Endo Flashcards
(45 cards)
Metabolic Syndrome definition, sx, dx, tx
Syndrome of multiple metabolic abnormalities that increase the risk for complications such as DM & CVD
PATHO: insulin resistance is the key component
*free fatty acids are released, which causes an increase in triglyceride & glucose production as well as reduction in insulin sensitivity, leading to insulin resistance & hyperinsulinemia
*the high levels of insulin cause sodium reabsorption, leading to HTN
dx
At least 3/5:
HDL: <40mg/dL men; <50mg/dL women
BP: ≥135/85 (or drug tx for HTN)
Fasting triglyceride levels: ≥150mg/dL (or drug tx)
Fasting blood sugar: ≥100mg/dL (or drug tx for high glucose)
Waist circumference: >40in (102cm) men; >35in (88cm) women
tx
Lifestyle: weight reduction, exercise & ↑ physical activity, diet (rich in fruits, vegetables, lean poultry, fish, whole grains)
Weight loss meds: phentermine and lorcaserin MOA
Phentermine: 3mo short-term use ONLY
MOA: unknown; sympathomimetic
Lorcaserin: MOA: selective serotonin agonist (5-HT2C receptor) that induces satiety. Inhibits fat absorption
Acromegaly/Gigantism definition, sx, dx, tx
Gigantism: child (before fuse)
Acromegaly: adult (after fuse)
Etiologies: MCC by pituitary adenoma that secretes excessive amounts of GH
sx: Large hands, feet, nose, lips, ears, jaw, tongue
dx
*increased IGF-1
*GH test 2hr after glucose load
MRI/CT: pituitary tumor
tx: Pituitary tumor removal
Diabetes Insipidus definition, sx, dx, tx
*inability of the kidney to concentrate urine, leading to production of large amounts of dilute urine
2 TYPES:
Central: no production of ADH (MC)
*idiopathic MCC, destruction of posterior pituitary, head trauma, CNS tumor, infection
Nephrogenic: partial or complete renal insensitivity to ADH
*lithium, amphotericin B, hypokalemia, hypercalcemia, acute tubular necrosis, hyperparathyroidism
sx
*polyuria + polydipsia
*high-volume nocturia
Neurologic sxs of hypernatremia
*confusion, lethargy, disorientation
*seizures, coma
PE:
*dehydration, hypotension, rapid vascular collapse
dx
*increased serum osmolarity
*decreased urine osmolality & specific gravity
*increased urine volume
Fluid deprivation test: *establishes dx
*continued production of large amounts of dilute urine (low urine osmolality)
ADH stimulation test: *distinguishes central v. nephro
*central: responds to ADH
*nephrogenic: continued production of large amounts of dilute urine (no response to ADH)
tx
Central:
*desmopressin (DDAVP) first line
*carbamazepine second line
Nephrogenic:
*correct underlying cause
*hydrochlorothiazide, indomethacin, or amiloride is sxs persist
*sodium & protein restriction
Primary Hyperaldosteronism
(Conn Syndrome) definition, sx, dx, tx
▪︎Caused by autonomous overproduction of aldosterone in zona
glomerulosa of one or both adrenal glands
MCC:
▪︎bilateral idiopathic hyperplasia of the adrenal glands (~60%)
▪︎aldosterone-producing adrenal adenomas (~30%)
sx
▪︎HTN & hypokalemia
HTN:
▪︎resistant to 3 drugs, onset <30yo
▪︎SBP ≥150mmHg or DPB ≥100mmHg
Features of hypokalemia:
▪︎fatigue, muscle weakness, cramping
▪︎HA, palpitations, constipation
dx
▪︎plasma aldosterone concentration (PAC)
▪︎plasma renin activity (PRA) or concentration (PRC)
8AM PAC & PRA or PRC from seated patient
