Endocrinology Flashcards

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1
Q

Adrenal Insufficiency - Addison’s Disease

eti, sxs

A

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
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2
Q

Adrenal Insufficiency - Addison’s Disease

dx, tx

A

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
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3
Q

Cushing’s Disease

eti, sxs

A

HIGH cortisol

Eti:

  1. Cushing Syndrome
    • sxs from prolonged exposure to excess cortisol
  2. Cushing’s Disease
    1. ACTH secreting pituitary microadenoma, usu on v small anterior pituitary
    2. F 3x > M

Sxs:

  • Obesity - buffalo hump, moon facies, supraclavicular pads
  • HTN
  • Thirst
  • Pigmented striae
  • oligomenorrhea/amenorrhea
  • polyuria
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4
Q

Cushing’s Disease

dx, tx

A

Dx:

  1. 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
  2. Low dose Dexamethasone Suppresion Test
    • failure of steroid to decrease cortisol = diagnostic
  3. High dose Dexamethasone Supression test
    • no suppression (cortisol still high) = Cushing’s syndrome

Tx for Cushing’s Disease - Transsphenoidal resection

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5
Q

Diabetes Inspidus

eti, Sxs

A

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
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6
Q

Diabetes Inspidus

dx, tx

A

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
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7
Q

Diabetic Mellitus Type 1

eti, sxs, dx, tx

A

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
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8
Q

Diabetes Mellitus Type 2

eti, sxs, tx (no meds)

A

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
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9
Q

Diabetes Mellitus T2

Meds

A

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
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10
Q

Diabetic Ketoacidosis

A

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!

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11
Q

NonKetotic Hyperglycemia

A

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
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12
Q

Hypothyroidism

A

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
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13
Q

Hyperthyroidism

A

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
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14
Q

Thyroiditis - Hashimoto’s

A

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

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15
Q

Thyroiditis - Postpartum thyroiditis

A

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

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16
Q

Thyroiditis - Subacute thyroiditis (Quervain’s Thyroiditis)

A

MCC of thyroid pain, mc in F>M

Eti - post infectious and muscle aches - following symptoms of fever, myalgias, & pharyngitis

Sxs:

  • Inflamed, painful thyroid
  • fever and muscle aches

Early hyperthyroid course, then hypothyroidism

Increased ESR 60-100

17
Q

Thyroiditis - Drug induced and Infectious

A

Drug Induced

  • antithyroid meds - methimazole and PTU
  • lithium - bipolar
  • amiodarone - antiarrhythmic
  • Interferon alpha
  • Tyrosine kinase inhibitors - anticancer
  • TSH recheched q 6-12 mos

Infectious

  • Hematogenous spread of staph or strep
  • Inflammation - fever, heat, pain, redness, swelling
  • Incr WBC
18
Q

Hyperparathyroidism

A

Overactive parathyroid gland - secrete too much PTH = incr level of Ca

increase PTH => bone breakdown => Ca rise

Primary - d/t parathyroid adenoma

Secondary - physiologic resposnse to hypoCa or Vit D deficiency (MCC kidney disease)

Sxs: same as hypercalcemia

  • bone loss (incr PTH and Ca abs from bones) = pain in bones
  • renal loss of Ca = kidney stones
  • incr GI abs of Ca = abd groans
  • irritability, psychosis, depression = moans

Dx:

  • Incr Ca, PTH, decr phosphorus
  • urine - hyperphosphaturia, hypercalciuria

Tx:

  • Primary = surgical resection, if all 4, remove 3.5 glands
  • Secondary = replace cause (vit D/Ca supp)
  • if Ca very high = IV fluids, Lasix, calcitonin
    • tx osteoporosis with bisphosphonates