IM Endo Flashcards
1
Q
panhypopituitarism
etiology
A
caused by any condition that compresses or damages the pituitary gland. tumors of many types can copmress the gland such as mets, adenomas, rathke cleft cysts, meningiomas, craniopharyngiomas, or lymphoma. trauma and radiation are damaging to the pituitary. conditions such as hemochromatosis, sarcoidosis, and histiocytosis x or infection with fungi, tb, and parasites infiltrate the pituitary destroying its function. finally, ai and lymphocytic infilatration can damage the gland
2
Q
panhypopituitarism
presentation
A
the sx are based on the deficiencies of the specific hormone
3
Q
ultimately, anything that damages the brain, from tumor to stroke to infection can cause
A
panhypopituitarism
4
Q
panhypopituitarism
prolactin deficiency
A
there are never any symptoms of prolactin deficiency in men
in women prolactin deficiency inhibits lactation after childbirth
5
Q
panhypopituitarism
lh and fsh
A
women will not be able to ovulate or menstruate normally and will become amenorrheic
men will not make testosterone or sperm, ed and decreased muscle mass
both will have decreased libido and decreased axillary pubic and body hair
6
Q
kallman syndrome
A
decreased fsh and lh from decreased gnrh
anosmia
renal agenesis in 50%
7
Q
panhypopituitarism
gh deficiency
A
children present with short stature and dwarfism
adults have fewer sx of GH deficiency bc several other hormones such as catecholamines, glucagon, and cortisol act as stress hormones:
central obesity
increased ldl and cholesterol levels
reduced lean muscle mass
8
Q
hyponatremia is common secondary to hypothyroidism and isolated glucocorticoid underproduction
A
k levels remain normal bc aldosterone is not affected and aldosterone excretes k
9
Q
mri detects compressing mass lesions on the
A
pituitary
10
Q
low tsh and thyroxine
confirmatory test
A
decreased tsh response to trh
11
Q
decreased acth and decreased cortisol
confirmatory test
A
normal response to cosyntropin stimulation of the adrenal. cortisol will rise (adrenal is normal) in recent disease, but abnormal in chornic disease bc of adrenal atrophy
no response in acth level with crh
an elevated baseline cortisol level excludes pituiatry insufficiency
12
Q
decreased lh and fsh levels
decreased testosterone levels
confirmatory test
A
no confirmatory test
13
Q
G levels low, but this finding is not helpful since GH is pulsatile and maximum at night
confirmatory test
A
no response to arginine infusion
no response to GH releasing hormone
14
Q
prolactin level low, but not helpful
confirmatory test
A
no response to TRH
15
Q
metyrapone
A
inhibits 11 beta hydroxylase. this decreases the ouput of the adrenal gland, so it should cause ACTH levels to rise bc cortisol goes down and it negatively inhibits ACTH
16
Q
insulin stimulation
A
when insulin decreases glucose levles, GH should usually rise. Failure of GH to rise in response to insulin indicates pituitary insufficiency
17
Q
treatment for panhypopituarism
A
replace deficient hormones with:
cortisone
thyroxine
testosterone and estrogen
recombinant human growth hormone
18
Q
replace cortisol before starting
A
thyroxine
19
Q
posterior pituitary
A
the 2 products of the posterior pituitary are ADH and oxytocin, there is no deficiency disease described for oxytoxin. oxytocin helps uterine contraction during delivery but delivery still occurs even if it is absent. adh deficiency is also known as central diabetes insipidus
20
Q
diabetes insipidus
definition
A
a decrease in either the amount of ADG from the pituitary (central) or its effect on the kidney (nephrogenic)
21
Q
diabetes insipidus
etiology
A
Central: any destruction of the brain from stroke tumore trauma hypoxia or infilatration of the gland from sarcoidosis or infection can cause CDI
Nephrogenic: a few kidney disease such as chronic pyelonephritis amyloidosis myeloma or sickle cell disease will damage the kidney enough to inhbit the effect of ADH. Hypercalcemia and hypokalemia alo inhibit adh’s effect on the kidney
22
Q
diabetes insipidus
presentation
A
di presents with extrmeely high-volume urin and excesssive thirst resulting in volume depletion or hypernatremia, when hypernatremia is severe there will be neurological sx such as confusion disorientation lethargy and evventually seizures and coma. neurological sx occure only when volume losses are not matched with drinking enough fluid
23
Q
lithium is a classic cause of
A
NDI
24
Q
when to do a vasopressin test
A
excessive thirst > increase in urine volume, and decrease in urine osmolarity and sodium > decrease in serum volume and a increase in serum osmolality and sodium > do desmopressin stimulation test
25
diabetes insipidus
diagnostic tests
serum sodium is elevated when oral replacement is insufficient. Urine osmolality and urine sodium are decreased. serum osmolailty which is largely a function of serum sodium is eleveated. urin volume is enormous
the difference between central and nephrogenic di is determined by the response to vasopressin. in central di urine volume will decrease and urine osmolality will increase. with nephrogenic di there is no effect of vasopressing on urine volume or osmolality
26
diabetes insipidus
treatment
central di is treated with long term vasopressin (desmopressin) use.
