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PANCE Practice > PANCE Prep- Endocrine > Flashcards

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
Q

MC of hypocalcemia w/ decrease PTH and increased PTH

A

Decreased PTH: hypoparathyroidism (autoimmune, post surgical)

Increased PTH: chronic renal dz, liver dz, hypomagnesemia

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26
Q

EKG findings of hypoCa++ and hyperCa++

A

Hypo: prolonged QT

hyper: shorten QT interval

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27
Q

TX of hypercalcemia

A

Mild: nothing- tx underlying cause

Sever/symptomatic: IV saline–> furosemide 1st line
*avoid hydrochlorothiazide

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28
Q

DEXA scan of what indicates osteoporosis and what is the tx

A

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
Q

SE of Bisphosphonates

A
  1. Pill esophagititis
  2. jaw osteonecrosis
  3. pathologic fx of femur
30
Q

Blue-tinted sclerae and presenile deafness

A

Osteogenesis imperfecta

31
Q
  • 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
A

Renal osteodystrophy
*Osteitits fibrosis cystica and osteomalacia

TX: phosphate binders: Calcium carbonate, calcium acetate, Sevelamer
2. vit. D active forms (Calcitriol)

32
Q

How can you differentiate osteoporosis and osteomalacia

A

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
Q

Describe what layers of the adrenal cortex produce each hormone

A

G- glomerulosa (outer)= A-aldosterone
F- fasiculata= C-Cortisol
R- reticularis = E-estrogen/androgen

34
Q

MC causes of primary and secondary adrenocortical insufficiency

A

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
Q
  1. Hyperpigmentation
  2. Orthostatic hypotension (decreased aldosterone)
  3. HyperK+, hypoNA+, Hypoglycemia
  4. Metabolic acidosis
A

Primary (Addison’s disease) adrenocortical insuff.

36
Q

How to dx and tx adrenocortical insuff.

A
  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
Q

Tx of Adrenal (Addisonian) Crisis

A
  1. IV fluids: normal saline or D5 if hypoglycemic
  2. IV hydrocortisone
  3. fx electrolytes
  4. Fludrocortisone
38
Q

Causes of Cushing’s Syndrome

A

*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
Q

How do you dx Cushing’s Syndrome

A

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
Q

Tx of

  1. Cushings DZ
  2. Ectopic ACTH-secreting or adrenal tumor
  3. Iatrogenic steroid tx (hypercortisolism)
A
  1. Transsphenoidal surgery
  2. tumor removal
    3 .GRADUAL steroid taper
41
Q

Causes of primary and secondary hyperaldosteronism

A

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
Q
  • Proximal muscle weakness, polyuria*, fatigue, constipation
  • Hypertension** HA**, flushing of face
  • NOT EDEMATOUS
  • Labs: HypoK+ w/ metabolic alkalosis
A

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
Q

How to tx hyperaldosteronism

  1. Conn’s syndrome
  2. Hyperplasia
  3. Secondary (renovascular HTN)
A
  1. excision of adrenal aldosteronoma + spironolactone (blocks aldosterone)
  2. Spironlactone, ACEI, CCB
  3. Angioplasty definitive, ACEI
44
Q

How do you dx and tx PCC

A
  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
Q

s/s of hyperprolatinemia include: amenorrhea, galactorrhea, infertility because prolactin inhibits gonadotropin-releasing hormone (FSH/LH)

TX ?

A

TX:

  1. stop offending drugs (dopamine antagonists)
  2. Dopamine agonists: Cabergoline* or bromocriptine
46
Q

What is the difference between type 1 and 2 DM

A

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
Q

What is the first sign of diabetic nephropathy?

A

microalbuminuria

TX: ACEI

*DM is most common cause of ESRD (HTN is 2nd MC)

48
Q

DX of DM

  1. Fasting plasma glucose:
  2. 2hr GTT:
  3. HgbA1c:
  4. Random plasma glucose:
A
  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
Q

Management and goals of DM

A
  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
Q

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

A

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
Q

What type of anti-hyperglycemic med?
Benefits and SE?

