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Rotation 2: Adult Primary Care > Endocrinology (5%) > Flashcards

Endocrinology (5%) Flashcards

1
Q

What are some examples of hyperthyroid d/o?

A

Grave’s Dz

Toxic multinodular goiter

Toxic adenoma

TSH Secreting pituitary adenoma

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2
Q

What will TSH levels be in Hyperthyroidism?

Hypothyroidism?

A

Low in Hyperthyroidism

High in Hypothyroidism

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3
Q

Describe the HPT (hypothalamus, pituitary, thyroid) axis

A
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4
Q

Toxic multinodular goiter, Grave’s, toxic adenoma, or normal RAIU?

A

A. Normal

B. Grave’s

C. Toxic multinodular goiter

D. Toxic adenoma

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5
Q

Will Free T3 and Free T4 be elevated or low in hyperthyroidism?

Hypothyroidism?

A

Elevated in Hyperthyroidism

Low in Hypothyroidism

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6
Q

Tx for Grave’s?

Tx for Toxic multinodular goiter?

Tx for toxic adenoma?

Tx for pituitary adenoma?

A

Grave’s: Radioactive iodine, Methimazole, Propylthiouracil, BB for sx relief

TMG and TA: Radioactive iodine, Methimazole, PTU, BB for sx

Pituitary adenoma: Transspenoidal surgery to remove

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7
Q

What are some examples of hypothyroid d/o?

A

Hashimoto’s

Silent (lymphocytic) thyroiditis

Postpartum thyroiditis

deQuervain’s Thyroiditis

Medicaiton induced

Acute thyroiditis

Riedel’s thyroiditis

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8
Q

The MC cause of hypothyroidism in the US…

The MC cause of hypothyroidism worldwide is…

A

Hashimoto’s thyroiditis

iodine deficiency

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9
Q

Tx for hypothyroidism?

A

Levothyroxine

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10
Q

______ thyroiditis = fibrous thyroid

A

Riedel’s thyroiditis

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11
Q

Which type of hypothyroidism occurs post-virally?

A

deQuervain’s thyroiditis

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12
Q

What medications can cause hypothyroidism?

A

Amiodarone (contains iodine)

Lithium

Alpha interferon

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13
Q
A
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14
Q

What condition is described below?

Caused by pancreatic beta cell destruction (pt no longer able to produce insulin)

Most commonly presents in children/young adults (onset usually <30y)

Type 1A autoimmune beta cell destruction triggered by 1+ environmental factors

Type 1B: non-autoimmune beta cell destruction

A

Type 1 DM

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15
Q

What condition is described below?

Combo of insulin resistance and relative impairment of insulin secretion

Etiology likely due to genetic and environmental factors: especially weight gain and decreased physical activity

90% of pts are overweight

MC >40y/o

A

Type II DM

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16
Q

What are potential risk factors for developing Type II DM?

What does CHAOS stand for?

A

H/o impaired glucose tolerance, FHx, 1° relative, Hispanic, African American, Pacific Islander, HTN, HLD, delivery of baby >9lbs

Syndrome X/insulin resistance: CHAOS –> Chronic HTN, Atherosclerosis, Obesity (central), Stroke

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17
Q

What is the development of DM during pregnancy called?

A

Gestational DM

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18
Q

What are classic sx of pts with Type I DM?

A

polyuria, polydipsia, polyphagia, weight loss

Diabetic ketoacidosis, HHS

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19
Q

What is HHS?

How is it different from DKA?

A

Hyperosmolar hyperglycemic state (HHS) is a complication of DM in which high blood sugar results in high osmolarity w/o significant ketoacidosis

Sx include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness

Differences: see picture

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20
Q

What are potential complications of DM?

A

Neuropathy: “stocking glove”, orthostatic hypotension, CN III palsy w/ nml pupil size

Retinopathy: cotton wool spots, hard exudates, neovascularization, central vision loss

Nephropathy: microalbuminuria, kimmelstiel wilson on kidney bx (condition associated w/ long-standing DM that affects the network of tiny blood vessels in the glomerulus, which is critically necessary for the filtration of the blood –> “nodular glomerulosclerosis”)

Macrovascular: CAD

23
Q

_______ is the most common cause of end stage renal dz

A

DM

24
Q

Why are pts with DM at an increased risk of infections?

A

D/t vascular insufficiency and immunosuppresion from hyperglycemia

25
Q

_______ is a complication of the management of DM

A

Hypoglycemia

usually d/t too much insulin use, too little food, or excess exercise

26
Q

What results on each of the following tests will help make the dx of DM in a pt?

Fasting plasma glucose

2 hour glucose tolerance test

Hemoglobin A1c

Random plasma

A

Fasting plasma glucose: >/= 126

2 hour glucose tolerance test: >/= 200

Hemoglobin A1c: >/= 6.5%

Random plasma: >/= 200

27
Q

Dx of hypoglycemia: Random blood sugar ____-____ mg/dL

Sx occur at ____ mg/dL

Brain dysfunction begins at ____ mg/dL

A

50-60 mg/dL

60

50

28
Q

What is a normal fasting blood glucose level?