nephrogenic di is managed by trying to correct the underlying cause, it also responds to hctz, amiloride and prostaglanding inhibitors such as nsaids (eg indomethacin)
27
Vasopressin (desmopressin) stimulation test
Urine volume decrease and osmolality increase > dx is central diabetes insipidus > treat with vasopressin
No effect on urine > dx is nephrogenic diabetes insipidus > treatment is to treat underlying cause, hctz, amiloride and nsaids
28
acromegaly
definition
the overproduction of gh leading to soft tissue overgrowth throughout the body
29
acromegaly
etiology
alnost always caused by a pituitary adenoma, can be associated with multiple endocrine neoplasias when it is combined with parathyroid and pacreatic disorder like gastrinoma or insulinoma. rarely it is caused by ectopic gh or ghrh production from a lymphoma or bronchial carcinoid
30
acromegaly
presentation/what is the most likely dx
causes enlargement in soft tissue like cartilage and bone:
increased ring hat and shoe size
carpal tunnel sydrome and obstuctive sleep apnea from soft tissues enlarging
body odor from sweat glandy hyptertrophy
coarsening facial features and teeth widening from jaw growth
deep voice and macroglossia (big tongue)
colonic polyps and skin tags
arthalgias from joints growing out of alignment
htn for unclear resons in 50%
cardiomegaly and CHF
ed from incrased prolactin taht is cosecreted with the pituitary adenoma
31
GH abuse can give the same presentation of
acromegaly
32
acromegaly
diagnostic tests
lab tests will show glucose intolerance and hyperlipidemia, which contribute to cardiac dysfunction.
the best inital test is a level of insulinlike growth factor (IGF-1).
the most accurate test is the glucose suppression test. normally glucose should suppress growth hormone levels
mri should be done only after the laboratory identification of acromegaly
33
acromegaly
treatment
surgery: it resonds to transpenoidal transection of the pituitary in 70% of cases. larger adenomas are harder to cure
medications
cabergoline: dopamine will inhibit GH release
octreotide or lanreotide: somatostatin inhibits GH release
pegvisomat: a gh receptor antagonist it inihbits IGF release from the liver
radiotherapy: radiation is used only in those who do not respond to surgery or medications
34
prolactin levels are tested bc of cosecretion with
growth hormone
35
hyperprolactinemia
etiology
high prolactin levels can seem confusing bc so many causes have nothing to with a pituitary adenoma. prolactin can be cosecreted with GH, and increase simplybecause of acromegaly. hypothyroidism lease to hyperprolactinemia bc extremely high trh levels will stimulate prolactin secretion
36
physiologic causes of hyperprolactinemia
pregnancy
intense exercise
renal insufficiency
increased chest wall stimulation
cutting the pituitary stalk eliminated dopamine delivery to the anterior pituitary. dopamine inhibits prolactin release
37
drugs taht cause hyperprolactinemia
antipsychotic medications, methyldopa, metoclopromide, opiods, tca's, and verapamil all raise prolactin levels
38
verapamil is the only ccb to raise
prolactin level
39
hyperprolactinemia
presentation
women present with glactorrhea, amenorrhea, and infertility.
men have ed and decreased libido, gynecomastia, galactorrhea is rare
40
do not do an mri of the head first in
any endocrine disorder
41
Hyperprolactinemia
diagnostic tests
after the prolactin level is found to be high, perform:
thyroid function tests
pregnancy test
BUN/creatinine (kidney disease elevates prolactin)
liver function tests (cirrhosis elevates prolactin)
MRI is done after:
high prolatin level is confrimed
secondary causs liek medication are excluded and
the pt is not pregnant
42
hyperprolactinemia treatment
Dopamine agonists: cabergoline is better tolerated than bromocriptine
transphenoidal surgery is appropriate for those not repsonidng to medications
radiation is rarley needed
43
always exclude pregnancy first in any woman with a high
prolactin level
44
hypothyroidism
etiology
hypothyroidism is almost always from a single cause: failure of the thyroid gland from burnt-out hashimoto thyroiditis. the acute phase is rarely perceived. occasionally pts have hypthyroidism from:
dietary deficiency of iodine
amiodarone
45
hypothyroidism
what is the most likely dx
hypothyroidism is characterized by almost all bodily processes being slowed down-except mentrual flow, which is increased
when TSH is bery high (more than double th eupper limit of normal) with normal T4, replace hormone.
when TSG is ess than double the normal, get antithyroid peroxidase/antithyroglobulin antibodies. if antibodies are positivt, replace thyroid hormone.
