Endocrinology Flashcards
diagnosis for diabetes made by ONE of the following (4 different ways)
- 2 FASTING glucose greater than or equal to 126
- ONE RANDOM glucose greater than or equal to 200 WITH symptoms (polyuria, polydipsia, polyphagia)
- ABNORMAL GTT (2-hour GTT with 75G glucose load)
- HbA1c greater than 6.5%
STRONGEST indication for screening for diabetes
HTN
mechanism for type 2 diabetes
excess fat = insulin deficiency
best INITIAL treatment for type 2 diabetes
- DIET
- EXERCISE
- WEIGHT LOSS
best INITIAL MEDICAL treatment for type 2 diabetes
metformin (biguanide)
metformin MOA
blocks gluconeogenesis
main advantages of metformin (2)
- no risk of hypOglycemia
- does NOT increase obesity
metformin CONTRAindications (2 main ones)
- renal insufficiency
- use of contrast
name the sulfonylureas (3)
- glyburide
- glimepiride
- glipizide
sulfonylurea MOA
increase insulin RELEASE from pancreas
sulfonylurea ADVERSE EFFECTS (2 main ones)
- hypOglycemia
- SIADH
name the dipeptidyl peptidase 4 (DPP-4) inhibitors
- sitaGLIPTIN
- linaGLIPTIN
- aloGLIPTIN
- saxaGLIPTIN
dipeptidyl peptidase 4 (DPP-4) inhibitor MOA
block metabolism of INCRETINS
mechanism of incretins (GLP and GIP)
```
GLP = glucagon-like peptide
(GIP = glucose insulinotropic peptide)
~~~
increase insulin and decrease glucagon secretion from pancreas
name the thiazolidinediones
- rosiGLITAZONE
- pioGLITAZONE
thiazolidinedione MOA
increase PERIPHERAL insulin sensitivity
thiazolidinediones CONTRAindication
CHF
name the a-glucosidase inhibitors
- acarbose
- miglitol
a-glucosidase inhibitor MOA
block glucose ABSORPTION in intestinal lining
name the insulin secretagogues
- nateGLINIDE
- repaGLINIDE
secretagogue MOA
increase insulin RELEASE from pancreas
name the SGLT inhibitors (sodium-glucose transport)
- canaGLIFLOZIN
- dapaGLIFLOZIN
- empaGLIFLOZIN
SGLT inhibitor MOA
inhibits glucose reabsorption in kidneys
name the GLP (glucagon insulinotropic peptide) analogs
- exenaTIDE
- liragluTIDE
GLP analog MOA
slow gastric emptying and promote weight loss
name long-acting insulin
- glargine (daily)
- detemir (daily, or Q12H)
- NPH (Q12H)
name short-acting insulin
- aspart
- lispro
- glulisine
mechanism for type 1 diabetes
underproduction of insulin d/t destruction of pancreas
DKA presentation
- hyperventilation d/t metabolic acidosis
- “fruity” breath from acetone
- confusion from hyperosmolar state
best INITIAL tests for DKA
- chemistry
- arterial blood gas
- acetone level
marker of ketone production
B-hydroxybutyrate
DKA lab findings
- hyperglycemia (> 250)
- hyperkalemia
- low bicarb
- low pH
- elevated AG
- elevated acetone, acetoacetate, and B-hydroxybutyrate
- +/- pseudohyponatremia
INITIAL treatment for DKA
NS bolus
once DKA is confirmed, next step in management
IV insulin
complications of diabetes:
BP goal
less than 140/90
complications of diabetes:
LDL goal
diabetes = CAD
less than 100
if BOTH DM AND CAD, less than 70
complications of diabetes:
retinopathy
ANNUAL dilated eye exam to detect PROLIFERATIVE RETINOPATHY
treatment for proliferative retinopathy in DM
laser photocoagulation
complications of diabetes:
nephropathy
microalbumin
if ANY protein is found in urine of DM patient, should be treated with
ACEI/ARB
complications of diabetes:
neuropathy
ANNUAL foot exam
treatment for diabetic neuropathy
gabapentin, or pregabalin
complications of diabetes:
erectile dysfunction
no routine screening test: just ask
treatment for erectile dysfunction
PDE inhibitor (e.g. sildenafil)
n.b. CI with nitrates
complications of diabetes:
“bloating,” constipation, abdominal fullness, and diarrhea
gastroparesis
treatment for gastroparesis
metoclopramide, or erythromycin
hypOthyroidism:
- weight =
- intolerance =
- hair =
- skin =
- mental =