-Stimulates pancreatic insulin release from beta cells

A

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
Q

What type of anti-hyperglycemic med?
Benefits and SE?

-Stimulates pancreatic beta cell insulin release

A

Meglitindies
ex. Repaglinide, Nateglinide

SE: hypoglycemia (less than sulfonylurea), Wt gain

53
Q

What type of anti-hyperglycemic med?
SE?

-Delays intestinal glucose absorption (inhibits pancreatic alpha amylase and intestinal alpha-glucosidase hydrolase)

A

Alpha-glucosidase inhibitors
ex. acarbose, Miglitol

SE: Hepatitis (increased LFTs), GI upset

54
Q

What type of anti-hyperglycemic med?
Benefits and SE?

-Increase insulin sensitivity at peripheral receptor site-adipose and muscle tissue

A

Thiazolidinediones

ex. Pioglitazone, Rosiglitazone
* no effect on pancreatic beta cells

SE: fluid retention and edema, cardiovascular toxicity w. Avandia, MI

55
Q

What type of anti-hyperglycemic med?
Benefits and SE?

  • Mimics incretin–> increase insulin secretion, decrease glucagon secretion
  • Delays gastric emptying
A

Glucoagon-like peptide (GLP-1) Agonists
ex. Exenatide, Liraglutide

Benefit: no wt gain

SE: hypoglycemia, pancreatitis,
*CI if hx of gastroparesis**, thyroid CA

56
Q

What type of anti-hyperglycemic med?
Benefits and SE?

-Lowers renal glucose threshold–> increased urinary glucose excretion

A

SGLT-2 inhibitor
ex. Canagliflozin, Dapaglifozin

SE: thirst, Nausea

57
Q

Give examples of

  1. Rapid acting insulin
  2. Short-acting insulin
  3. Intermediate acting
  4. Long acting
A
  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
Q

Normal glucose until rise in serum glucose levels btwn 2am-8am. results from decreased insulin sensitivity and nightly surge of counter regulatory hormones

A

Dawn Phenomenon

TX: betime injection of NPH (to blunt moring hyperglycemia) aoviding carbs late at night

59
Q

Noctural hypoglycemia followed by rebound hyperglycemia (due to surge in GH)

A

Somogyi effect

TX: prevent hypoglycemia by decreasing bedtime NPH dose or give bedtime snack

60
Q

Progressive rise in glucose from bed to morning

A

Insulin waning
*seen when NPH dose given before dinner

TX: move insulin dose to bedtime or increase the evening dose

61
Q

what are kussmaul respirations

A

deep continuous respirations as lung attempts to blow off excess CO2 to reduce acidemia

**seen w/ DKA

62
Q

for DKA and HHS, describe:

  1. plasma glucose
  2. arterial pH
  3. Serum bicarb
  4. ketones
A

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
Q

Tx of DKA/HHS

A

*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
Q

Multiple Endocrine Neoplasia I (MEN I) are rare inherited disorders of 1 or more overactive endocrine gland tumors:

A
  1. Parathyroid 90%
  2. Pancrease 60%
  3. Pituitary 55%
  • Most tumors are benign
  • associated w/ Menin gene defect
65
Q

___ associated w/ presence mucosal neuromas and Marfan-like body habitus

__ have more aggressive form of medullary thyroid carcinoma (presents in infancy)

A

MEN 2B

MEN 2B

66
Q

_____ seen only in MEN 2A

____ seen only in MEN 2B

A

hyperparathryoidism= 2A

Neuromas, marfan-like body habitus= 2B

67
Q

Multiple Endocrine Neoplasia II (MEN 2) are rare inherited autosomal dominant disorders that are associated w/ what types of tumors?

A

MEN2 (90%): medullary thyroid carcinoma, PCC, hyperPTH

MEN1 (5%): medullary thyroid carcinoma, PCC, neuromas, Marfanoid

68
Q

Management of Metabolic Syndrome

A
  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
Q

___ waist circumference of men and __ for women are possible criterias for metabolic syndrome

A

> 40 inches for men

>35inches for women

PANCE Practice (26 decks)

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