▪︎PAC ≥10ng/dL, PRA <1ng/mL/hr, PRC < lower limit of normal
Confirmatory: 3d high-sodium diet, then 24h urine aldosterone
▪︎urinary aldosterone >12mcg/d
tx
Bilateral or surgery not possible:
▪︎Spironolactone (preferred)
▪︎Eplerenone (less effective at ⇣ BP)
Unilateral, adenoma, carcinoma:
▪︎laparoscopic unilateral adrenalectomy
Chronic Adrenal Insufficiency definition, sx, dx, tx
*adrenal gland does not produce enough hormones
Hypothalamus (CRH) 🡪 pituitary (ACTH) 🡪 adrenal (cortisol)
RAAS 🡪 aldosterone
Primary (Addison Disease): adrenal gland destruction
*lack of cortisol & aldosterone
Etiologies:
*autoimmune MCC in the US
*infection (TB, HIV) MCC in developing countries
*vascular: thrombosis or hemorrhage 🡪 Waterhouse-Friderichsen
*others: trauma, metastatic disease, meds (ketoconazole)
Secondary: pituitary failure of ACTH secretion
*lack of cortisol ONLY; aldosterone intact due to RAAS
Etiologies:
*hx of exogenous glucocorticoid use MCC overall
*hypopituitarism
sx
Sxs due to lack of cortisol:
*weakness, myalgias, fatigue
*GI: weight loss, anorexia, N/V/D, abdominal pain
*HA, sweating, abnormal menstruation
*mild hyponatremia, salt craving
*hypotension, hypoglycemia
Addison: sxs due to lack of sex hormones & aldosterone
*hyperpigmentation (↑ ACTH stimulates melanocyte-stimulating hormone secretion)
*orthostatic hypotension
*women: loss of libido, amenorrhea, loss of axillary/pubic hair
dx
Baseline labs: 8am ACTH, cortisol, renin
*↑ renin (esp. w/ primary)
*cortisol <3µg/dL = (+) adrenal insufficiency
*Primary: ↑ ACTH
*Secondary: ↓ ACTH
Labs:
*hypoglycemia
Addison:
*hyponatremia, hyperkalemia
*non-anion gap metabolic acidosis
Screening: high-dose ACTH (Cosyntropin)
*no rise in cortisol 🡪 Addison (primary)
*destroyed adrenal gland = no response
*normal rise in cortisol 🡪 secondary
*adrenal gland in intact = responds
tx
Glucocorticoid replacement:
*hydrocortisone first line
*dexamethasone
Addison 🡪 (+) mineralocorticoid
*fludrocortisone
Illness, surgery, high fever, stress:
*3x the normal PO dose
Adrenal (Addisonian) Crisis definition, sx, dx, tx
*sudden worsening of sxs
*precipitated by a “stressful” event (illness, surgery, trauma, volume loss, hypothermia, MI, fever, sepsis, hypoglycemia, steroid withdrawal, etc.)
Etiologies:
*abrupt withdrawal of steroids (w/o tapering) MCC
*previously undiagnosed + subject to stress
*diagnosed + no increase in meds during stress
*bilateral adrenal infarction (hemorrhage)
sx
Shock:
*hypotension
*hypovolemia
Profound weakness, severe abdominal pain, peripheral vascular collapse, electrolyte abnormalities, shock
dx
Labs:
*hyponatremia
*hyperkalemia
*hypoglycemia
*cortisol, aldosterone, ACTH, renin, CBC
tx
*isotonic fluids (NS or D5NS) plus
*IV hydrocortisone
*dexamethasone if undiagnosed
*reversal of electrolyte disorders
*fludrocortisone
Cushing’s Syndrome definition, sx, dx, tx
*s/sxs related to cortisol excess
Etiologies:
*long-term high-dose steroid therapy MCC overall
*exogenous
*Cushing’s Disease: pituitary ACTH overproduction
*ectopic ACTH-producing tumor (SCLC)
*adrenal tumor (adenoma)
sx
Fat redistribution:
*central obesity, “moon facies”
*buffalo hump, supraclavicular fat pads
*thin extremities
Skin:
*thin skin (atrophy), striae (red or purple, 1cm wide)
*easy bruising, ↓ wound healing