A

70-100 mg/dL

30
Q

What is the recommended managment for and goals of DM?

A

Diet, exercise, lifestyle changes: should be tried first in Type II DM

  • ± insulin if unable to control glucose with trial of diet, exercise, lifestyle changes, meds

Insulin therapy initiated in Type I DM

Insulin preferred for glucose control in gestational DM

Glucose control: Hgb A1c <7.0%

Lipid control: LDL<100; HDL 40; TG<150

Neuropathy: Gabapentin, ±TCAs, Foot care (wide, loose-fitting shoes, nail trimming, podiatrist monitoring at least yearly)

Retinopathy: DM control, laser photocoagulation tx, Bevacizumab (proliferative), Vitrectomy, Yearly eye screening by an ophthalmologist

Nephropathy: DM control, ACE Inhibitors if microalbuminuria, Low sodium diet, yearly screening for microalbuminemia, yearly checks of BUN & creatinine

31
Q

What are some examples of Biguanides?

A

Metformin

32
Q

What are some examples of Sulfonylureas?

A

Glipizide, Glyburide, Glimepiride

33
Q

What are some examples of Meglitinides?

A

Repaglinide, Nateglinide

34
Q

What are some examples of Alpha Glucosidase Inhibitors?

A

Acarbose, Miglitol

35
Q

What are some examples of Thiazolidinediones?

A

Pioglitazone, Rosiglitazone

36
Q

What are some examples of GLP-1 Agonists?

A

Exenatide, Liraglutide

37
Q

What are some examples of DPP-4 Inhibitors?

A

Sitagliptin, Linagliptin, Saxagliptin

38
Q

What is the dawn phenomenon?

Management?

A

Normal glucose until rise in serum glucose levels between 2am - 8 am

Results from decreased insulin sensitivity and nightly surge of counter regulatory hormones (during nighttime fasting)

Management: bedtime injxn of NPH, avoiding carb heacy snacks before bed, insulin pump use early in the AM

39
Q

What is the somogyi effect?

Management?

A

Nocturnal hypoglycemia followed by rebound hyperglycemia (due to surge in growth hormone)

MANAGEMENT: prevent hypoglycemia by decreasing nighttime NPH dose or give bedtime snack

40
Q

What are some examples of SGLT-2 Inhibitors?

A

Canagliflozin, Dapagliflozin

41
Q

Lab values that indicate DKA?

HHS?

A
42
Q

What are some examples of Rapid Acting Insulins?

Short Acting?

Intermediate?

Long Acting?

A

Rapid: Lispro (humalog), Aspart (Novolog)

Short: Regular (Humulin-R)

Intermediate: NPH (Humulin N, Novolin N), Lente (Humulin L, Novolin L)

Long: Detemir (Levemir), Glargine (Lantus)

43
Q

What are some examples of pre mixed insulins?

A

Humulin 7/30

Novolin 70/30

Novolog 70/30

Humulin 50/50

<em>administered 2x daily before meals</em>

46
Q

_____ and _____ are results of INSULIN DEFICIENCY and counterregulatory hormonal excess in diabetics as a direct response to stressful triggers (most commonly ______)

A

DKA and HHS

infection

48
Q

How to tell the difference between DKA and HHS?

A

DKA: Ketoacidosis

HHS: higher severity of hyperglycemia

49
Q

______: younger pts with type I DM

______: usually older w/ T2DM (higher mortality)

A

DKA

HHS

50
Q

Describe the pathophysiology of DKA

A

Insulin deficiency

hyperglycemia

dehydration

ketonemia (high anion gap metabolic acidosis)

potassium deficit

Usually occurs in Type I (may occur in some type 11).

51
Q

Describe the pathophysiology of HHS

A

Usually occurs in pts with type 2 DM w/ some illness leading to reduced fluid intake (MC infection)

dehydration, increased osmolarity, hyperglycemia

potassium deficit

absence of severe ketosis (Type II DM make enough insulin to prevent ketogenesis usually)

52
Q

Hyperglycemia is observed in both DKA and HHS with sx such as….

With sx of ______ seen in pts with DKA and ______ in pts with HHS

A

thirst, polyuria, polydipsia, nocturia, weakness, fatigue, confusion, nausea, vomiting, CP

abd pain: DKA

mental status changes: HHS

53
Q

What two findings on PE are pathognomonic for DKA?

A

KETOTIC BREATH (fruity with acetone smell) & KUSSMAUL RSESPIRATIONS (deep and labored)

54
Q

What are the tx goals for DKA?

HHS?

A

Closing of the anion gap in DKA

Normal mental status in HHS

55
Q

What four things are recommended for management of DKA and HHS?

A
  1. IV FLUIDS: Critical 1st step
  2. INSULIN (REGULAR)
  3. POTASSIUM: (1st verify renal output) Despite serum K levels, patient is always total body potassium deficient

<em>Correction of DKA invariably will cause hypokalemia</em>

  1. Bicarbonate: only in severe acidosis (especially since the acidosis usually resolves w/ IV fluids & insulin)

<em>Associated w/ many complications (ex. increased rate of cerebral edema)</em>

Rotation 2: Adult Primary Care (14 decks)

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