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PANCE Prep- Endocrine Flashcards

1
Q

Labs:

  1. increased ACTH and cortisol= ?
  2. increased ACTH and decreased cortisol = ?
  3. Decreased ACTH and increased cortisol= ?
A
  1. Cushings Disease (pituitary adenoma)
  2. Addison’s Disease
  3. Adrenal adenoma
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2
Q

Describe the lab findings for

  1. primary hypothyroidism
  2. subclinical hypothyroidism
  3. TSH-mediated hyperthryoidism
  4. primary hyperthryoidism
A
  1. High TSH, low fT4
  2. High TSH, normal ft4
  3. High TSH, high fT4 (2ry or 3ry- same direction)
  4. Low TSH, high fT4
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3
Q

What do the following thyroid Ab typically mean?
Anti-thyroid peroxidase Ab
Anti-thyroglobulin Ab
Thyroid stimulating Ab (TSH receptor Ab)

A
  1. Hashimoto’s or other autoimmune thyroiditis
  2. Hashimoto’s or other autoimmune thyroiditis
  3. Specific for Graves disease
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4
Q

RAdioactive iodine test:

  1. Diffuse uptake
  2. Decreased uptake
  3. Hot nodule
  4. multiple nodules
  5. cold nodule
A
  1. Graves or TSH-secreting pit. adenoma
  2. Thyroiditis (Hashimotos, postpartum, deQuervain)
  3. Toxic adenoma
  4. Toxic Multinodular goiter
  5. r/o malignancy
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5
Q
  • Congential hypothyroidism due to maternal hypothyroidism or infant hypopituitarism
  • Macroglossia, hoarse cry, coarse facial features, umbilical hernia, weight gain, mental delay
A

Cretinism

TX: levothyroxine

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6
Q

How do you dx Euthryoid sick syndrome

A

Decreased fT4/T3, TSH
Abnormally low T3
Increased reverse T3

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7
Q

How do you treat thyroid storm

A
  1. Anti-thyroid meds: IV PTU or Methimazole
  2. BB for symptomatic tx
  3. Supportive: IV glucocorticoid (inhibits conversion of T4 into T3), Antipyretics (avoid ASA) , cooling blankets
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8
Q

Tx of Myxedema crisis and who is MC seen in

A
  • extreme form of hypothyroidism
  • MC seen in elderly women w/ longstanding hypothyroidism in winter (cold weather)

TX:

  1. IV levothyroxine
  2. passive warming w/ blankets- avoid rapid rewarming
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9
Q
  • Diffuse, enlarged thyroid
  • Thyroid bruits*
  • Ophthalmopathy: lid lag, exophthalmos/proptosis
  • ***Pretibial myxedema
A

Grave’s disease
*MC cause of hyperthryoidism

DX: +Thyroid-stimulating immunoglobulins (Ab)
-Low TSH, high fT4/fT3
RAIU: Diffuse uptake

TX: radioactive iodine (MC tx)

  1. Methimazole or PTU
  2. BB- sx
  3. Thryoidectomy
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10
Q

+/- dyspnea, dysphagia, stridor, hoarseness

  • No skin/eye changes
  • Labs: low TSH, high fT4/T3
  • RAIU: PATCHY areas of both increased decreased uptake
A

Toxic multinodular Goiter

TX: Radioactive iodine

  • Methimazole or PTU
  • BB
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11
Q

+/- dyspnea, dysphagia, stridor, hoarseness

  • No skin/eye changes
  • Labs: low TSH, high fT4/T3
  • RAIU: increased LOCAL uptake
A

Toxic adenoma

TX: Radioactive iodine

  • Methimazole or PTU
  • BB
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12
Q
  • Diffuse, enlarged thyroid
  • Bitemporal hemianopsia
  • Mental disturbance
  • Labs: high TSH and fT4/T3
  • RAIU: DIFFUSE uptake
A

TSH secreting pituitary adenoma

TX: Transsphenoidal surgery to remove pit. adenoma

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13
Q

TX of postpartum thyroiditis

A
  • return to euthyroid state in 12-18 months w.o tx
    1. ASA
    2. No anti-thyoroid meds

*Have + thyroid Ab present

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14
Q

Firm hard, ‘woody’ nodule

A

Riedels thyroiditis

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15
Q

MC cause of hypothyroidism in the US= ?

