Endocrine Diseases Flashcards
Adrenal Insufficiency causes :
- primary
- secondary and tertiary
- acute
- chronic
primary–addisons disease–MCC is autoimmune destruction of adrenal gland–>lack of cortisol and aldosterone
secondary–pituitary failure to secrete ACTH or suppression of HPA axis–>lack of androgens and cortisol
tertiary–hypothalamic disease and decr in CRH
acute–addisonians crisis
what happens if a PT is abruptly stopped on steroid tx?
adrenal insufficiency
- bc steroids provide exogenous negative feedback to the pituitary
- if steroids are stopped…the pituitary takes time to recover function–and during that time–adrenal insufficency can occur
in secondary adrenal insufficiency– ACTH is H/L and aldosterone is H/L??
ACTH–low
aldosterone–not affected so its normal
*of course low cortisol
MCC for acute adrenal insufficiency–Addisonians crisis
abrupt withdrawl of corticoid tx or a skipped dose of steroids
precipitating factors for addisonian crisis?
stressful event
- surgery
- illness
- trauma
- volume loss
- hypothermia
- MI
- fever
- hypoglycemia
- steroid withdrawl
MCC for addisonian crisis
abrupt withdrawl of glucocorticoids
imaging for chronic and acute adrenal insufficiency
CT: of the adrenal glands if unsure if insuff is autoimmune or not
CT imaging findings for Addison disease
small noncalcified adrenal glands
when do you see adrenal calcifications?
- tuberculous addison dz
- hemorrhage
- fungal infection
- pheochromocytoma
- melanoma
how to test for adrenal insufficiency (AI)
- order basic metabolic panel and do 8am measure of serum cortisol
- ->If results inconsistent with AI: consider other diagnosis
- ->If low cortisol levels, normal to high K and low to normal Na are found then go to: - Cosyntropin ACTH stimulation test: where we measure basal ACTH levels B4 administering IV ACTH–then we measure the cortisol levels after 30-60 mins
- –>if normal: consider other diagnosis
- –>LOW cortisol and HIGH acth–PRIMARY AI
- –>LOW cortisol and LOW acth–secondary AI - If primary AI:
- measure 21-hydroxylase antibody
- CT of adrenal glands
lab findings for primary adrenal insuff
- CRH
- ACTH
- cortisol
- Aldosterone
- Renin
- what would the ACTH stimulation test results show?
high CRH high ACTH low cortisol Low aldosterone high renin
ACTH stim tests would show: high ACTH
lab findings for secondary adrenal insuff
- CRH
- ACTH
- cortisol
- aldosterone
- Renin
- what would the ACTH stimulation test results show?
CRH: high ACTH: low Cortisol: low aldosterone: low Renin: normal to low
ACTH stim test: absent/low ACTH
lab findings for tertiary adrenal insuff
- CRH
- ACTH
- cortisol
- aldosterone
- Renin
- what would the ACTH stimulation test results show?
CRH: low ACTH: low Cortisol: low Aldosterone: low Renin: normal to low
ACTH stim test: exaggerated or prolonged
BMP results for adrenal insufficiency
- k
- na
- glucose
hyponatremia
hyperkalemia
hypoglycemia
list the disorders of HYPOfunction of adrenal glands
-both primary and secondary
PRIMARY
- ACUTE adrenal insufficiency–addisonian crisis
- addison’s disease
SECONDARY:
-pituitary failure of ACTH secretion–aka CHRONIC adrenocortical insufficiency
List the disorders of HYPERfunction of adrenal glands
-primary and secondary
- Cushing’s disease–SECONDARY
- Cushing’s syndrome
- Primary hyperaldosteronism
- Pheochromocytoma
Manifestations of ________ cause Cushing’s syndrome
Hypercortisolim
Hypercortisolism aka?
Cushing Syndrome
Different b/w Cuhsing’s DZ and Syndrome?