*hyperpigmentation if ↑ ACTH
Acanthosis nigricans: epidermal hyperplasia & thickening of the skin esp. around neck/armpit w/ hyperinsulinemia
Androgen excess: hirsutism, acne, oily skin
*HTN
dx
Screening tests:
(1) 24hr urinary-free cortisol (most specific)
(2) nighttime salivary cortisol
(3) low-dose (1mg) overnight dexamethasone suppression test
*elevated cortisol/no suppression = (+) syndrome
Differentiating tests: ACTH + high-dose dex suppression test
*Cushing’s Disease: ↑ ACTH + SUPPRESSION
*Ectopic ACTH-producing tumor: ↑ ACTH + no suppression
*Adrenal tumors, steroids: ↓ ACTH + no suppression
Labs: hyperglycemia, dyslipidemia, leukocytosis, hypokalemia, metabolic alkalosis
Cushing’s Disease 🡪 pituitary MRI
Adrenal tumor 🡪 abdominal CT
Ectopic ACTH-producing lung tumor 🡪 CXR
tx
Corticosteroid use:
*gradual taper to prevent Addisonian crisis
Cushing’s Disease:
*transsphenoidal resection
*inoperable 🡪 radiation, Pasireotide
Adrenal tumor: tumor excision
Ectopic tumor: resection
*unresectable 🡪 Ketoconazole, Metyrapone
DM Type 1 defintion and DKA
90% autoimmune – pancreatic β cells fail to respond to stimuli & undergo autoimmune destruction
Onset: usually <30 (3/4 diagnosed in childhood)
*peaks at 4-6y then again at 10-14y
*NOT associated w/ obesity
Type 1A: autoimmune (MC); HLA-DR3 & HLA-DR4 association
Type 1B: non-autoimmune β cell destruction
Main RF: family hx (first-degree relative)
Diabetic Ketoacidosis (DKA):
*infection MCC – others: D/C or inadequate insulin therapy, undiagnosed DM, MI, CVA, pancreatitis
DMT1 sx
3 initial presentations:
*Classic new onset: polydipsia, polyuria, & weight loss + hyperglycemia & ketonemia (or ketonuria)
*DKA
*Silent (asymptomatic) incidental discovery
*perineal candidiasis – common in young children/girls
*acute visual disturbances
DKA: sxs evolve rapidly over 24h
Child appears acutely ill & suffers from moderate to profound dehydration
*polyuria, polydipsia
*fatigue, HA, AMS
*N/V, abdominal pain
PE: tachycardia, tachypnea, hypotension, ↓ skin turgor
*fruity (acetone) breath
*Kussmaul respirations (deep, labored breathing)
DM1 Associations & Solutions:
Dawn Phenomenon: normal glucose until 2-8am when it rises; results from ↓ insulin sensitivity & a nightly surge of counter-regulatory hormones during nighttime fasting
TX: bedtime injection of NPH to blunt morning hyperglycemia; avoid carbs late at night
Somogyi Effect: nocturnal hypoglycemia followed by rebound hyperglycemia d/t surge in growth hormone
TX: ↓ nighttime NPH dose or give bedtime snack
Insulin Waning: a progressive rise in glucose from bed to morning
TX: change of insulin dose to bedtime
DMT1 dx
Criteria: one of the following
1) Fasting plasma glucose ≥126mg/dL on >1 occasion
2) Random plasma glucose ≥200mg/dL + classic s/sxs of hyperglycemia
3) OGTT – plasma glucose ≥200mg/dL after 2hr
4) HbA1C ≥6.5% confirmed by repeat testing
Autoantibodies: GAD65, IA2, insulin
*any (+) autoantibodies 🡪 assume DM1
LOW insulin & C-peptide
*urine: glucose, ketones
DKA:
*BG >250mg/dL (usually <800mg/dL)
*acidic pH <7.3, anion gap usually >20mEq/L
*bicarb <15-18
*(+) urine/serum ketones
Potassium: total body K is depleted, but serum K is normal/elevated (K shift from intracellular fluid to extracellular fluid)
DMT1 tx
INSULIN THERAPY!!