MC cause of hypothyroidism in the world = ?

A

Hashimoto’s Thyroiditis

Iodine deficiency

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16
Q

MC type of benign and malignant thyroid nodules

A 
Benign: 
Follicular adenoma (colloid)-MC

Malignant: Papillary Carcinoid (80%)
**Only 5% of thyroid nodules are malignant

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17
Q

What thyroid carcinoma?

  • Hx of radiation exposure
  • young female
  • Local cervical lymph node METS
A

Papillary (MC-80%)

  1. MC after radiation exposure
    * least aggressvie and distant METS are uncommon
    * excellent prognosis
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18
Q

What thyroid carcinoma?

  • Associated with MEN2
  • Secretes Calcitonin
A

Medullary

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19
Q

What thyroid carcinoma?

  • Mc in males >65y/o
  • rapid growth w/ compressive sx
  • May invade trachea
A

Anaplastic

*Most aggressive

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20
Q

__ is required for intestinal Ca2+ absorption

What hormones regulate Ca2+ levels

A

Vit. D

PTH and Calcitriol (Vit. D) increased blood Ca++ (via GI, kidney absorption and increased osteoclast activity)

Calcitonin decreased blood Ca++ (via decrease GI, kidney absorption and increased bone mineralization)

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21
Q

MC causes of primary hyperPTH and secondary hyperPTH

A

primary: parathryoid adenoma (80%)
Parathyroid hyperplasia/enlargement
-Lithium

secondary: hypocalcemia or vit. D def.
- Chronic kidney failure (MC)

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22
Q

S/S of primary hyperparathyroidism

A

HYPERcalcemia: “stone, bones, abdominal groans, psychic moans” (kidney stones, bone pain/fractures, ileus, constipation, weakness, fatigue)
-decreased DTR

Labs: TRIAD: HyperCa++, increased PTH, decreased phosphate
-increased 24hr urine calcium excretion

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23
Q

S/S of hypoparathryoidism

A

HYPOcalcemia: carpopedal spasm, Trousseau’s and Chvosteks sign
-Increased DTR

Labs: TRIAD: HypoCa++, decreased PTH, increase phospate

TX: Ca and Vit. D supp.