46
High TSH (double normal) + normal T4 =
treatment
47
what to look for in hypothyroidism
```
bradycardia
constipation
weight gain
fatigue, lethargy, coma
decreased reflexes
cold intolerance
hypothermia (hair loss, edema)
```
48
what to look for in hyperthyroidism
```
tachycardia, palpitations, arrhythmia (atrial fibrillation)
diarrhea (hyperdefecation)
weight loss
anxiety, nervousness, restlessness
hyperreflexia
heat intolerance
fever
```
49
antithyroid peroxidase antibodies tell who needs thyroid replacement when
T4 is normal and TSH is high
50
hypothyroidism
diagnostic tests
all thyroid disorders are best tested first with a TSH. if the TSH level is supressed, measure T4 levels. TSG levels are markedly elevated if the gland has failed
51
hypothyroidism
treatment
replacing thyroid hormone with thyroxine (synthroid) is sufficient
52
Hyperthyroidism types
graves
subacute thyroiditis
painless "silent" thyroiditis
exogenous thyroid hormone use
pituitary adenoma
53
only graves disease has
eye and skin abnormalities
TSH receptor antibodies
54
what is the most likely dx
graves disease
eye (proptosis) (20-40%) and skin (5%) findings
55
what is the most likely dx
subacute thyroiditis
tender thyroid
56
what is the most likely dx
painless "silent" thryoiditis
nontender, normal exam results
57
what is the most likely dx
exogenous thyroid hormone use
involuted gland is not palpable
58
what is the most likely dx
pituitary adenoma, thyroid
high TSH level
59
hyperthyroidism
diagnostic tests
all forms of hyperhytoidism have an elevated T4 (thyroxine) level.
only pituitary adenomas will ahve a high TSH level. in all others the pituitary release of TSH is inhibited
60
Lab findings in hyperthyroidism
graves disease
TSH: low
RAIU: elevated
Confirmatory: positive antibody testing
61
Lab findings in hyperthyroidism
subacute thyroiditis
TSH: low
RAIU: decreased
Confirmatory: tenderness
62
Lab findings in hyperthyroidism
painless "silent" thyroiditis
TSH: low
RAIU: decreased
Confirmatory: none
63
Lab findings in hyperthyroidism
exogenous thyroid hormone use
TSH: low
RAIU: decreased
Confirmatory: history and involuted nonpalpable gland
64
Lab findings in hyperthyroidism
pituitary adenoma
TSH: high
RAIU: not done
Confirmatory: mri of head
65
Treatment
graves disease
radioactive iodine
66
Treatment
subacute thyroiditis
aspirin
67
Treatment
painless silent thyroidis
none
68
Treatment
exogenous thyroid hormone use
stop use
69
Treatment
pituitary adenoma
surgery
70
Treatment of acute hyperthyroidism and "thyroid storm"
Propranolol: blocks target organ effect, inhibits peripheral conversion of T4>T3
Thiourea drugs (methimazole and ptu): blocks hormone production
iodinated contrast material (iopanoic acid and ipodate): blocks the peripheral conversion of T4 to the more active T3, also blocks the release of existing hormoen
steroids (hydrocortisone)
radioactive iodine: ablates the gland for a permanent cure
71
graves ophthalmopathy
steroids are the best initial therapy. radiation is used in those not responding to steroids. severe cases may need decompressive surgery
72
Thyroid nodules
these are incredible common, and are palpable in as much as 5% of women and 1% of men. 95% are benign (adenoma, colloid nodule, cyst). thyroid nodules are rarely associated with clinically apparent hyperfunctioning or hypofunctioning
73
methimazole is preferred of
ptu
74
if the pt has a hyperfunctioning thyroid do they need a needle biopsy
no bc malignancies of the thyroid or not hyperactive
75
Thyroid US
only gives you size still have to do thyroid function testing or biopsy
76
thryoid nodule
diagnostic tests
thyroid nodules grater than 1 cm must be biopsied with a fine needle aspirate if there is normal thyroid funtion (t4/TSH)
nodules in those who are euthyroid should be biopsied
there is no need to ultrasound or do radionuclide scanning bc these tests cannot exclude cancer
77
needle biopsy is the mainstay of
thyroid nodule management
78
when a pt has a thyroid nodule
perform thyroid function tests (TSH and T4)
if tests are normal, biopsy the gland
79
thyroid follicular adenoma
