Endocrinology Flashcards
Adrenal Insufficiency - Addison’s Disease
eti, sxs
LOW cortisol d/t autoimmune destruction of adrenal cortex
can be precipitated by stress, illness, trauma, infection, met cancer
Sxs:
- hyperpigmentation - bronze
- weakness
- anorexia, wt loss
- Pain - athralgias, myalgias
- Anxiety, irritability, depression
Adrenal Insufficiency - Addison’s Disease
dx, tx
Dx:
- 8AM Serum cortisol < 3mcg/dL and ele ACTH > 200 pg/mL
-
ACTH Stimulation Test
- Primary/Addison’s - high ACTH, low cortisol
- Secondary/pituitary - low ACTH, low cortisol
-
Cosyntropin Stimulation Test**
- Cortisol serum should rise > 20 ug/dL
- Primary/Addison’s: high ACTH, low cortisol
- Secondary/pituitary: low ACTH, low cortisol
- Serum Dehydroepiandrosterone (DHEA) < 1000 mg/dL
- HypoNa
- HyperKalemia
- CT of Adrenal gland
- Adrenal Autoantibodies
Tx:
- Addison’s - Glucocorticoid + mineralcorticoid replacement therapy
- Hydrocortisone 1st line
- Fludrocortisone
- Secondary/pituitary - fix pituitary
Cushing’s Disease
eti, sxs
HIGH cortisol
Eti:
-
Cushing Syndrome
- sxs from prolonged exposure to excess cortisol
-
Cushing’s Disease
- ACTH secreting pituitary microadenoma, usu on v small anterior pituitary
- F 3x > M
Sxs:
- Obesity - buffalo hump, moon facies, supraclavicular pads
- HTN
- Thirst
- Pigmented striae
- oligomenorrhea/amenorrhea
- polyuria
Cushing’s Disease
dx, tx
Dx:
-
24 hr urine free cortisol collection
- if ele cortisol => ACTH level
- high plasma or serum ACTH = ACTH dependent cause
- MRI of brain => pituitary adenoma (Cushing Disease)
- low plasma or serum ACTH = ACTH independent cause
- CT of adrenals => adrenal mass/adenoma
- high plasma or serum ACTH = ACTH dependent cause
- if ele cortisol => ACTH level
-
Low dose Dexamethasone Suppresion Test
- failure of steroid to decrease cortisol = diagnostic
-
High dose Dexamethasone Supression test
- no suppression (cortisol still high) = Cushing’s syndrome
Tx for Cushing’s Disease - Transsphenoidal resection
Diabetes Inspidus
eti, Sxs
Deficiency of or resistance to Vasopressin (ADH) - decr kidney’s ability to reabsorb water = massive polyuria
Eti: MC dx in children
Central DI
- deficiency of ADH from posterior pituitary/hypothalamus
- no ADH production MCC idiopathic
- autoimmune destruction of posterior pituitary from trauma, infx, sarcoidosis
Nephrogenic DI
- lack of reaction to ADH
- partial or complete Insensitivity to ADH
- Drugs (Lithium, Amphoterrible)
- HyperCa and hypoK - can’t concentrate urine
- Acute tubular necrosis
Sxs:
- polyuria
- polydipsia
Diabetes Inspidus
dx, tx
Dx:
- Serum osmolality (blood) is high - blood gets thicker bc water is not getting reabsorbed
- Urine osmolality is low - too much water:solute ratio
-
Water Deprivation Test
- establish diagnosis of DI - urine continues to be dilute
- r/o psychogenic - ADH working so urine osmolality would increase
-
Desmopressin Stimulation Test -differentiates btwn Central or Nephrogenic
- Central - urine concentration increase = response to ADH
- Nephrogenic - continue production of dilute urine bc kidneys do not respond
Tx:
- Central - desmopressin/DDAVP
- Nephrogenic - Na and protein restriction, HCTZ, indomethacin
Diabetic Mellitus Type 1
eti, sxs, dx, tx
Type 1 - MC in young people
- Immune mediated - pancreatic islet B cells destruction via autoimmune (type 1A) and idiopathic (type 1B, MC in Asian and African)
Sxs:
- Polyuria
- Polydipsia
- wt loss despite normal or increased appetite (polyphagia)
- Blurred vision
- Glucosuria
Dx
- Random glucose > 200mg/dL
- fasting glucose > 126 on > 1 occassion
- HbA1c > 6.5%
Tx
- Mediterranean diet
- Insulin - regular insulin - in abd
- Daily asp to decr DVT risk
- Opthal exam
- Mod exercise
- prompt tx of infx
Diabetes Mellitus Type 2
eti, sxs, tx (no meds)
Type 2 - younger persons who are overwt/obese; central obesity
Sxs:
- Polydipsia
- Polyuria
- Fatigue
- Candida vaginitis
- Skin infx
- blurred vision
- poor wound healing
Dx
- Random glucose > 200
- Fasting > 126
- If btwn 100-125, PO glucose tolerance test - 3 hr plasma glucose > 200
- A1c > 6.5%
- A1c 5.7-6.4 = Prediabetes
- Fasting glucose - 100-125
- 2 hr PO glucose tolerance test 140-199
Tx:
- Weight loss - diet, exercise
- monitor eyes/feet
- control BP
- Urine Albumin/Cr screening
Diabetes Mellitus T2
Meds
Metformin
- decr hepatic glucose production & intestinal absorption
