Endocrinology (5%) Flashcards by Laura Gardner

What are some examples of hyperthyroid d/o?

Grave’s Dz

Toxic multinodular goiter

Toxic adenoma

TSH Secreting pituitary adenoma

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What will TSH levels be in Hyperthyroidism?

Hypothyroidism?

Low in Hyperthyroidism

High in Hypothyroidism

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Describe the HPT (hypothalamus, pituitary, thyroid) axis

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

A. Normal

B. Grave’s

C. Toxic multinodular goiter

D. Toxic adenoma

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

Hypothyroidism?

Elevated in Hyperthyroidism

Low in Hypothyroidism

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Tx for Grave’s?

Tx for Toxic multinodular goiter?

Tx for toxic adenoma?

Tx for pituitary adenoma?

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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What are some examples of hypothyroid d/o?

Hashimoto’s

Silent (lymphocytic) thyroiditis

Postpartum thyroiditis

deQuervain’s Thyroiditis

Medicaiton induced

Acute thyroiditis

Riedel’s thyroiditis

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The MC cause of hypothyroidism in the US…

The MC cause of hypothyroidism worldwide is…

Hashimoto’s thyroiditis

iodine deficiency

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Tx for hypothyroidism?

Levothyroxine

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______ thyroiditis = fibrous thyroid

Riedel’s thyroiditis

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Which type of hypothyroidism occurs post-virally?

deQuervain’s thyroiditis

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What medications can cause hypothyroidism?

Amiodarone (contains iodine)

Lithium

Alpha interferon

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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

Type 1 DM

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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

Type II DM

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What are potential risk factors for developing Type II DM?

What does CHAOS stand for?

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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What is the development of DM during pregnancy called?

Gestational DM

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What are classic sx of pts with Type I DM?

polyuria, polydipsia, polyphagia, weight loss

Diabetic ketoacidosis, HHS

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What is HHS?

How is it different from DKA?

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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What are potential complications of DM?

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

_______ is the most common cause of end stage renal dz

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

D/t vascular insufficiency and immunosuppresion from hyperglycemia

_______ is a complication of the management of DM

Hypoglycemia

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

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

Fasting plasma glucose: >/= 126

2 hour glucose tolerance test: >/= 200

Hemoglobin A1c: >/= 6.5%

Random plasma: >/= 200

Dx of hypoglycemia: Random blood sugar \_\_\_\_-\_\_\_\_ mg/dL Sx occur at ____ mg/dL Brain dysfunction begins at ____ mg/dL

50-60 mg/dL 60 50

What is a normal fasting blood glucose level?

70-100 mg/dL

What is the recommended managment for and goals of DM?

**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

What are some examples of Biguanides?

Metformin

What are some examples of Sulfonylureas?

Glipizide, Glyburide, Glimepiride

What are some examples of Meglitinides?

Repaglinide, Nateglinide

What are some examples of Alpha Glucosidase Inhibitors?

Acarbose, Miglitol

What are some examples of Thiazolidinediones?

Pioglitazone, Rosiglitazone

What are some examples of GLP-1 Agonists?

Exenatide, Liraglutide

What are some examples of DPP-4 Inhibitors?

Sitagliptin, Linagliptin, Saxagliptin

What is the dawn phenomenon? Management?

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

What is the somogyi effect? Management?

Nocturnal hypoglycemia followed by rebound hyperglycemia (due to surge in growth hormone) MANAGEMENT: prevent hypoglycemia by decreasing nighttime NPH dose or give bedtime snack

What are some examples of SGLT-2 Inhibitors?

Canagliflozin, Dapagliflozin

Lab values that indicate DKA? HHS?

What are some examples of Rapid Acting Insulins? Short Acting? Intermediate? Long Acting?

**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)

What are some examples of pre mixed insulins?

Humulin 7/30 Novolin 70/30 Novolog 70/30 Humulin 50/50 ^{administered 2x daily before meals}

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

DKA and HHS infection

How to tell the difference between DKA and HHS?

DKA: Ketoacidosis HHS: higher severity of hyperglycemia

\_\_\_\_\_\_: younger pts with type I DM \_\_\_\_\_\_: usually older w/ T2DM (higher mortality)

DKA HHS

Describe the pathophysiology of DKA

Insulin deficiency hyperglycemia dehydration ketonemia (*high anion gap metabolic acidosis*) potassium deficit Usually occurs in Type I (may occur in some type 11).

Describe the pathophysiology of HHS

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)

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

thirst, polyuria, polydipsia, nocturia, weakness, fatigue, confusion, nausea, vomiting, CP abd pain: DKA mental status changes: HHS

What two findings on PE are pathognomonic for DKA?

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

What are the tx goals for DKA? HHS?

Closing of the anion gap in DKA Normal mental status in HHS

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

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 ^{Correction of DKA invariably will cause hypokalemia} 4. **Bicarbonate**: only in severe acidosis (especially since the acidosis usually resolves w/ IV fluids & insulin) ^{Associated w/ many complications (ex. increased rate of cerebral edema)}