Disease: Pituitary Gland overprodues ACTH(due to hyperplasia or adenoma)—secondary cause of Hypercortisolim
Syndrome: s/s related to cortisol excess…..does not specify a cause of source of why excess cortisol.. has 4 main causes.. .ONE Of them is Cushing Disease
Four main causes of Cushing Syndrome
- Exogenous sources: long-term high dose glucocorticoids tx—-MCC overall!!!**
- Endogenous:
- over secretion of ACTh from AP—-cushing’s disease–MC endogenous cause!!!!!*******
* secondary
or
- Ectopic ACTH producing tumor/adenoma (MEN, SCLC)
- secondary
or
-Adrenal Tumor/adenoma (primary)
MC place for an ectopic tumor secreting ACTH
lungs—small cell lung Ca
low dose dexamethasone test is used as?
screening test for Cushing syndrome
when do we do high dose dexamethasone test??
after we get a negative result on low dose—- aka elevated cortisol levels
**used to distinguish a pituitary cause AKA cushing dz from an adrenal cause/other cause
Dexamethasone test results below indicate what cause of Cushing Syndrome:
- high ACTH with suppression of Cortisol
- High ACTH with no suppression of cortisol
- Low ACTH with no suppression of cortisol
- Cushing Dz (bc adrenals are sending neg feedback to AP—but AP is not listening)
- Ectopic ACTH producing tumor
- Adrenal tumor and/or exogenous steroids
list the three screening tests for cushing syndrome
*which is the most specific
- 24 hour urine test to test for cortisol-MOST SPECIFIC
- Nighttime salivary cortisol (11pm)
- Low dose 1 mg overnight dexamethasone test
if a low dose dexamethasone test does NOT suppress ACTH…..
indicates that cushing syndrome exists
but does not tell us the SOURCE of the increased cortisol—– why we do the high dose dex test
does an ectopic ACTH producing tumor respond to the negattive feedback?
NO
*why this test result will show as HIGH acth and no suppression of cortisol
When localizing the ACTH for dex test—- _____ responds to the negative feedback and _____ does not
Cushings disease DOES respond to neg feedback (why cortisol is supressed)
ECtopic ACTH prod tumor does not (why cortisol not supressed)
MCC of primary hyperaldosternoism
Bilateral adrenal hyperplasia
primary hyperaldosternoism is renin indep or dependen?
independent
Renin levels are NOT increased.. only seen with secondary
Conn syndrome is?
Adrenal Aldosternonoma—tumor in the zona glomerulosa secreting aldosterone
*primary form of hyperaldosteronism
triad for hyperaldosteronsm?
HTN— very very very drug resistant
HyPOkalemia
Metabolic alkalosis
PTs usually present how for hyperaldosteronism?
usually asympto
lab results for primary hyperaldosternoism?
HIGH aldosterone and normal renin 20:1 ratio -Hypok -hypernatremia high ph
labs for secondary hyperaldosternoism?
High aldosteron
high plasma renin levels—–because RAAS is activated due to renal artery stenosis– and increase in RAAS–increase renin–increase aldosterone
**NOT an adrenal issue here
define adenoma
a tumor that is non cancerous
Most common place for neuroendocrine tumors to arise?
why?
lungs and GI tract
WHY? because THEY LOVE BLOOD– love to grow in vascularized areas
**but since they are from neuroendocrine cells– they can arise technically anywhere
Characteristics of carcinoid tumors can cause?
carcinoid syndrome
carcinoid syndrome manifestations
flushing
diarrhea
wheezing
TSH secreting pituitary adenoma
- what is it
- size?
- invasive?