cannot exclude cancer so you must remove the entire nodule, this is an indeterminate finding on fine needle apsiration. a sonogram cannot exclude cancer
80
hypercalcemia
etiology
the omst common cause of hypercalcemia is primary hyperparathyroidism (PTH). most of the pts are asymptomatic. For those with severe, acute symptomatic hypercalcemia, there is a high prevalence of cancer and the hypercalcemia of malignancy which is from a pth like particle. other causes are:
```
vit d intoxication
sarcoidosis and other granulomatous diseases
thiazide diuretics
hypthyroidism
mtastases to bone and multiple myeloma
```
81
hypercalcemia
presentation
acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy, and constipation
short QT and htn
osteoporosis
nephrolithiasis
diabetes inspidus
renal insufficiency
82
hypercalcemia
treatment
acute hypercalcemia is treated with:
saline hydration at high volume
bisphosphonates: pamidronate, zoledronic acid
83
the mechanism of htn in what is not clear
hypercalcemia
84
primary hyperparathyroidism and cancer account for 90% of
hypercalcemia pts
85
prednisone controls hypercalcemia when it is from
sarcoidosis or any granulomatous disease
86
give calcitonin when
when hypercalcemia is not controlled with saline and bisphosphonates, if it is from malignancy (give cinacalcet if not), use dialysis if renal failure
87
hpyerparathyroidsim
etiology
Primary is from:
```
solitary adenoma (80-85%)
hyperplasia of all 4 glands (15-20%)
parathyroid malignancy (1%)
```
88
hyperparathyroidism presentation
primary hyperparathyroidism often presents as an asymptomatic elevation in clacium elvels found on routine blood testing. when there are symptoms, it can occationally present with the signs of acute, severe hypercalcemia previously described. more often there are slower manifestations such as:
osteoporosis
nephrolithiasis and renal insufficiency
muscle weakness, anorexia, nausea, vomiting, and abdominal pain
peptic ulcer disease (calcium stimulated gastrin)
89
hyperparathyroidism diagnostic tests
besides high calcium and PTH levels, you will also find a low phosphate level, low chloride level, EKG with a short QT, and sometimes an elevated BUN and creatinine. alkaline phosphatase may be elevated from the effect of PTH on bone
90
bone x ray is not a good test for what
effects of high PTH, dexa densitometry is better
91
when hyperparathyroid what will help before surgery
preop imaging of the neck with us or nuclear scanning to help determine the approach.
92
hyperparathyroidism treatment
surgical removal of the involved parathyroid gland is the standard of care
when surgery is not possible give cinacalcet
93
hypocalcemia
etiology
primary hyperparathyroidism is most often a complication of prior neck surgy, such as thyroidectomy, in which the parathyroids have been removed
other causes are:
hypomagnesemia: magneisum is necessary for PTH to be released from the lgand. low magnesium levels also lead to increased urinary loss of calcium
Renal Failure: other causes include vitamin D deficiency, genetic disorders, fat malabsorption, and low albumin states.
94
for every pon decrease in albumin the calcium level decreases by
0.8
95
low albumin causes a decrease in total calcium but the free calcium level
is normal hence no symptoms
96
hypocalcemia
presentation
signs of neural hyperexcitability in hypocalcemia:
```
chvostek sign (facial nerve hyperexcitability)
carpopedal spasm
perioral numbness
mental irritability
seizures
tetany (trousseau sign)
```
97
hypocalcemia
diagnostic tests
ekg shows a prolonged QT
slit lamp exam shows early cataracts
98
hypocalcemia
treatment
replace calcium and vitamin D this is done orally if sx are mild or absent and iv if sx are severe
99
low calcium =
twitchy and hyperexcitable
100
high calcium =
lethargic and slow
101
hypercortisolism
definition
cushing syndrome can be sued interchangeably iwth the term hypercotisolism, cushing disease is a term used for the pituitary overproduction of ACTH from carcinoid or cancer or from overproduction autonomously in the adrenal gland. prednisone and other glucocorticoid use can cause the same manifestation.