- heart =
- muscle =
- reflexes =
- fatigue? =
- menstrual changes =
- gain
- cold
- coarse
- dry
- depressed
- bradycardia
- WEAK
- diminished
- yes
- yes
hypERthyroidism:
- weight =
- intolerance =
- hair =
- skin =
- mental =
- heart =
- muscle =
- reflexes =
- fatigue? =
- menstrual changes =
- loss
- heat
- fine
- anxious
- tachycardia, tachyarrhythmias (e.g. atrial fibrillation)
- WEAK
- N/A
- yes
- yes
mechanism of weight gain in hypOthyroidism
low thyroid = decreased metabolic rate (decreased use of glucose and FFA) = weight gain
best INITIAL tests for hypothyroidism
- free T4 (decreased)
- TSH (increased)
treatment for hypothyroidism
levothyroxine (T4 replacement, which gets converted in tissues to T3)
4 forms of hyperthyroid
- Graves (diffuse toxic goiter)
- silent thyroiditis
- subacute
- pituitary adenoma
Graves disease (diffuse toxic goiter):
- physical findings
- RAIU (radioactive iodine uptake)
- treatment
- eye, skin, and nail findings
- elevated
- radioactive iodine ablation (RAI)
silent thyroiditis
- physical findings
- RAIU (radioactive iodine uptake)
- treatment
- none
- low
- none
subacute thyroiditis
- physical findings
- RAIU (radioactive iodine uptake)
- treatment
- tender thyroid gland
- low
- aspirin
pituitary adenoma
- physical findings
- RAIU (radioactive iodine uptake)
- treatment
- none
- elevated
- surgery
ophthalmopathy seen in Graves disease
- exophthalmos (eyes are bulging)
- proptosis (eyelids are retracted)
dermopathy seen in Graves disease
pretibial myxedema
nail finding seen in Graves disease
onycholysis (separation of nail from nailbed)
ACUTE treatment for Graves disease
PTU (propylthiouracil), or methimazole
definitive treatment for Graves disease
radioactive iodine ablation (RAI)
treatment for symptoms in Graves disease (tremor, and palpitations)
propranolol
PTU (propylthiouracil) MOA
inhibits thyroid peroxidase:
- iodination of tyrosine residues of thyroglobulin
- coupling of DIT and MIT
- decreases PERIPHERAL conversion of T4 to T3
methimazole MOA
inhibits thyroid peroxidase:
- iodination of tyrosine residues of thyroglobulin
- coupling of DIT and MIT
silent thyroiditis may have which antibodies?
- thyroid peroxidase Ab
- antithyroglobulin Ab
ONLY cause of hyperthyroidism with ELEVATED TSH
pituitary adenoma
treatment for pituitary adenoma
- MRI of brain
- surgery
- elevated T4
- low TSH
- nonpalpable thyroid d/t atrophy of gland
exogenous thyroid hormone abuse
- acute
- SEVERE
- life-threatening hypERthyroidism
thyroid storm
treatment for thyroid storm
- iodine (blocks iodine uptake and hormone release)
- PTU, or methimazole (blocks thyroxine production)
- dexamethasone (blocks PERIPHERAL conversion of t$ to T3)
- propranolol (blocks PERIPHERAL EFFECTS)
can you determine etiology thyroid function from presence of goiter?
NO, can hypOthyroidism, hypERthyroidism, or normal thyroid
next best in management if there is a solitary thyroid nodule
fine needle biopsy (FNA)
if solitary thyroid nodule shows cancer, next step in management
surgery
MCC of hypercalcemia
PRIMARY hyperparathyroidism
other causes of hypercalcemia
- malignancy
- granulomatous disease
- vitamin D toxicity
- thiazide diuretics
- TB
- histoplasmosis
- berylliosis
mechanism of PTH (parathyroid hormone) (4 effects)
- reabsorbs Ca++ at DISTAL tubule
- excretes phosphate at PROXIMAL tubule
- activates vitamin D
- reabsorbs Ca++ and phosphate from bone
target organ damage from hyperparathyroidism
- kidney stones
- osteoporosis/osteomalacia/fractures
- confusion
- constipation (initially, diarrhea)
diagnostic tests for hyperparathyroidism
- PTH (elevated)
- Ca++ (elevated)
treatment for hyperparathyroidism
surgery
when is surgical removal the answer for hyperparathyroidism?
