ENDOCRINE

Question 1

What kind of antigens and antibodies are most associated with type 1 diabetes?

Answer 1

human leukocyte antigens

Islet cell antibodies

Question 2

What is a unique development for Type 1 DM?

Answer 2

ketone development

Question 3

What is the pathology of type 2 DM?

Answer 3

Tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/ or impaired insulin production

Question 4

What is syndrome X

Answer 4

DM II and associated with obesity, HTN, and abnormal lipid profiles (low HDLs and high triglycerides)

Question 5

What does metabolic syndrome entail and how is the diagnosis made

Answer 5

3 or more of the following:

1) wait circumference >40inches (102cm) in men and >35inches (89cm) in women
2) BP>130/85
3) triglycerides >150
4) FBG>100
5) HDL

Question 6

Diagnostics for DM type 1 and type II

Answer 6

• Random plasma glucose >200 with polyuria, polydipsia and weight loss
• Serum fasting (8hrs) blood sugar >126 on 2 separate occasions
• Kenonemia, ketouria, or both for type 1
• Oral glucose tolerance test>200 2 hours post-prandial
• Hbg A1C- ROUTINE Diagnosis- normal 5.5-7%
• Impaired glucose tolerance test FBG >100and

Question 7

Dietary teaching for diabetics

Answer 7

carb intake 55-60%
fats 20-30%
protein 10-20%
Fiber 25g/1000 calories

Question 8

When is insulin therapy warranted and how do you start insulin?

Answer 8

if a patient presents with ketones

0.5units/kg/day giving 2/3 dose in the morning and 1/3 dose in the evening

Question 9

What is the conventional split dose mixtures of insulin

Answer 9

morning dose of insulin is 2/3 NPH and 1/3 regular

evening dose of insulin is 1/2 NPH and 1/2 regular

Question 10

What are the insulin analogs

Answer 10

Aspart (novolog)
Glargine (Lantus)- prolonged duration
Lispro (Humalog)- rapid onset

Question 11

What are the 5 classes of oral antidiabetics?

Answer 11

Sulfonylureas
Biguanides 
Alph-glucosidase inhibitors 
Thiazolidinediones
Non-sulfonylurea insulin release stimulators

Question 12

Sulfonylureas- how it works and names

Answer 12

stimulate the pancreas to release more insulin

2nd generations: glipizide(glucotrol), glyburide, glimepride

Question 13

Biguanides- how it works and names

Answer 13

decreases hepatic glucose production and intestinal glucose absorption
Metphormin (glucophage)
Good adjunct to the sulfonylureas but can be used alone especially in obese patients

Question 14

How do alpha-glucosidase inhibitors work and give some names

Answer 14

bind to disaccharides more readily than sucrose, so less glucose is absorbed by the gut
acarbose (precose)
miglitol (glyset)

Question 15

What is a common thiazolidinediones and whats the popular brand?

Answer 15

glitazones decrease gluconeogenesis
Pioglitazone hydrochloride (actos)

Question 16

How do the non-sulfonylurea insulin release stimulators work and what are 2 brands

Answer 16

Rapidely absorbed from the intestine and mimics the effects of rapidly acting insulin
Repaglinide (Prandin)
Nateglinide (starlix)

Question 17

How does Exenatide ( Byetta) work?

Answer 17

Injectable that mimics the effects incretins (signals pancreas to increase insulin secretion and the liver to stop producing glucagon). Causes n/v/d

Question 18

How does Sitagliptin (Januvia) work?

Answer 18

DD-4 inhibitor, breaks down incretins

Question 19

How does Pramlintide (Symlin) work?