- C/I if eGFR < 30ml/min; not rec’d with 30 to 45 ml/min
- dc 24 hrs before contrast and resume 48 hrs after
- monitor Cr, stop if Cr > 1.5
Sulfonylureas
- stimulates pancreatic B-cell Insulin release
- oldest DM drugs - risk of hypoglycemia
- Glipizide, Glyburide, Glimepiride
Thiazolidinediones
- Increase Insulin sensitivity in peripheral receptor site adipose and muscle tiissues; has no effect on pancreatic beta cells
- C/I - CHF, liver disease, fluid retnetion, wt gain, bladder cancer (pioglitazone), increase in MI (rosigilitazone)
Alpha glucosidase Inhibitors
- Delays Intestinal glucose absorption
- GI side effects - TID dosing
- Acarbose, miglitol
GLP-1 Agonists
- lower blood sugar by mimicking incretin -causes insulin secretion and decreased glucagon, delays gastric emptying
- SE - req’s injection, freq GI SE,
- benefits of weight loss, reduced CV mortality (semaglutide)
- Dulaglutide (trulicity), Exenatide (bydureon)
DPP-4 Inhibitors
- inhibits degradation of GLP1 so more circulating GLP1
- expensivie, incr risk of HF (sxagliptin)
- Sitagliptin (januvia)
SGLT2 Inhibitors
- lowers renal glucose threshold, Increases urinary glucose excretion
- SE - vulvovaginitis, UTI, lower limb amps, AKI, DKA
- Benefits - wt loss, reduction in systolic BP, reduce CV risk
Insulin
- add in blood sugar A1C > 9
Diabetic Ketoacidosis
Medical emergency - complications of Diabetes
Increased insulin req’s = shortage. Body starts to use excess fat => ketone accumulations
Insulin deficiency => hyperglycemia => deH2O => ketonemia (anion gap Met Acidosis) => potassium def
Younger pts w/ Type 1 DM
Sxs:
- thirst, polyuria, polydipsia, nocturia
- weakness, fatigue, confusion
- N/V
- Chest pain/ abd pain
- Signs - tachypnea/tachycardia, hypotension, decreased skin turgor, fruity breath/Kussmaul’s respiration
Dx:
- Blood sugars > 250 mg/dL
- anion gap Met acidosis pH < 7.3 and HCO3 < 18
- Plasma ketones
Tx: IV fluids & insulin!
NonKetotic Hyperglycemia
MC in DM T2 during physiological stress
high blood sugar = high osmolarity w/o significant ketoacidosis
Eti
- acute infx/med conditions
- drugs that impair glucose tolerance - glucocorticoid, or increase fluid loss (diuretics)
Sxs:
- days to weeks
- Altered LOC
- signs of deH2O, weakness
- leg cramps
- vision problems
Dx:
- Blood sugar > 600 mg/dL or 30 mmol/L
- Osmolarity > 320 mOsm/kg
- pH > 7.3
Tx
- IV NS 0.9%
- IV insulin (if K > 3.3 mEq/L)
- LMWH - risk of clots
- decrease slowly - risk of cerebral edema if not
- K replacement as needed
- target plasma glucose in acute tx is 250-300 mg/dL
Hypothyroidism
95% Autoimmune - MC Hashimoto’s or prev thyroidectomy/iodine ablation, congenital
Sxs: - everything LOW OR SLOW
- Weakness, lethargy
- dry/coarse hair
- slow speech
- cold intolerance
- weight gain
- depression
- anemia, bradycardia, hyporeflexia
Dx
- TSH high
- T4 and T3 low
- Antithyroid peroxidase
- Antithyroglobulin ABs
Tx
- Levothyroxine/Synthroid
Hyperthyroidism
Production of too much thyroxin hormone - increase metabolism
Eti - MCC Grave’s disease (autoimmune), toxic adenoma, thyroiditis, pregnancy, amiodarone
Sxs:
- weight loss, anxiety
- warm, moist skin
- insomnia
- fine tremor, muscle cramp, hyperreflexia
- amenorrhea
- tachycardia/palpitations
- Graves - diffuse goiter w/ bruit, exopthalmos, pretibial myxedema
- heat Intolerance
Dx:
- TSH low and T4 high - primary disease
- TSH high and T4 high - secondary dz
- Anti-thyrotropin antibodies
- RA Iodine uptake = increased uptake in
- Graves = diffusely high uptake
- Toxic Multinodular goiter = Discrete areas of high uptake
Tx:
- BB symptomatic
- Methimazole
- Propylthiouracil (PTU) - safe for pregnancies in the first trimester, then switch to Methimazole
- Thyroidectomy - complication recurrent laryngeal
Thyroiditis - Hashimoto’s
Inflammation of the thyroid gland - multiple etiologies
Hashimoto’s thyroiditis
autoimmune form - thyroid tissue is destroyed by antibodies over time = chronic hypothyroidism
Sxs:
- goiter on PE
- high levels of anti-TPO antibodies
Tx
euthyroid - no treatment
Chronic hypothyroidism - lifelong sub w/ T4 aka levothyroxine
Thyroiditis - Postpartum thyroiditis
2-12 months after giving birth
Immune system diminished after pregnancy => after birth immune system becomes more active and attacks thyroid
Hyperthyroid phase 5-7 mos after birth followed by normal thyroid function