102
hypercortisolism
etiology
pituitary ACTH (cushing disease) 70%
adrenals 15%
unknown source of ACTH 5%
ectopic ACTH (cancer, carcinoid)
103
hypercortisolism
presentation
fat redistribution: Moon face, truncal obesity, buffalo hump, thin extremitites, increased abdominal fat
Skin: striae, easy bruising, decreased wound healing, adn thinning of skin
osteoporosis
htn: from increased sodium reabsorption in th ekideny and increased vascular reactivity
menstural disorders in women
ed in men
cognitive disturbance: from decreased concentration to psychosis
polyuria: from hyperglycemia and increased freee water clearance
104
hypercortisolism
diagnostic tests
1. Establish the presence of hypercortisolism
| 2. establish the cause of hypercortisolism
105
Establish the presence of hypercortisolism
the best initial test for the presence of hypercortisolism is the 24 hour urin cortisol. if this is not in the choices then andwer is the 1 mg overnight dexamethasone suppression test. the 1 mg overnight dexamethason suppression test should normally suppress the omrning cotisol level. if this suppression occurs, hypercortisolism can be excluded
there are false positives on the 1 mg overnight dexamethasone suppression test
the 24 hour urin cortisol is a more specific test of hypercortisolism if the 24 urin cortisol is elevated the presence of hypercortisolism is confirmed
106
causes of false positive 1 mg overnight suppression testing
depression
alcoholism
obesity
107
establish the cause of hypercortisolism
ACTH testing is the best inital test to determine the cause or location of hypercortisolism
Low ACTH means an adrenal source
if the ACTH level is elevated teh source coudl be from:
Pituitary (suppresses with high dose dexamethasone)
ectopic production: lung cancer, carcinoid (dexamethasone does not suppress)
once the ACTH level is elevated and does not suppress with high dose dexamethasone, scan the brain with an MRI. if the mri does not show a clear pituitary lesion, sample the inferior petrosal sinus for ACTH, possibly after stimulating the pt with corticotropin-releasing hormone (CRH). An elevated ACTH from the venous drainage of the pituitary confirs the pituitary as the source. the petrosal venous sinus must be sampled bc some pituitary lesions are too small to be detected on MRI.
108
Decreased ACTH =
adrenal source
109
if the ACTH is elevated and you cannot find a defect in the pituitary either by MRI or samplingthe petrosal sinus
scan the chest looking for an extopic source of ACTH production. you can always confirm teh source of hypecortisolism with biochemical tests before you perform imagins studies
110
CC: I feel weak and tired, and I notice hair growth on my face and strance marks on my stomach
low-dose (1 mg) dexamethasone suppression test
decreased=disease excluded
111
CC: I feel weak and tired, and I notice hair growth on my face and strance marks on my stomach
cortisol testing:
24 urine
late-night salivary
increased
do ACTH testing if high:
ACTH dependant cushing syndrom
if low:
ACTH independant cushing syndrome
112
at least 10% of the population has an abnormality of what on MRI
the pituitary so if you start with a scan you may removed the pituitary when the source is in the adrenals
113
ACTH high?>high dose dexamethasone
suppresses: pituitary
Dose not suppress: ectopic + cancer
114
Other lab testing for hypercortisolism
cortisol is a stress hormone that is an antiinsulin. in addition, there is some aldosteronelike effect of cortisol that has an effect on the kidneys distal tubule of excreting potassium and hydrogen ions
115
effects of hypercortisolism include
```
hyperglycemia
hyperlipidemia
hypokalemia
metabolic acidosis
leukocytosis from demargination of white blood cells, at least half of white cells in the blood are on the vessel wall waiting for an acute stress to come into circulation. they are like parked police cars wiating to be called
```
116
hypercortisolism
treatment
surgically remove the source of hypercortisolism. transphenoidal surgery is done for pituitary sources whereas laparoscopic removal is done for adrenal sources
117
evaluation of adrenal incidentaloma
how far should you go in the evaluation of an unexpected, asyptomatic adrenal lesion found on CT
metanephrines of blood or urine to exclude pheochromocytoma
renin and aldosterone levels to exclude hyperaldosteronism
1 mg overnight dexamethasone suppresion test
118
4% of the population has adrenal incidenaloma
do not start with a scan or you will remove the wrong organ
119
laboratory finding in adrenal disorders
ACTH level
Adrenal: low
Pituitary: high
Ectopic: high
120
laboratory finding in adrenal disorders
Petrosal Sinus
Adrenal: not done
Pituitary: high ACTH
Ectopic: low ACTH
121
laboratory finding in adrenal disorders
Gigh dose dexamethasone
Adrenal: no suppression
Pituitary: suppresses
Ectopic: no suppression
122
ACTH independent cushign syndrome
Adrenal mass?