- symptoms
- renal insufficiency
- markedly elevated 24H URINE Ca++
- serum Ca++ more than 12.5
acute, severe hypercalcemia presentation
- confusion
- constipation
- polyuria/polydipsia (from nephrogenic DI)
- short QT syndrome
- renal insufficiency (ATN/kidney stone)
treatment for acute, severe hypercalcemia
- hydration (high volume: 3-4 liters of NS)
- bisphosphonate (very potent, but slow)
- furosemide (ONLY AFTER hydration)
- calcitonin (IF hydration and furosemide do NOT work quickly enough)
- steroid (IF etiology is granulomatous disease)
mechanism of volume depletion in hypercalcemia
- inhibits ADH effect in collecting duct = nephrogenic DI
- high Ca++ filtration promotes osmotic diuresis
causes of hypocalcemia
- surgical removal of parathyroid glands
- hypomagnesemia (PTH needs magnesium to work)
- vitamin D deficiency
- acute hyperphosphatemia (binds Ca++)
- fat malabsorption (binds Ca++ in gut)
- PTH resistance (pseudohypoparathyroidism)
presentation of severe hypocalcemia
- seizures
- neural twitching (Chvostek’s and Trousseau’s signs)
- arrhythmia/prolonged QT
treatment for hypocalcemia
- replace Ca++
- vitamin D if deficient, or hypoparathyroidism
clinical presentation, regardless of cause, of hyperadrenalism AKA hypercortisolism (Cushing syndrome)
- fat REdistribution
- easy bruising and striae
- HTN
- muscle wasting
- hirsutism
name the 3 sources of Cushing disease
- pituitary tumor
- ectopic ACTH production
- adrenal adenoma
Cushing disease: pituitary tumor
- ACTH level
- effect of high-dose dexamethasone
- specific test for diagnosis
- treatment
- high
- suppression
- MRI, or petrosal vein sampling
- removal
Cushing disease: ectopic ACTH production
- ACTH level
- effect of high-dose dexamethasone
- specific test for diagnosis
- treatment
- high
- NO suppression
- scan chest and abdomen
- removal
Cushing disease: adrenal adenoma
- ACTH level
- effect of high-dose dexamethasone
- specific test for diagnosis
- treatment
- LOW
- NO suppression
- scan adrenals
- removal
lab findings in hypercortisolism
- hyperglycemia
- hyperlipidemia
- osteoporosis
- leukocytosis
- metabolic alkalosis (d/t increased urinary loss of H+)
mechanism of metabolic alkalosis in hypercortisolism
cortisol = mineralocorticoid/aldosterone effects
increased H+ excretion at a-intercalated cell of late distal/early collecting duct
best INITIAL diagnostic tests
- 1 mg overnight dexamethasone suppression testing
- 24-hour urine cortisol
LOW ACTH level
adrenal gland ORIGIN
HIGH ACTH level
either pituitary gland or from ECTOPIC production
- fatigue
- anorexia
- weight loss
- weakness with hypOtension
- thin patient with hyperpigmented skin
- hypERkalemia, with mild metabolic acidosis
- hyponatremia
- may have hypoglycemia and neutropenia
adrenal insufficiency (Addison disease)
MOST ACCURATE test for adrenal insufficiency
- cosyntropin (synthetic ACTH) stimulation test
- CT scan of adrenal glands
treatment for ACUTE addisonian (hypoadrenal) CRISIS
- check cortisol level
- IVF and hydrocortisone
treatment for STABLE (nonhypotensive) adrenal insufficiency
prednisone
treatment for adrenal insufficiency, if patient is STILL hypotensive AFTER prednisone
fludrocortisone
- HTN
- hypOkalemia
- metabolic alkalosis
hyperaldosteronism (Conn syndrome)
diagnostic tests for hyperaldosteronism
- LOW renin
- HIGH aldosterone
- HTN
how do you confirm diagnosis for hyperaldosteronism
CT scan of adrenal glands
treatment for hyperaldosteronism: solitary adenoma
surgical resection
treatment for hyperaldosteronism: hyperplasia
spironolactone
- HA, palpitations, tremors, anxiety, flushing (all nonspecific)
- EPISODIC HYPERTENSION
pheochromocytoma
best INITIAL tests for pheochromocytoma
- serum and urinary catecholamine levels (HIGH)
- serum free metanephrine and VMA levels
MOST ACCURATE test for pheochromocytoma
CT or MRI of adrenal glands
what test is used to detect metastatic disease in pheochromocytoma?