TSH producing adenoma… rare
- large
- very invasive
presentation for TSH secreting pituitary adenoma
diffuse goiter >95% of time
- hyperthyroid s/s
- pituitary adenoma s/s
lab work for tsh secreting pit adenoma
High TSH and High free T3/T4
- also can have some vision disturbances if its obstruction optic chiasm
- **because it is secondary hyperthyroidism
how to diagnose TSH secreting pituitary adenoma
MRI***
2. radioactive iodine uptake scan–will note diffuse uptake
radioactive iodine uptake scan–how does it work and for what hormone
TSH
-when TSH rises–thyroid gland uses iodine to make the T hormones–RAIU tests use a radioactive tracer (iodine) to measure how much tracer the thyroid gland absorbs
what disease will have diffuse uptake for RAIU
graves or TSH secreting pituitary adenoma
what disease will have decreased uptake for RAIU
thyroiditis
-hashimoto, postpartum
what disease will have “hot nodule or hot spot” uptake for RAIU
toxic adenoma
hot spot= focal area of increased uptake
what disease will have multiple nodules uptake for RAIU
toxic multinodular goiter
list the well differentiated thyroid CAs
papillary throid carcinoma
follicular thyroid Carcinoma
list the invasive and poorly differentiating thyoid CAs
Medullary thyroid carcinoma
anaplastic thyroid carcinoma
if she shows a pathology pic– which thyroid CA would it be?
papillary thyroid carcinoma
pathology shows “orphan Annie eye Nuclei”— what CA?
papillary thyroid carcinoma
which the MC thyroid CA?
papillary thyroid carcinoma
who have a poorer prognosis for papillary thyroid carcinoma.. men or women?
MEN**
who has a higher incidene rate for papillary thyroid CA?
WOMEN
which of the thyroid cancers is least aggressive and highest cure rate?
papillary thyroid carcinoma
which of the subtypes for DM1 is MC?
subtype 1A
when does 1A usually peak for onset?
young… ages 4-14
trigger for subtype 1A?
outside factors
- infection
- gene mutation: HLA DR3-DQ2 and DR4
MC clin man for DM1
hyperglycemia without acidosis
second MC clin man for DM1
DKA
normal body ph
- 35-7.45
* **7.40
DKA is MC seen with? and Hyperglycemic Hyperosmolar state MC seen with?
DKA–DM1
HHS–DM2
anion gap equation
+
normals for anion gap
[NA+] - [Cl-] - [HCO3]
normals range from 3-11 or 8-16
explain the presentation of diabetic neuropathy
stocking glove distribution–finger tips–fingers–hands—arms—–
or
toe tip–toes—foot–calfs—etc
*progresses distal–>proximal SYMMETRICALLY
what test is done to test for DM neuropathy
- monofilament test
- also can use the vibration sense test with tuning fork—if the PT cannot feel the vibrations from the fork… then move the fork proximally until they do feel it to sense their degree of neuropathy
target A1C to be below??
7
lab vlaues for DKA
pH <7.3 Bicarb <22 \+ketones in urine BGL >250... but usually not above 600 increased serum osmolarity
dawn phenomenon
- define
- describe patho behind it
- management
- normal glucose levels UNTIL
- ->2-8am
*results from decrease insulin sensitivity and nightly surge of counterregulatory hormones during nighttime fasting–>cortisol, glucagon, GH
- tx:
- bedtime injection of insulin (NPH) to blunt morning hypergycemia
- avoid nighttime snacks or CHO snacks late at night
Somogyi effect
- define
- describe patho behind it
- management
nocturnal hypoglycemia followed by rebound hyperglycemia
*due to surge in GH after the early AM hypoglycemia
tx:
- decrease nighttime insulin (NPH) dose
- give bedtime snack
- move evening dose of NPH to earlier
insulin waning
- define
- describe patho
- tx
progressive rise in glucose from bed–> morning
- seen when NPH evening dose is administered before dinner
- due to ineffective dosing of NPH insulin
tx:
-move NPH insulin dose to bedtime
or
-increase the evening dose
*happens a lot with newly diagnosed diabets who are unsure how todo nightttime dose
what is the main reason for delayed diagnosis of DM2
lack of overt s/s in the early disease process
**many PTs are diagnosed during anual screeings or incidentally with blood tests
ADA screening for DM
all adults greater than or equal to 45 X3 years
OR
BMI >25 in adults
explain patho behind poor wound healing in DM
DM patients have poor circulation bc their BVs are narrower–>glucose damages endothelium (constant inflammation)–>not enough oxygen is bound to hemoblogin–>less going to the area to be fixed