CT adrenal
123
ACTH-dependent Cushing Syndrome
pituitary vs ectopic ACTH production?
high dose dexamethasone suppression test
suppression of cortisol?
pituitary adenoma? (cushing disease)
pituitary mass?
pituitary MRI
no mass seen?
pterosal sinus sampling for ACTH
124
ACTH-dependent Cushing Syndrome
pituitary vs ectopic ACTH production?
high dose dexamethasone suppression test
increase ACTH and cortisol?
ectopic ACTH secreting tumor
chest CT
125
Hypoadrenalism
definition
chronic hypadrenalsim is also called ADDison disease. acute adrenal insufficiency is an adrenal crisis. these conditions are different severities of the same disorder
126
Hypoadrenalism
etiology
Addison disease is caused by autoimmune destruction of the gland in more than 80% of cases.
less common causes are:
infection (tb)
adrenoleukodystophy
metastatic cancer to the adrenal gland
127
acute adrenal crisis is cause by
hemorrhage
surgery
hypotension
trauma that rapidly destroys the gland
the sudden removal of chronic high dose prednisone (steroid) use can precipitate acute adrenal crisis
it is less comman to have an acute adrenal crisis from the loss of the pituitary bc aldosterone is not under the control o fACTH
128
Hypoadrenalism
presentation
weakness
fatigue
altered mental status
nausea
vomiting
anorexia
hypotension
hyponatremia
hyperkalemia
hyperpigmentation is just chronic
129
if hypoadrenalism is from pituitary failure
ACTH level is low
130
high acth level means the etiology of adrenal insufficinecy is
a primary adrenal failure
131
eosinophilia is common in
hypoadrenalism
132
hypoadrenalism diagnostic tests
pats have the hooposit of hypercortisolism so they have
hypoglyxemia
hyperkalemia
metabolic acidosis
hyponatremia
high bun
133
what is more important than testing in acute adrenal crisis
treatment
134
hypoadrenalism treatment
1. replace steroids with hydrocortisone
2. fludrocortisone is a steroid hormone that is particularly high in mineralocorticoid or aldosterone-like effect. fludricortisone is most useful if the pt still have evidence of postural instability. mineralocorticoid cupplements hsould be used in primary adrenal insuffciiency when the pat is on oral steroids such as cortisone
135
Signs and sx of hypoadrenalism
weakness hypotension weight loss hyperpigmentation
then to the cosyntropin stimulation test (plasma cortisol before and after cosyntropin IM or IV)
cortisol fails to rise
high ACTH
aldosterone also low
primary adrenal insufficiency
136
Signs and sx of hypoadrenalism
weakness hypotension weight loss hyperpigmentation
then to the cosyntropin stimulation test (plasma cortisol before and after cosyntropin IM or IV)
cortisol fails to rise
low ACTH
aldosterone an increase
secondary adrenal insufficiency or adrenal atrophy from pituitary insufficiency
137
Primary hyperaldosteronism
etiology
Primary hyperaldosteronism is the autonomous overproduction of aldosterone despire a high pressure with a low renin activity. eighty percent are from solitary adenoma. most of the rest is from bilateral hyperplasia. it is rarely malignant
138
Primary hyperaldosteron
| what is the most likely dx
all forms of secondary htn are more likely in those whose onset:
is under age 30 or above 60
is not controlled by 2 antihypertensive meds
has a characteristic finding on the hx physical or labs
139
Primary hyperaldosteronism
presentation
there is high bp in association with a low potassium level.the low potassium level is either found on routine lab testing or bc of sx of muscular weakness or diabetes insipidus from the hypokalemia
140
Primary hyperaldosteronism
diagnostic tests
the best initial test is to measure the ration of plasma aldosterone to plasma renin. an elevated plasma renin excludes primary hyperaldosteonism.
the most accurate test to confirm the presence of a unilateral adenoma is a sample of the venous blood draining the adrenal. it will show a high aldosterone level.
141
Primary hyperaldosteronism
CT
Ct scan of the adrenals should only be done after biochemical testin confirms:
low potassium
high aldosterone despite a high salt diet
low plasma renin level
142
high bp + hypokalemia =
primary hyperaldosteronism
143
never start with what in endocrinology?
