Endocrinology (5%) Flashcards
What are some examples of hyperthyroid d/o?
Grave’s Dz
Toxic multinodular goiter
Toxic adenoma
TSH Secreting pituitary adenoma
What will TSH levels be in Hyperthyroidism?
Hypothyroidism?
Low in Hyperthyroidism
High in Hypothyroidism
Describe the HPT (hypothalamus, pituitary, thyroid) axis
Toxic multinodular goiter, Grave’s, toxic adenoma, or normal RAIU?
A. Normal
B. Grave’s
C. Toxic multinodular goiter
D. Toxic adenoma
Will Free T3 and Free T4 be elevated or low in hyperthyroidism?
Hypothyroidism?
Elevated in Hyperthyroidism
Low in Hypothyroidism
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
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
The MC cause of hypothyroidism in the US…
The MC cause of hypothyroidism worldwide is…
Hashimoto’s thyroiditis
iodine deficiency
Tx for hypothyroidism?
Levothyroxine
______ thyroiditis = fibrous thyroid
Riedel’s thyroiditis
Which type of hypothyroidism occurs post-virally?
deQuervain’s thyroiditis
What medications can cause hypothyroidism?
Amiodarone (contains iodine)
Lithium
Alpha interferon
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
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
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
What is the development of DM during pregnancy called?
Gestational DM
What are classic sx of pts with Type I DM?
polyuria, polydipsia, polyphagia, weight loss
Diabetic ketoacidosis, HHS
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
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
DM
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
<em>administered 2x daily before meals</em>
_____ 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?
- IV FLUIDS: Critical 1st step
- INSULIN (REGULAR)
- 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>
- 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>