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24
Q

What is Chvostek’s sign and Trousseau’s sign

A

Chvosteks: facial spasm with tapping of the facial nerve

Trousseau: inflation of BP cuff above systolic BP causes carpal spasm

*seen in hypocalcemia

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25
MC of hypocalcemia w/ decrease PTH and increased PTH
Decreased PTH: hypoparathyroidism (autoimmune, post surgical) Increased PTH: chronic renal dz, liver dz, hypomagnesemia
26
EKG findings of hypoCa++ and hyperCa++
Hypo: prolonged QT hyper: shorten QT interval
27
TX of hypercalcemia
Mild: nothing- tx underlying cause Sever/symptomatic: IV saline--> furosemide 1st line *avoid hydrochlorothiazide
28
DEXA scan of what indicates osteoporosis and what is the tx
T score = -2.5 TX: 1. Bisphosphonates (inhibits osteoclasts) (Alendronate, Risedronate, Ibandronate) 2. Vit D (Ergocalciferol) 3. Selective Estrogen Receptor Modulator (SERM)- Raloxifene 4. Estrogen 5. PTH tx 6. Calcitonin (last line tx)
29
SE of Bisphosphonates
1. Pill esophagititis 2. jaw osteonecrosis 3. pathologic fx of femur
30
Blue-tinted sclerae and presenile deafness
Osteogenesis imperfecta
31
- Bone and prox. muscle pain - Labs: low Ca and high phosphate, PTH - Radiographs: periosteal erosions, bony cysts, "salt and pepper" appearance of skull - Cystic brown tumors on biopsy
Renal osteodystrophy *Osteitits fibrosis cystica and osteomalacia TX: phosphate binders: Calcium carbonate, calcium acetate, Sevelamer 2. vit. D active forms (Calcitriol)
32
How can you differentiate osteoporosis and osteomalacia
Osteoporosis: (bone breakdown) mineral and matrix loss is proportional -"brittle bones" Osteomalacia: (vit D def) decreased mineralization of bone osteoid only - cortical thinning -XRAY: looser lines (zones) and "pseudofracture" lines "soft bones"
33
Describe what layers of the adrenal cortex produce each hormone
G- glomerulosa (outer)= A-aldosterone F- fasiculata= C-Cortisol R- reticularis = E-estrogen/androgen
34
MC causes of primary and secondary adrenocortical insufficiency
Primary (Addison's disease) adrenocortical insuff. = lack cortisol AND aldosterone 1. Autoimmune- MC in industrialized countries (causes adrenal atrophy) 2. Infection- MC worldwide- TB, HIV (adrenal calcifications) Secondary= lack of cortisol (MC than primary) 1.Exogenous steroid use
35
1. Hyperpigmentation 2. Orthostatic hypotension (decreased aldosterone) 3. HyperK+, hypoNA+, Hypoglycemia 4. Metabolic acidosis
Primary (Addison's disease) adrenocortical insuff.
36
How to dx and tx adrenocortical insuff.
1. HD ACTH stimulation test--> little/no increase in cortisol levels= Adrenal insuff 2. CRH stimulation test--> Increased ACTH levels but LOW cortisol = primary/Addison OR low ACTH and low cortisol= secondary TX: primary: Glucocorticoids (Hydrocortisone) + mineralocorticoids (fludrocortisone) secondary: glucocorticoids only **During illness/surgery/high fever oral dosing needs to be adjusted to recreate the normal adrenal gland response to stress (ie. 3x normal dose)
37
Tx of Adrenal (Addisonian) Crisis
1. IV fluids: normal saline or D5 if hypoglycemic 2. IV hydrocortisone 3. fx electrolytes 4. Fludrocortisone
38
Causes of Cushing's Syndrome
*hypercortisolism Exogenous: LT HD corticosteroid (MC cause overall) Endogenous: 1. Cushings Disease (70%)- Benign pit. adenoma or hyperplasia (secretes ACTH) 2. Ectopic ACTH- small cell lung CA (secretes ACTH) 3. Adrenal tumor
39
How do you dx Cushing's Syndrome
Screen: 1. LD dexamethasone suppression test--> No suppression = Cushings syndrome 2. 24hr urinary free cortisol levels --> increased urinary cortisol= Cushings syndrome 3. Salivary cortisol levels--> increased cortisol = C.S Differentiating 1. HD dexamethasone suppression test --> Suppression = Cushings Disease OR --> no suppression= adrenal or ectopic ACTH producing tumor 2. ACTH levels--> decreased ACTH= adrenal tumors OR --> normal/increased ACTH= Cushings disease or ectopic ACTH producing tumor