a scan there are too many incidental lesions of the adrenal
144
Primary hyperaldosteronism
treatment
unilateral adenoma is resected by laparoscopy
bilateral hyperplasia is treated with eplerenon or spironolactone
145
spironolactone causes
gynecomastia and decreased libido bc it is antiadrenergic
146
pheochromocytoma
definition and etiology
pheochromocytoma is a nonmalignant lesion of the adrenal medulla autonomously overproducing catecholamines despite a high bp
147
pheochromocytoma
what is the most liekly diagnosis
htn that is episodic in nature
ha
sweating
palpitations and tremor
148
pheochromocytoma
diagnostic tests
the best inital test is the level of free metanephrines in plasma. this is confirmed with a 24 hour urine collection for metanephrines. this is more sensitive than the urine vanillylmandelic acid level. direct measurement of epinephrine and norepineprhine are useful as well
imaging of the adrenal glands with CT or MRIis done only after biochemical testing
mibg scanning: this is a nuclear isotype scan that detects the locationo fo pheochromocytoma that originates outside the adrenal gland
149
pheochromocytoma
treatment
phenoxybenzamine is an alpha blocker htat is the best initial therapy. of pheochromocytoma. calcium channel blocekr and beta blockers are used afterward
pheos are removed surgically or by laparoscopy
150
Diabetes Mellitus
definition etiology
dm is defined as persistently high fasting glucose levels greater than 126 on at least 2 separate occasions
151
Type 1 DM
onset in childhood
insulin dependent from an early age
not related to obesity
defined as insulin deficiency
152
Type 2 DM
onset in adulthood
directly related to obesity
defined as insulin resistance
153
Diabetes Mellitus
presentation
polyuria, polyphagia, and polydipsia are the most common presentation. Type 1 diabetics are generally thinner than Type 2 diabetics. Type 2 DM is more resistant to diabetic ketoacidosis (DKA). both types present with decreased wound healing. Type 2 diabetics are much less likely to present iwth polyphagia.
154
Diabetes Mellitus
diagnostic tests
diabetes is defined/diagnosed as:
two fasting blood glucose measurements greater than 125mg/dl
single glucose level above 200mg/dl with above symptoms
increased glucose elvel on oral glucose tolerance testing
hemoglobin a1c greater than 6.5% is a diagnostic criterion and is the best test to follow response to therapy over the last several months.
155
Diabetes Mellitus
treatment
Diet exercise and weight loss - weight loss can control asm uch as 25% of cases of Type 2 DM without the need for medications, since decreasing the amoun of adipose tissue helps to decrease insulin resistance. Exercising muscle dose not need insulin.
Oral hypoglycemic medication - the best initial drug therapy is with oral metformin. Sulfonylureasare not used as first line therapy bc they increase insulin release from the pancreas, thereby driving the glucose intracellularly and increasing obesity. The goal of therapy is Hga1c less than 7%
156
Metformin
works by blocking gluconeogenesis. it does not increase weight gain. in the absence of renal failure, metformin is clearly the best inital therapy for diabetes
157
metformin is contraindicated in who
people with renal dysfunction bc it can accumulate and cause metabolic acidosis
158
DPP-IV inhibitors
sitaglipitin, linagliptin, alogliptin
block the metabolism of the incretins, also called insulinotropic peptide (GIP) and glucagon-like peptide (GLP). the term glucagon like peptide is confusing, bc GLP actually inhibits or suppresses glucagon.
159
Incretin Mimetics
exenatide, liraglutide, albiglutide
are a direct replacement of incretins. They are generally not gien before the DPP-IV inhibitors, bc they must be administerd by injection. incretin agonists also markedly slow gastric motility and decrease weight. the management of incretins is confusing bc they have seversal names
160
The incretins (GIP and GLP) increase
insulin release and decrease glucagon release from the pancreas. They are secreted into the bloodstream when food (especially carbohydrates) enters the duodenum and is metabolized by dipeptidyl peptidase IV (DPPIV). the incretins normally have a half life of only 1-2 minutes. Giving DPP-IV inhibitors- such as sitagliptin, saxaglipitin, and linagliptin-markedly lengthens the half life of incretins.
161
Incretins =
glucose insulinotropic peptide (GIP) and glucagon-like peptide (GLP)
DPP-IV inhibitors block their metabolism
all slow gi motility
162
Thiazoladinediones (glitazones)
provide no clear benefit over the hypoglycemic medications. they are relatively contraindicated in CHF bc they increase fluid overload.
163
Nateglinide and repaglinide
they are stimulators of insulin release in a manner similar to sulfonylureas, but do not contain sulfa. they do not add any therapeutic benefit to sulfonylureas
164
alpha glucosidase inhibitors (acarbose and miglitol)
they are agents that block glucose absorption in the bowel. they add about half a point decrease in HgA1C . they cause flatus, diarrhea, and abdominal pain. they can be used with renal insufficiency.