MIGB scan
FIRST treatment used for pheochromocytoma
phenoxybenzamine (alpha blockade)
treatment for pheochromocytoma AFTER a-blocker
propranolol
definitive treatment for pheochromocytoma
surgery
ALL forms of congenital adrenal hyperplasia (CAH)
- elevated ACTH
- low aldosterone
- low cortisol
- treatable with prednisone
name the 3 kinds of CAH
- 21-hydroxylase deficiency
- 11-hydroxylase deficiency
- 17-hydroxylase deficiency
MOST COMMON TYPE of CAH
21-hydroxylase deficiency
- hirsutism (virilization)
- HYPOTENSION
21-hydroxylase deficiency
diagnostic test for 21-hydroxylase deficiency
increased 17-hydroxyprogesterone level
- hirsutism (virilization)
- HYPERTENSION
11-hydroxylase deficiency
- HYPERTENSION ONLY
- NO hirsutism (virilization)
17-hydroxylase deficiency
MC pituitary tumor
prolactinoma
presentation for prolactinoma: men
- impotence
- decreased libido
- gynecomastia
- presents LATE
- MORE LIKELY to have signs of mass effect (HA, and visual disturbance)
presentation for prolactinoma: women
- amenorrhea
- galactorrhea in ABSENCE of pregnancy
- presents EARLY
MOST ACCURATE test for prolactinoma
MRI of brain
best INITIAL treatment for prolactinoma
- dopamine agonist (bromocriptine, or cabergoline)
- surgery, if medicine doesn’t work
- growth hormone-secreting adenoma in pituitary
- excess production of growth hormone (GH)
acromegaly
acromegaly presentation
- enlarged head, fingers, feet, nose, and jaw
- intense sweating (enlarged sweat glands)
acromegaly also causes
- joint abnormalities
- amenorrhea
- cardiomegaly
- HTN
- colonic polyps
- DM
best INITIAL test for acromegaly
insulinlike growth factor (IGF)
which test is NOT done first for acromegaly, and why?
- growth factor
- bc max secretion is in middle of night and has short half-life
MOST ACCURATE test for acromegaly
GH suppression with glucose EXCLUDES acromegaly
treatment for acromegaly
transsphenoidal resection
somatostatin analog that has some effect on inhibiting GH release
octreotide
dopamine agonists that inhibit GH
bromocriptine, and cabergoline
GH receptor antagonist
pegvisomant
primary amenorrhea causes
- Turner syndrome
2. testicular feminization
secondary amenorrhea causes
- pregnancy (MCC)
- exercise
- extreme weight loss
- hyperprolactinemia
- polycystic ovary syndrome (PCOS)
- short stature
- webbed neck
- wide-spaced nipples
- scant pubic and axillary hair
- XO karyotype
TURNER SYNDROME
- genetically male, but looks/acts/feels female
- does not menstruate (no cervix, fallopian tubes, ovaries, or top 1/3 of vagina)
testicular feminization
- obesity
- amenorrhea
- hirsutism
- increased adrenal androgens
PCOS
treatment for glucose intolerance and DM in PCOS
metformin
treatment for virilization in PCOS
spironolactone
- tall male
- insensitivity of FSH and LH receptors in testicles
- XXY karyotype
- VERY HIGH FSH and LH levels, BUT NO testosterone is produced from testicles
Klinefelter’s syndrome
treatment for Klinefelter’s syndrome
testosterone
- ANOSMIA (key to diagnosis)
- hypogonadism
- LOW GnRH, FSH, and LH
Kallman’s syndrome