40
Tx of 1. Cushings DZ 2. Ectopic ACTH-secreting or adrenal tumor 3. Iatrogenic steroid tx (hypercortisolism)
1. Transsphenoidal surgery 2. tumor removal 3 .GRADUAL steroid taper
41
Causes of primary and secondary hyperaldosteronism
Primary: renin-independent 1. idiopathic or idiopathic bilateral adrenal hyperplasia 2. Conn's syndrome: Adrenal aldosteronoma Secondary: due to increased renin 1. renal artery stenosis 2. decreased renal perfusion (CHF, hypovolemia)
42
- Proximal muscle weakness, polyuria*, fatigue, constipation - Hypertension** HA**, flushing of face - NOT EDEMATOUS - Labs: HypoK+ w/ metabolic alkalosis
Hyperaldosteronism DX: - Labs: hypoK+ w/ metabolic alkalosis - Aldosterone:renin ratio screening if hypertensive (ARR>20 and plasma aldosteron >20 and *low plasma renin levels= primary) - DEFINITIVE TEST: saline infusion test: no decrease in aldosterone level= primary
43
How to tx hyperaldosteronism 1. Conn's syndrome 2. Hyperplasia 3. Secondary (renovascular HTN)
1. excision of adrenal aldosteronoma + spironolactone (blocks aldosterone) 2. Spironlactone, ACEI, CCB 3. Angioplasty definitive, ACEI
44
How do you dx and tx PCC
1. increased 24hr urinary catecholamines including metanephrine and vanillymandelic acid 2. MRI/CT 3. S/S= HTN, palpitations, HA, excessive sweating TX: complete adrenalectomy ***Preoperative nonselective alpha-blockade w/ PHEnoxybenzamine or PHEntolamine x7-14days followed by BB (do not initiate w/ BB to prevent unopposed alpha-constriction)
45
s/s of hyperprolatinemia include: amenorrhea, galactorrhea, infertility because prolactin inhibits gonadotropin-releasing hormone (FSH/LH) TX ?
TX: 1. stop offending drugs (dopamine antagonists) 2. Dopamine agonists: Cabergoline* or bromocriptine
46
What is the difference between type 1 and 2 DM
Type 1: Pancreatitc beta cell destruction (inability to produce insulin) (MC dx <30y/o) Type 2: insulin resistance and relative impairment of insulin secretion (MC dx >40y/o)
47
What is the first sign of diabetic nephropathy?
microalbuminuria TX: ACEI *DM is most common cause of ESRD (HTN is 2nd MC)
48
DX of DM 1. Fasting plasma glucose: 2. 2hr GTT: 3. HgbA1c: 4. Random plasma glucose:
1. Fasting plasma glucose: (Gold standard)- 126 or higher (fasting at least 8 hrs on 2 occasions) 2. 2hr GTT: 200 or higher (3 hr GTT is GS for gestational DM) 3. HgbA1c: 6.5% or higher 4. Random plasma glucose: 200 or higher
49
Management and goals of DM
1. Diet, exercise, lifestyle changes (Carbs 50-60%, protein 15-20%, 10%unsaturated fats) 2. HgbA1c <7% 3. Lipid control LDL<100 4. Neuropathy: Gabapentin, podiatrist x1yr 5. Retinopathy: opthalmologist x 1yr 6. Nephropathy: ACEI, yearly screening for microalbuminemia and BUN/creatinine
50
What type of anti-hyperglycemic med? Benefits and SE? MOA: decreased hepatic glucose production and increases peripheral glucose utilization -decrease GI intestinal glucose absorption, increase insulin sensitivity no effect on pancreatic beta cells
Biguanides ex. Metformin Benefits: NO WT GAIN, 1st line PO meds SE: Lactic acidosis (don't give w/ hepatic or renal impairment), GI upset, Macrocytic anemia*
51
What type of anti-hyperglycemic med? Benefits and SE? -Stimulates pancreatic insulin release from beta cells
Sulfonylureas (insulin secretagogue) ex. 1st gen: Tolbutamide 2nd gen: Glipizide, glyburide, glimepiride Benefits: 2nd gen have less SE SE: Hypoglycemia** (MC), GI upset, disulfiram reaction*, WT GAIN
52
What type of anti-hyperglycemic med? Benefits and SE? -Stimulates pancreatic beta cell insulin release
Meglitindies ex. Repaglinide, Nateglinide SE: hypoglycemia (less than sulfonylurea), Wt gain
53