Answer 19

Injectable for type 1&2DM, resembles human amylin, slows the absorption of glucose and inhibits the actions of glucagons: promotes weight loss while decreased glucose levels

Question 20

What happens during the somogyi effect

Answer 20

nocturnal hypoglycemia and morning hyperglycemia

Question 21

treatment of the somogyi effect

Answer 21

reduce or omit the HS insulin

Question 22

what happens during the dawn phenomenon

Answer 22

tissue becomes desensitized to insulin nocturnally, becomes progressively elevated throughout the night and morning hyperglycemia

Question 23

How do you tx the dawn phenomenon

Answer 23

add or increase the HS dose of insulin

Question 24

Diabetic Ketoacidosis (DKA) is a complication of

Answer 24

DM1

Question 25

what state is DKA

Answer 25

intracellular dehydration

Question 26

What is hyperosmolar hyperglycemic non-ketosis a complication of?

Answer 26

DMII

Question 27

What happens in HHNK?

Answer 27

PAtients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis and extracellular depletion

Question 28

When is kussmauls breathing seen?

Answer 28

in DKA

Question 29

When is fruity breath seen?

Answer 29

DKA

Question 30

What are the labs/ diagnostics for DKA

Answer 30

hyperglycemia (>250) ketonemia, ketonuria Marked glucosuria metabolic Acidosis (Ph

Question 31

What are the labs/ diagnostics for HHNK?

Answer 31

``` serum blood glucose >600 Hyperosmolality elevated BUN and cr elevated hbg a1c normal Ph Normal anion gap ```

Question 32

What is the most common form of hyperthyroid

Answer 32

graves disease

Question 33

What are some other causes of hyperthyroid

Answer 33

toxic adenoma, subacute thyroiditis, TSH, secreting tumor of the pituitary, high doses of amiodorone

Question 34

Patho causes of hypothyroidism

Answer 34

``` pituitary deficiency of TSH hypothalamic deficiency of TRH iodine deficiency hashimotos throiditis damage to the gland idiopathic ```

Question 35

What is the most sensitive test for hyperthyroidism

Answer 35

TSH assay

Question 36

What is the most important test for hyperthyroidism

Answer 36

t3

Question 37

What else can elevate the ANA

Answer 37

lupus or collagen disease

Question 38

What test should be performed to establish etiology of hyperthyroidism

Answer 38

thyroid radioactive iodine uptake

Question 39

What 2 drug classes are used for hyperthyroidism

Answer 39

propranolol for symptomatic relief (especially for subacute) | Thiourea drugs for patients with mils cases, small goiters or fear of isotopes (Methimazole, propylthiouracil/ PTU)

Question 40

Treatment dosing with levothyroxine

Answer 40

50-100mcg every day, increasing the dosage by 25mcg every 1-2 weeks until symptoms stabilize decrease dosing for >60yo

Question 41

Causes of Cushings syndrome

Answer 41

ACTH hyper secretion by the pituitary, adrenal tumor, chronic administration of glucocorticoids

Question 42

S/SX of Cushing's syndrome

Answer 42

central obesity, moon face with buffalo hump, acne, poor wound healing, purple strake, hirsutism, HTN, weakness, amenorrhea, impotence, HA, polyuria and thirst, labile mood, frequent infections

Question 43

Labs for Cushing's syndrome

Answer 43

``` HYPERGLYCEMIA HYPERNATREMIA HYPOKALEMIA leukocytosis elevated plasma cortisol in the morning dexamethasone suppression test serum ACTH glycosuria ```

Question 44

Causes of addisons disease

Answer 44

deficient cortisol, androgens, and aldosterone Autoimmune destruction of the adrenal gland CA with mets Bilateral adrenal hemorrhage (from anticoagulation tx) pituitary failure resulting in ACTH

Question 45

s/sx addisons disease

Answer 45

``` hyperpigmentation in buccal mucosa and skin creases diffuse tanning and freckles orthostasis and hypotension scant axillary and pubic hair rapid worseing acute fever change in LOC ```

Question 46

labs for addisons disease

Answer 46

``` HYPOGLYCEMIA HYPONATREMIA HYPERKALEMIA elevated ESR Lymphocytosis ```

Question 47

management of addisons disease

Answer 47

glucocorticoid and mineralcortiocoid replacement (aldosterone and androgen)

Question 48

what is the pathophysiology of graves disease

Answer 48

hyperthyroidism: when the thyroid gland overproduces the hormone thyroxine as a result of an immune system attack