*Multiple Daily Injections (MDI): long-acting insulin injections 1-2x/d + rapid or short-acting insulin before each meal/snack
*Insulin Pump: delivers continuous SC infusion of rapid or short-acting insulin + supplemented boluses before each meal/snack
DKA: SIPS – saline, insulin (regular), potassium repletion, search for underlying cause
Saline: isotonic 0.9% (normal saline) until hypotension & orthostasis resolves
*then switch to ½ NS (0.45%)
*once serum glucose reaches ~200-250, add dextrose (to prevent hypoglycemia from insulin)
Insulin: for pts w/ K ≥3.3mEq/L – regular insulin continuous infusion; 2 regimens
*0.1units/kg IV bolus then continuous IV infusion 0.1units/kg/h
*NO BOLUS, start continuous IV infusion 0.14units/kg/h
*if serum glucose doesn’t fall by at least 50-70mg/dL in the first hour, DOUBLE rate of insulin infusion
Potassium: regardless of serum K, pts have a large total body K deficit
*K <3.3mEq/L – HOLD INSULIN; give IV KCl 20-40mEq/L until K above 3.3mEq/L
*K 3.3-5.3mEq/L – give KCl 20-30mEq/L IV fluid
*maintain SERUM K 4-5mEq/L
*K >5.3mEq/L – DO NOT GIVE K; check serum K q2h & delay KCl admin until serum K <5.3mEq/L
Sodium Bicarbonate: ONLY GIVEN TO PTS W/ pH <6.90 (admin associated w/ complications of overcorrection & increased cerebral edema)\
DM Type II definition and HHS
Combination of insulin insensitivity (resistance) & relative impairment of insulin secretion
Risk Factors: obesity greatest RF, decreased physical activity, family hx, metabolic syndrome
Hyperosmolar Hyperglycemic State (HHS): seen in older patients, associated w/ more severe dehydration; no ketosis or acidosis
DMT2 and HHS sx, dx, tx
3 Ps: polyuria, polydipsia, polyphagia
*poor wound healing
*increased infections
HHS: s/sxs develop more insidiously
*polyuria, polydipsia, weight loss, profound dehydration
*NEURO SXS – mental obtundation, coma, seizures
*fatigue, weakness, N/V
PE: tachycardia, hypotension, ↓ skin turgor, ↑ capillary refill time
dx
Criteria: one of the following
1) Fasting plasma glucose ≥126mg/dL on >1 occasion
2) Random plasma glucose ≥200mg/dL + classic s/sxs of hyperglycemia
3) OGTT – plasma glucose ≥200mg/dL after 2hr
4) HbA1C ≥6.5% confirmed by repeat testing
HIGH insulin & C-peptide
HHS:
*BG >600mg/dL, often >1000mg/dL
*Plasma osmolality >320
*pH >7.3, bicarb >18
*ketones: small
tx
Initial: diet, exercise, lifestyle changes
Asymptomatic:
*metformin MC initial
*intolerance/CI: GLP-1 receptor agonists, SGLT2 inhibitors
Symptomatic: insulin indicated as initial therapy
HHS: fluids most important management!!