What type of anti-hyperglycemic med? SE? -Delays intestinal glucose absorption (inhibits pancreatic alpha amylase and intestinal alpha-glucosidase hydrolase)
Alpha-glucosidase inhibitors ex. acarbose, Miglitol SE: Hepatitis (increased LFTs), GI upset
54
What type of anti-hyperglycemic med? Benefits and SE? -Increase insulin sensitivity at peripheral receptor site-adipose and muscle tissue
Thiazolidinediones ex. Pioglitazone, Rosiglitazone * no effect on pancreatic beta cells SE: fluid retention and edema**, cardiovascular toxicity w. Avandia, MI**
55
What type of anti-hyperglycemic med? Benefits and SE? - Mimics incretin--> increase insulin secretion, decrease glucagon secretion - Delays gastric emptying
Glucoagon-like peptide (GLP-1) Agonists ex. Exenatide, Liraglutide Benefit: no wt gain SE: hypoglycemia, pancreatitis, *CI if hx of gastroparesis**, thyroid CA
56
What type of anti-hyperglycemic med? Benefits and SE? -Lowers renal glucose threshold--> increased urinary glucose excretion
SGLT-2 inhibitor ex. Canagliflozin, Dapaglifozin SE: thirst, Nausea
57
Give examples of 1. Rapid acting insulin 2. Short-acting insulin 3. Intermediate acting 4. Long acting
1. Rapid: Lispro, Aspart (give at the same time of meal- often used w/ long acting) 2. Short- regular (given 30-60min prior to meal) 3. Intermediate: NPH, Lente (covers insulin for about 1/2day or overnight) 4. Long: Detemir, Glargine/Lantus (covers insulin for 1 day, ie. basal insulin)
58
Normal glucose until rise in serum glucose levels btwn 2am-8am. results from decreased insulin sensitivity and nightly surge of counter regulatory hormones
Dawn Phenomenon TX: betime injection of NPH (to blunt moring hyperglycemia) aoviding carbs late at night
59
Noctural hypoglycemia followed by rebound hyperglycemia (due to surge in GH)
Somogyi effect TX: prevent hypoglycemia by decreasing bedtime NPH dose or give bedtime snack
60
Progressive rise in glucose from bed to morning
Insulin waning *seen when NPH dose given before dinner TX: move insulin dose to bedtime or increase the evening dose
61
what are kussmaul respirations
deep continuous respirations as lung attempts to blow off excess CO2 to reduce acidemia **seen w/ DKA
62
for DKA and HHS, describe: 1. plasma glucose 2. arterial pH 3. Serum bicarb 4. ketones
HHS: 1. plasma glucose: over 600 2. arterial pH: >7.3 3. Serum bicarb: >15 4. ketones: small DKA: 1. plasma glucose: >250 2. arterial pH: <7.3 3. Serum bicarb: 15-18 4. ketones: Positive
63
Tx of DKA/HHS
*DKA= DM1, HHS= DM2 1. IV fluids** (isotonic 0.9% NS--> then 0.45% NS after hypotension resolves--> then D5 0.45 1/2 NS when glucose reaches 250 2. Insulin (regular) 3. K+ repletion (despirt serum K elvels, pt always has total K+ def.)
64
Multiple Endocrine Neoplasia I (MEN I) are rare inherited disorders of 1 or more overactive endocrine gland tumors:
1. Parathyroid 90% 2. Pancrease 60% 3. Pituitary 55% * Most tumors are benign * associated w/ Menin gene defect
65
___ associated w/ presence mucosal neuromas and Marfan-like body habitus __ have more aggressive form of medullary thyroid carcinoma (presents in infancy)
MEN 2B MEN 2B
66
_____ seen only in MEN 2A ____ seen only in MEN 2B
hyperparathryoidism= 2A Neuromas, marfan-like body habitus= 2B
67
Multiple Endocrine Neoplasia II (MEN 2) are rare inherited autosomal dominant disorders that are associated w/ what types of tumors?
MEN2 (90%): medullary thyroid carcinoma, PCC, hyperPTH MEN1 (5%): medullary thyroid carcinoma, PCC, neuromas, Marfanoid
68
Management of Metabolic Syndrome
1. Lifestyle 2. weight loss - phentermine - Lorcaserin: induces satiety - Orlistat: inhibits fat absorption 3. LDL Tx 4. TG tx 5. Increase HDL 6. BP managment 7. Insulin resistance: metformin
69
___ waist circumference of men and __ for women are possible criterias for metabolic syndrome
>40 inches for men | >35inches for women

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