165
pramlintide
it is an analog of a protein called amulin that is secreted normally with insulin. amylin decreases gastric emptying, decreases glucagon levels, and decreases appetite
166
insulin
insulin is added if the pt is not controlled with oral hypoglycemic agents. insulin glargine gives a steady state of insulinfor the entire day. dosing is not tested. glargine provides much more steady blood levels than NPH insulin, which is dosed twice a day. long acting insulin is combined with a short acting insulin such as lispro, aspart, or glulisine. regular insulin is sometimes used as the short acting insulin, goal of therapy is A1C less than 7%
167
lispro, aspart, glulisine
Onset: 5-15 minutes
Peak action: 1 hour
Duration: 3-4 hours
168
Regular insulin
Onset: 30-60 minutes
Peak action: 2 hours
Duration: 6-8 hours
169
NPH
Onset: 2-4 hours
Peak action: 6-7 hours
Duration: 10-20 hours
170
Glargine
Onset: 1-2 hours
Peak action: 1-2 hours
Duration: 24 hours
171
Diabetic Ketoacidosis
more common in those with Type 1 diabetes, diabetic ketoacidosis (DKA) can definitely present in those with Type 2 diabetes
```
Hyperventilation
possibly altered mental status
metabolic acidosis with an increased anion gap
hyperkalemia in blood, but decreased total body potassium bc of urinary spillage
increased anion gap on blood testing
serum is positive for ketones
nonspecific abdominal poin
acetone odor on breath
polydipsia and polyuria
```
172
Diabetic Ketoacidosis
treatment
treat with large-volume saline and insulin replacement. replace potassium when the potassium level comes down to a level approaching normal. correct the underlying cause: noncompliance with medications, infection, pregnancy, or any serious illness.
173
Decrease insulin
Increase synthesis of glucose
increase breakdown of glycogen
decrease uptake of glucose by tissues
increase breakdown of fats
174
Increase synthesis of glucose
increase breakdown of glycogen
increase liver output of glucose> hyperlgycemia
175
decrease uptake of glucose by tissues
hyperglycemia
176
increase breakdown of fats
increase free fatty acids in plasma > increase liver output of ketone bodies >ketoacidosis
177
Increase breakdown of proteins
increase synthesis of glucose> increase liver output of glucose> hyperglycemia
178
what is the most accurate measure of the severity of dka
hyperglycemia is not the best measure of the severity of DKA. the glucose level can be markedly elevated without the presence of ketoacidosis. urine ketones mean very little. although blood ketones are important, they are not all detected. if the serum bicarbonate is very low, the pt is at risk of death. if the serum bicarbonate is high, it does not matter how high the glucose level is, in terms of severity. serum bicarbonate level is a way of saying anion gap. if the bicarbonate level is low, the anion gap is increased.
179
Health Maintenance
all pts with DM should receive:
pneumococcal vaccine
yearly eye exam to check for proliferative retinopathy, which needs laser therapy
stain medication if the ldl is above 100mg/dl
ace inhibitors and arbs if the blood pressure is greater than 140/90 mmhg
acei or arb if urine tests positive for microalbuminuria
aspirin, used regularly in all diabetic pts abov the age of 30
foot exam for neuropathy and ulcers
180
Complications of Diabetes
Cardiovascular complications
diabetic nephropathy
gastroparesis
retinopathy
neuropathy
181
Complications of Diabetes
Cardiovascular complications
diabetic pts are at significantly increased risk of mi, stroke, and CHF from premature atherosclerotic disease. this is why the goal of blood pressure in these pts (below 140/90 mmhg) is lower than in the general population. in addition, diabetes is considered an equivalent of coronary disease for treatment of ldl, and the goal is less than 100mg/dl when initiating treatment with statins
182
Complications of Diabetes
diabetic nephropathy
diabetes leads to microalbuminuria early in the disease. the dipstick for urine becomes trace positive at 300 mg per 24 hours. pts with dm should be screened annually for microalbuminuria and started on an ace inhibitor or arb when it i spresent. these agents are proven to decrease the rate of progression of nephropathy by decreasing intraglomerular hypertension and decreasing damage to the kidney.
183
Complications of Diabetes
gastroparesis
after several years, DM decreases the ability of the gut to sense the stretch of the walls of the bowel. stretch is the main stimulant to gastric motility. gastroparesis is an immobility of the bowls that leads to bloating, constipation,, early satiety, vomiting, and abdominal discomfort. treatment is with metoclopromide and erythromycin, which increase gastric motility.
184
Complications of Diabetes
retinopathy
DM's effect on microvasculature is especially apparent in the eye. in the united states, nearly 25,000 people go blind from DM each year. the only management for nonproliferative retinopathy is tighter control of glucose. aspirin does not help retinopathy. when neovascularization and vitreous hemorrhages are present, it is called proliferative retinopathy. this is treated with laser photocoagulation, which markedly retards the progression to blindness.
185
Complications of Diabetes
neuropathy
damage to microvasculature damages the vasonervorum that surrounds large peripheral nerves. this leads to decreased sensation in the feet-the main cause of skin ulcers of the feet which lead to osteomyelitis. when the neuropathy leads to pain, treatment is with pregabalin, gabapentin, or tricyclic antidepressants.
