H20 retention
  • K excretion
  • increases blood volume -> increases blood pressure
  • vasoconstriction
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9
Q

What are the factors that increase aldosterone?

A
  • dehydration
  • hypovolemia
  • hyponatremia (decreased sodium)
  • hypotension
  • renin from the kidney -> increases angiotensinogen (liver) -> increases angiotensin I -> ACE (lungs) -> ANGIOTENSIN II -> increases aldosterone
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10
Q

What are the metabolic effects of cortisol?

A

1- on fat: mobilization
- if excess -> deposition in abnormal sites (face, neck, & abdomen)

2- on proteins -> anabolism
- if excess -> catabolism (muscle wasting & osteoporosis)

3- on carbs -> increase gluconeogenesis
- in excess -> decreased glucose uptake by muscles & hyperglycemia

4- on electrolytes -> Na & H20 retention & K excretion

5- on blood -> increases RBCs & decreases eosinophils & lymphocytes

6- androgenic
7- anti-allergic -> decreases Ag-Ab reaction
8- anti-inflammatory
- in excess -> decreases fibrous tissue formation (collagen) & destroys elastic fiber & decreases inflammatory cells

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11
Q

What are the functions of the Zona Reticularis hormones?

A

androgens & small amounts of estrogen & progesterone

  • dehydro-epiandrosterone -> enhances protein anabolism & promotes development of secondary sexual characters
  • end product (ketosteroids) are excreted in the urine (used for diagnosis)
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12
Q

What are the causes of Conn’s syndrome?

A

Primary hyperaldosteronism

  • adenoma
  • hyperplasia of Zona glomerulosa
  • carcinoma
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13
Q

What is the clinical picture of Conn’s syndrome?

A

1- hypertension: due to sodium retention

2- hypokalemia

  • apathy, paresthesia
  • arrhythmias (extrasystoles)
  • atony of the intestines (constipation & paralytic ileus)
  • muscle weakness & episodic paralysis (dyspnea)
  • impaired glucose tolerance test

3- alkalosis (metabolic)
- due to heavy loss of H+ with K in urine -> tetany due to decreased ionized calcium

4- NO EDEMA

  • K diuresis -> polyuria
  • impaired tubular reabsorption of water
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14
Q

What investigations are done in Conn’s disease?

A

1- BIOCHEMICAL

  • hypokalemia (N = 3.5 - 5)
  • hypernatremia (N=140)
  • alkalosis (increased serum HC03) (N= 22 - 30)

2- URINARY

  • polyuria -> due to K diuresis
  • increased K & decreased sodium
  • increased aldosterone excretion (N= 12-50 ug/24h)

3- MEASURE PLASMA LEVELS

  • decreased Renin
  • increased aldosterone despite high Na load

4- US & adrenal CT -> for adenoma & carcinoma

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15
Q

How is Conn’s syndrome treated?

A
  • Surgical removal of adenoma

- MEDICAL in bilateral & hyperplasia -> Amiloride (K-sparing diuretics)

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16
Q

What are the causes of Cushing’s syndrome?

A

ENDOGENOUS tumors
1- pituitary adenoma -> secondary hypercortisol
2- adrenal -> primary Cushing’s syndrome
3- paramalignant -> increases ACTH -> increases cortisol

EXOGENOUS -> corticosteroids (most imp)

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17
Q

What are the general clinical features of Cushing’s syndrome?

A

1- abnormal fat deposition

  • face -> moon face
  • neck -> buffalo hump
  • abdomen -> trunkal obesity (Samboxa shooed obesity)

2- protein catabolism

  • Muscle wasting & weakness
  • osteoporosis

3- hyperglycemia -> steroid diabetes (one of the most imp causes of secondary diabetes)

4- Hypertension (sodium & water retention) & hypokalemia (polyuria & alkalosis)

5- plethoric face due to polycythemia (increase RBCs)

6- in females -> amenorrhea, acne, & hirsutism
- in males -> decreased libido, impotence

7- decreases collagen & fibrous tissue formation (delayed wound closure)

  • bruises & purpura
  • STRIA RUBRA (rupture of weakened s.c tissue due to collagen deficiency)

8- decreases WBCs (eosinophils & lymphocytes) -> more prone to infection

8-

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18
Q

What are the clinical features that will help us identify the etiology?

A
  • virilization -> adrenal carcinoma (increase cortisol & androgens)
  • hypokalemic alkalosis, myopathy, & hyperpigmentation -> ectopic (paramalignant)
  • in children -> adrenal carcinoma
  • in males -> ectopic
  • in women -> pituitary
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19
Q

What are the investigations that suggest Cushing syndrome?

A

1- hypokalemic alkalosis & hypernatremia
2- increased RBCs & decreased lymphocytes & eosinophils
3- impaired glucose tolerance or DM
4- osteoporosis or unexpected fractures (in young patients too young for osteoporosis)

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20
Q

Which investigations confirm the diagnosis of Cushing syndrome?

