Transcript Document

Endocrine Physiology: Case
Studies in Adrenal Disorders
C.W. Spellman, PhD, DO
Assoc. Prof. Medicine
Assist. Dean, Dual Degree Program
Head, Endocrinology & Dir. Diabetes Clinics
UNTHSC
Reference Lab Values for Cases
Glucose
Na
K
HCO3
BUN
Creatinine
Calcium
Hb
60 -110 mg/dL
136 -144 mEq/dL
3.8 - 5.4 mEq/dL
23 - 26 m Eq/dL
8 - 14 mg/dL
0.6 - 1.5 mg/dL
8.5 - 10.5 mg/dL
13.5-15.5 g/dL
Reference Values, cont.
ACTH
TSH
a.m. Cortisol
ACTH Stim. cortisol
10 - 75 pg/ml
0.3 - 5.0 mIU/ml
5 - 25 g/dl
>18 - 20 g/dl or
7 g/dl > baseline
24 h urine free cortisol 10 - 50 ug/24 hr
Aldosterone
<10 ng/dl
Aldosterone : renin
<20
Cushing’s Syndrome
Cushing’s syndrome:
Excess glucocorticoids due to
Pituitary tumor
70 - 80%
Adrenal tumor
10 - 20%
Ectopic ACTH tumor
10%
Iatrogenic
“Classic” syndrome:
Weight gain, Plethora, Striae, HTN,
Proximal muscle weakness
Clinical Features of Cushing’s
Syndrome
Weight gain
“Moon face”
HTN
Striae
Hirsuitism
Glucose intol
Muscle weak.
Plethora
90%
75%
75%
65%
65%
65%
60%
60%
 Menses
60%
Acne
40%
Bruising
40%
Osteopenia 40%
Edema
40%
Hyperpig.
20%
K+ meta. alk. 15%
Case 1: Young Lady With Weight
Gain
A 24 y lady was in good health in the
Spring of 1999. She married in August and
her husband brought her to the Endocrine
clinic in December.
Complaints
80 lb weight gain
Fatigue
“Stretch marks”
Shortness of breath
Case 1, cont.
PE: BP=180/100 HR=84 RR=20 T=99
Ht=65” Wt=250 lbs
HEENT:  buccal fat
Neck:  dorsal fat
Chest:  supraclavicular
Lung: CTA
Cor:
RRR, no S3 or S4, normal PMI
Abd:
Obese
Extrem: Thin, prox. muscle weakness
Skin:
Wide red striae, ecchymoses
Neurol: normal
Case 1, cont.
Lab evaluations
Na
136
K
3.6
Gluc 190
Cr
0.9
Case 1, Questions
What do you think the diagnosis is?
If the lesion was in the pituitary, predict:
ACTH
Cortisol
If the disease was in the adrenals, predict:
ACTH
Cortisol
If the lesion was an ectopic tumor, predict:
ACTH
Cortisol
Case 1, Questions
How could you determine if this lady had
adrenal disease? Pituitary tumor? Ectopic
tumor?
Why is the glucose elevated?
Why is she weak?
What are the skin changes due to?
Why has she gained weight?
Why is the potassium low?
Clinical Features of Primary
Adrenal Insufficiency
Gradual onset
Weakness & fatigue
Wt loss/anorexia
Hyperpigmentation
Hypotension / tachycardia
Hyponatremia
Hyperkalemia
Muscle, GI pain
>95%
100%
100%
92%
88%
88%
64%
56%
Clinical Features of Secondary
Adrenal Insufficiency
Gradual onset
Weakness & fatigue
Wt loss/anorexia
Pale
Hair loss
Anemia
Electrolytes usually normal
>95%
100%
100%
100%
<50%
<50%
Case 2: Medical Student with
Weakness, Fatigue and Nausea
25 y 2nd y medical student develops
weakness, fatigue and nausea. She is
unable to complete the OB-GYN rotation.
The OB attending briefly evaluates the
student, suspects and endocrine problem
and refers her to our clinics.
Case 2, cont
PE: BP=90/60 HR=96 RR=16 T=98
Ht=68” Wt 130 lbs
HEENT: nor
Neck:
nor
Lung:
nor
Cor:
nor
Abd:
nor
Extrem: nor
Skin:
uniformly tan
Neurol: nor
Case 2, cont
Lab
Na
K
Glucose
TSH
Hb
124
5.9
70
1.55
15.4
Case 2, Questions
What do you think the diagnosis is?
If the lesion was in the adrenals, predict:
Cortisol
Aldosterone
ACTH
Why is the sodium low?
Why is the potassium high?
If the lesion was in the pituitary, predict:
Cortisol
Aldosterone
ACTH
Case 2, Questions
If the patient had secondary disease, how
would the physical examination have been
different?
If the patient had secondary disease, how
would the electrolytes have been different?
Aldosteronism
Old name: Conn’s syndrome
2x more common in ♀ than ♂
Occurs 30 – 50 y age group
Si/Sx
Diastolic HTN
Headache
Hypokalemia
LVH occurs
Renal disease
50% develop proteinuria
15% develop renal failure
Aldosteronism
Older data suggest that <1% of HTN is due
to aldosteronism
New data suggest that up to 10% of HTN is
due to aldosteronism
Suspect aldosteronism:
Diastolic HTN
Hypokalemia (K ~ ≤3 meq/L)
Causes of Aldosteronism
Aldosterone-producing adenoma
75% of cases of aldosteronism
Usually solitary nodules (0.5 - 2.5 cm)
Almost always benign
Causes of aldosteronism
Adrenocortical hyperplasia
a. 25% of cases of aldosteronism
b. Bilateral hyperplasia
c. Rarely produces hormones other
than aldosterone
Causes of Aldosteronism
Other causes
1. Adrenal carcinoma is extremely rare
2. Congenital adrenal hyperplasia
Produces mineralocorticoids
other than aldosterone
3. Secondary aldosteronism
High aldosterone is secondary to
high renin levels
Case 3: Young Man with
Hypertension
A 25 y male presents to the clinic as a
new patient. He takes no prescription
medications, over-the-counter products
or “alternative substances”
He came because his wife, a PA, noted
hypertension and scheduled the visit
Case 3, cont.
PE: BP=170/104 HR=72 RR=16 T=98
Ht=72” Wt=195 lbs
HEENT: nor
Neck:
nor
Chest: nor
Abd:
nor
Extrem: nor
Skin:
nor
Neurol: nor
Case 3, cont.
Lab
CMP
TSH
normal, except K=2.9
nor
Case 3, Questions
What do you think the diagnosis is?
How common is this disorder?
Predict the laboratory results of:
Aldosterone
Renin
Cortisol
Why does this patient have hypertension?
Why is the potassium low?
Case 3, Questions
What are possible causes of the problem?
Discuss primary causes
Discuss secondary causes
How would you differentiate primary from
secondary causes?
Can you illustrate the physiology of
primary and secondary disease?
Secondary Aldosteronism
Secondary aldosteronism refers to
appropriate increased production of
aldosterone in response to activation of the
renin-angiotensin system
Primary aldosteronism
Secondary Aldosteronism
 Vol
 Vol
 Na
 Renin
 Aldo
 Na
 Renin
 Aldo