*start IV fluids – 0.9% NaCl at 1L/h
*once glucose ~300mg/dL 🡪 5% dextrose w/ 0.45% NaCl at 150-250mL/h
Insulin: 0.1units/kg bolus then 0.1units/kg/h continuous IV infusion
Potassium: same guidelines as in DM1
Rapid acting insulin meds and their onset/duration
aspart (Novolog), lisper (Humalog), glulisine (apirdra)
onset: 10-20 mins
duration: 3-5 hours
long acting insulin meds, onset and duration
detemir, glargine, degladuc
onset: 1-4 hours
duration: 10-24 hours
Biguanides meds and MOA
metformin
MOA: Decreased hepatic glucose production
Sulfonylureas meds and MOA
- 2nd gen: glipizide, glyburide, glimepiride
- 1st gen: tolbutamide, chlorpropamide
Stimulates pancreatic beta cell insulin release
- hypoglycemia
Chlorpropamide: - hyponatremia, disulfiram reaction
GLP-1 Agonists meds and MOA
liraglutide, semaglutide, dulaglutide
MOA: Increased glucose-dependent insulin secretion
DPP4 Inhibitors meds and MOA
- sitagliptin
- linagliptin
- saxagliptin
MOA: Increases GLP-1 levels
SGLT-2 Inhibitors meds and MOA
- empagliflozin
- canagliflozin
- dapagliflozin
MOA: Lowers renal glucose threshold, leading to increased urinary glucose excretion
Hyponatremia sx, dx, tx
Acute: <48h ⇢ acute brain swelling, ⇡ ICP
Chronic: ≥48h ⇢ brain adapts to hypotonicity
S/SXS: HA, lethargy, N/V, confusion, seizures, brainstem herniation, coma, death
*often asymptomatic, may have mild concentration or cognitive defects, gait disturbances
dx
Normal Serum Sodium: 135-145mEq/L
SEVERE HYPONATREMIA: <125mEq/L
*urine osmolality (mOsm/kg)
≤100 ⇢ ADH-independent
>100 ⇢ ADH-dependent ⇢ look at urine sodium
*urine sodium (ref. ~20mEq/L)
tx
Symptomatic (seizures, confusion):
*emergent tx required regardless of etiology
*IV 3% NaCl in 100mL bolus over 10min
▪︎can repeat up to 2x if needed
*4-5mEq/L ⇡ of Na usually sufficient to promptly reverse neurological symptoms & ⇣ ICP
Hypovolemic: IV normal saline
Hypervolemic: fluid restriction +/- loop diuretics
Euvolemic: fluid restriction
Warning ⇢ osmotic demyelination syndrome and locked in syndrome
*result of overly rapid correction of sodium
*correction shouldn’t exceed 8mEq/L within 24h
Hypernatremia sx, dx, tx
S/SXS (Na >160mEq/L): lethargy, weakness, & irritability
▪︎lesions in hypothalamus (i.e., primary hypodipsia) sometimes progressing to ⇢ delirium, seizures, coma
*Diabetes Insipidus ⇢ ⊕polyuria, Uosm <300
▪︎Central: ⇣ pituitary release of ADH Chronic: >48h ⇢ Na levels slowly rise, brain adapts
▪︎Nephrogenic: renal resistance to ADH *often asymptomatic +/- signs of dehydration
SEVERE HYPERNATREMIA: ≥170mEq/L
DX: often from hx, MCC: water loss w/o replacement
*If Na >150 in alert patient w/ water access
⇢ suspect primary hypodipsia
*if etiology unclear ⇢ urine osmolality (mOsm/kg)
<300: diabetes insipidus ⇢ DDAVP challenge
▪︎Uosm ⇡ after DDAVP ⇢ central, if not ⇢ nephro
300-600: possible osmotic diuresis: ⊕glucosuria
>600: extrarenal ⇢ look at urine sodium
*urine sodium (mEq/L)
<20 ⇢ hypovolemia (e.g., vomiting, diarrhea, etc.)
>100 ⇢ sodium overload (i.e., iatrogenic)
tx
*requires induction of ⊕water balance
*calculate FWD
*hypotonic fluids ⇢ D5W most commonly used
If hypovolemic + hypernatremic
*FIRST: correct hypovolemia w/ ISOTONIC fluids
*then correction of sodium w/ hypotonic fluids
Hypokalemia sx, dx, tx
S/SXS: usually asymptomatic
*muscle weakness, cramps, ⇣ DTRs
*cardiac arrhythmias, rhabdomyolysis w/ AKI (K <2.5mEq/L)
dx
*normal K 3.6-5.0mEq/L
*24h-urinary K excretion >30mEq/d ⇢ renal wasting
*spot urine K/UCr ratio >13mEq/g ⇢ renal wasting
EKGΔ
*flat/inverted T waves ⇢ ST depression ⇢ U waves
*prolonged QT, PAC/PVCs, bradycardia, VT/VFIB
tx
*PO K replacement for mild/moderate
*IV KCl reserved for K <3.0mEq/L
▪︎avoid dextrose fluids ⇢ stimulates insulin release which shifts K intracellularly
*give Mg w/ potassium replacement