A

1- plasma cortisol level (N= 5 - 20) -> taken at 8am then 4pm

  • should be higher in the morning & 50% less in the afternoon
  • loss of diurnal variation suggests persistent elevation

2- urinary steroid excretion (24hr collection)

  • measure hydroxycorticosteroids or free urinary cortisol
  • if found in excess overnight
  • > do LOW DOSE dexamethasone suppression test (1mg ORAL at night)
  • after suppression test take a sample at 8am it SHOULD BE <7 (if not then Cushing’s)
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21
Q

What are the investigations that will help us differentiate between the 3 types of Cushing syndrome?

A

1- measure plasma ACTH

  • very high -> Ectopic
  • High -> pituitary
  • low or absent -> adrenal

2- HIGH DOSE dexamethasone suppression test

  • 2mg every 6hrs IV for 2 days
  • if pituitary Cushing’s -> plasma cortisol decreased
  • if ectopic or adrenal -> NO EFFECT

3- localization imaging

  • abdominal US, CT, retrograde venography -> adrenal tumors
  • sellar x-ray -> brain tumors (pituitary)
  • chest x-ray -> bronchogenic carcinoma (ectopic)
22
Q

What are the causes of pseudo-Cushing syndrome?

A
  • chronic alcoholism
  • severe illness
  • obesity
  • depression

increase in cortisol levels & absent diurnal variation

23
Q

What is the treatment for pituitary Cushing syndrome?

A

Surgical removal

24
Q

What is the treatment of adrenal cushing?

A

REMOVAL

  • pre-op -> give metyrapone to decrease cortisol levels
  • post-op -> give mitotane for residual disease
25
Q

What is the treatment for ectopic cushing’s?

A
  • treat original tumor
  • surgical removal
  • metyrapone +- mitotane
26
Q

How is exogenous Cushing’s treated?

A

STOP using corticosteroids

27
Q

What are the causes of Addison’s disease?

A

1- autoimmune adrenalitis (most common)
- can occur with other auto-immune diseases
2- miliary TB
3- following bilateral adrenalectomy & congenital enzymatic defects
4- amyloidosis, sarcoidosis, hemochromatosis
5- secondary to hypopituitarism (Simmonds disease)

28
Q

What are the clinical features of Addison’s disease?

A

deficiency in all hormones of the adrenal gland
ADDISONS TRIAD: hypotension + hypoglycemia + hyperpigmentation

1- asthenia: weakness of muscles & weight loss
2- hypotension: systolic BP <110mmg & postural hypotension (hypovolemia)
3- hypoglycemia
4- hyperpigmentation
5- loss of adrenal androgen: infertility & amenorrhea in females
6- GIT disturbances: nausea, vomiting, diarrhea
7- polyuria -> Na diuresis (could lead to severe dehydration)

29
Q

What is the cause of Asthenia in Addison’s disease?

A
  • lack of cortisol -> decreases RBCs -> anemia
  • hyperkalemia -> arrhythmia & muscle weakness
  • hypoglycemia
  • muscle cramps -> hyponatremia
30
Q

What is the cause of postural hypotension in Addison’s disease?

A
  • NO sodium -> NO vasoconstrictrion -> rapid drop of BP
    &
  • hypovolemia & dehydration
31
Q

What is the cause of hyperpigmentation in Addison’s disease?

A

1- hypocorticism -> increases ACTH -> increase melanocyte stimulating hormone -> increases pigmentation (primary hypoadrinalism)

2- destruction of adrenal medulla -> accumulation of tyrosine -> shifted to form melanin instead of epinephrine & norepinephrine

32
Q

What are the investigations preformed to diagnose Addison’s disease?

A

1- plasma cortisol level decreased
2- decreased 24hr urinary cortisol or ketosteroids
3- ACTH stimulation test
- normal response -> increase plasma cortisol by 6ug above basal value
- in primary adrenal insufficiency -> no response
- in secondary adrenal insufficiency -> normal response (increased cortisol)
4- biochemical changes: hyponatremia, hyperkalemia, acidosis, hypoglycemia
5- urine -> increased volume (Na diuresis) & decreased K excretion
6- blood
- normochromic anemia
- haemoconcentration
- eosinophilia & lymphocytosis

33
Q

What is the treatment of Addison’s disease?

A

1- replacement therapy -> prednisolone (cortisol)
-> fludrocortisone (aldosterone)
2- treat the cause

3- management during stressful conditions

  • MINOR illness -> double the dose until condition is resolved
  • MAJOR elective surgery -> 100mg (high dose) hydrocortisone the night before & 100mg every 8 hours after surgery -> taper it to reach the previous dose within the next 3 - 5 days
  • MAJOR emergencies (treated like addisonian crises) -> fluids, hydrocortisone & fludrocortisone, treat the cause
34
Q

What are the causes of Addisonian crises?

A

1- after sudden corticosteroid withdrawal (most imp)
2- previously undiagnosed patient
3- patient on treatment that underwent a major catastrophe without increasing their dose
4- Sheehan sydrome
5- after bilateral adrenalectomy
6- acute meningococcal septicemia (waterhouse friderichsen syndrome) -> hemorrhage -> acute adrenal failure
7- medical treatment for adrenal carcinoma (metyrapone or mitotane)
8- massive thrombosis of adrenal veins (during pregnancy, puerperium & burns)

35
Q

What are the clinical features of Addisonian crises?

A

sudden onset of

  • severe weakness
  • mental confusion
  • anorexia, nausea, vomiting, diarrhea
  • dehydration -> shock
  • coma & death within 24 hours if untreated (from severe hypoglycemia, hypotension, dehydration)
36
Q

What investigations are done to confirm addisonian crises?

A
  • severe hyponatremia
  • hyperkalemia
  • severe decrease in serum cortisol
37
Q

What is the treatment method for addisonian crises?

A

1- IV normal saline & glucose
2- hydrocortisone 100mg IV then every 8 hours 100mg-> taper until reaching the previous dose
3- fludrocortisone
4- treat cause

38
Q

What is the adrenogenital syndrome?

A

inherited enzymatic defects in the enzymes necessary for the synthesis of cortisol -> increased ACTH adrenal hyperplasia & synthesis of the other hormones

39
Q

What are the clinical features of enzyme 17 oH ase deficiency?

A

NO cortisol NO sex hormones INCREASED aldosterone

  • Hypertension
  • in females -> sexual infantilism
  • in males -> pseudohermaphroditism
40
Q

What are the clinical features of enzyme 21 oH ase deficiency?

A

most common
NO aldosterone NO cortisol INCREASED sex hormones
- hypotension
- hyperkalemia
- female pseudohermaphroditism (big clit, small vagina, libra majora are big & fused)
- male precocious puberty (macrojenitosmia praecox) but no spermatogenesis & dwarfism

41
Q

What are the clinical features of enzyme 11B oH ase deficiency?

A

NO cortisol NO aldosterone but deoxycorticosterone & deoxycortsol & androgens are present

  • hypertension
  • virilization in females pseudohermaphroditism
  • precocious puberty
42
Q

What is the treatment of adrenogenital syndrome?

A

1- replacement therapy -> prednisone (7.5mg/day) & fludrocortisone (o.1mg/day)
2- surgical correction -> female pseudohermaphroditism

43
Q

What is pheochromocytoma?

A 
catecholamine releasing tumor (commonly benign) 
rule of 90% 
- unilateral 90%- bilateral 10%
- benign 90% - malignant 10% 
- adrenal 90% - extra adrenal 10% 
- adults 90% - children 10%

Familial types -> MEN II

44
Q

What are the clinical manifestations of pheochromocytoma?

A

sympathetic overactivity
1- attacks of one or more times/week for < 1 hr
- vasoconstriction -> cold hands & feet & pallor
- hypertension
2- complications of hypertension on CVS & CNS
3- constipation & ischemic enterocolitis
4- diabetogenic (anti-insulin)

45
Q

What are the investigations done for pheochromocytoma?

A

1- urine examination

  • 24hr metanephrine (for diagnosis)
  • free urinary catecholamines
  • VMA 24hrs (only for screening)

2- plasma catecholamine

3- stimulation test is very dangerous

4- clonidine suppression test

  • in normal hypertension -> plasma NA decreases to normal rage 3 hours after taking clonidine
  • inn pheochromocytoma -> no response

5- localization of tumor

46
Q

How is pheochromocytoma treated?

A

1- MEDICAL

  • acute therapy for patients with severe hypertension: Phentolamine (a blocker) THEN propranolol
  • prolonged medical therapy -> if surgery is delayed

2- SURGICAL

  • PRE-OP -> Na nitroprusside or phentolamine to stabilize blood pressure
  • surgical removal of tumor
47
Q

What is the difference between MENI & MENII syndromes?

A

MEN I (Wermer’s syndrome)

  • parathyroid
  • pituitary
  • pancreas

MEN II (Simple’s syndrome)

  • pheochromocytoma
  • medullary thyroid carcinoma
  • parathyroid adenoma
48
Q

How do we diagnose hypogonadism?

A
  • decrease in LH & FSH -> pituitary cause (hypogonadotrophic gonadism)
  • increase LH & FSH but decreased testosterone -> primary testicular disease
  • normal or elevated LH & FSH & testosterone -> end organ resistance
  • decreased testosterone with no features of hypogonadism -> decreased sex hormone binding globulin (SHBG)
49
Q

How do we treat hypogonadism?

A
  • androgen replacement -> IM
  • pituitary causes -> like before
  • hypothalamic causes -> LHRH
50
Q

What are the types of hair?

A
  • Lanugo -> in fetus & newborn
  • Vellus -> fine adult hair covering body
  • Terminal hair -> thick pigmented hair on scalp & pubic area
51
Q

What are the causes of Hirsutism?

A

ANDROGEN INDEPENDENT

  • constitutional, familial, racial
  • starvation & anorexia
  • drugs: minoxidil, phenytoin, diazoxide

ANDROGEN DEPENDENT

  • ovarian -> arrenoblastoma, idiopathic hirsutism, PCO
  • adrenal -> virilizing adrenal tumor, congenital adrenal hyperplasia, Cushing’s
  • drugs -> androgens

drugs that hinder action of androgen on hair follicles

  • ketoconazol
  • spironolactone
  • cyproterone acetate

Internal Medicine pt.1 (33 decks)

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