Diagnosis and Management of Endocrine Disorders Flashcards

1
Q

Metabolic disease resulting form the breakdown in the body’s ability to either produce and/ or either produce and / or utilize insulin, resulting in inappropriate hyperglycemia ruffly 14 million American have diabetes; ruffly 50% of all persons with diabetes are undiagnosed

A

Diabetes Mellitus (DM)

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2
Q

Pathology:

1) Previously known as insulin-dependent or juvenile diabetes
b) Most common in adolescents but may occur in adulthood
c) Strongly associated with the presence of human leukocyte antigens (i.e. HLA-DRA3 or HLA-DRA4)
d) Islet cell antibodies found in approximately 90% of patients within 1st year of diagnosis
e) Ketone development usually occurs
f) Believed to be the result of an infectious or toxic environment insult to pancreatic B cells of genetically predisposed persons

A

Diabetes Mellitus (Type 1 DM)

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3
Q

Pathology:
1) Previously known as non-IDDM or adult-
onset DM
2) The most common type of diabetes: > 90%
diabetes in the United States
3) Circulating insulin exist enough to prevent
ketoacidosis but is inadequate to meet the
patient’s insulin needs
4) Caused by either tissue insensitivity to
insulin or an insulin secretory defect
resulting in resistance and/or impaired
insulin production
5) Not linked to human leukocytes antigens
or islet cell antibodies
6) Associate with obesity and Syndrom X:
obesity, hypertension, normal lipid profile
(low HDLs and high triglycerides)
7) Metabolic syndrome:
a) Waist circumference: > 40 inches (101.6
cm) in men and > 35 inches (88.9 cm) in
women
b) BP > 130/ 85
c) Triglycerides > 150
d) FBG > 100
e) HDL: < 40 in men and < 50 in women

A

Diabetes Mellitus (Type 2 DM)

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4
Q

Signs and symptoms of this: Type _____ DM

a) Polyuria
b) Polydipsia
c) Polyphagia
d) Nocturnal enuresis
e) Weight loss
f) Weakness/ fatigue
g) Other

A

Type 1 DM

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5
Q

Signs and symptoms of this: Type ____ DM

a) Insidious ones fo hyperglycemia; the patient may be asymptomatic
b) Polyuria
c) Polydipsia
d) Recurrent vaginitis often the first symptom in women
e) Peripheral neuropathies
f) Blurred vision
g) Chronic skin infections including pruritus
h) Increased risk of rectal cancer

A

2

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6
Q

Labs/ Diagnostics: DM type ___:
1) Random plasma glucose > 200 mg/dL with
polyuria, polydipsia, and weight loss
2) Serum fasting (at least 8 hrs) blood sugar >
126 mg/dL on two separate occasions
3) FBG may be elevated due to
corticosteroids, beta-blockers, thiazide
diuretics, statins
4) Ketonemia, ketonuria, or both
5) BUN/ creatinine elevated (dehydration)
6) Oral glucose tolerance test > 200 mg/dL
two hours postprandial- rarely used
7) Hbg A1c: Now use for routine diagnosis:
give an indication of glycemic control for
the past 2 to 3 months; normal = 5.5 to 7%
Impaired Glucose Tolerance: FBG > 100
and < 125

A

1

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7
Q

Labs/ diagnostics: DM type ____

1) Same as for type 1 DM except for no ketones in blood/ urine

A

type 2 DM

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8
Q
Management type 1 DM:
1) Treatment plans for all diabetes must be highly individualized
2) Analyze baseline studies
    a) Age of honest 
    b) 
    c) Cardiac risk factors
    d) Presence of ketones
    e) Diagnostic markers
    f) Cholesterol, triglycerides, ECG
    g) Renal studies, as needed
    h) Baseline physical exam noting 
       peripheral pulses, neurologic function. 
       eye and foot exams
A

2) b) Obesity

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9
Q

Dietary teaching: Consult dietitian/ DM 1
a) Total carbohydrate intake _____% total
calorie intake
b) Fats 20 to 30% total calories
c) Fibers 25 g/ 1000 calories
d) Protien 10 to 20% total calories

A

a) 55 to 60

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10
Q

Diabetes Mellitus (Type 1 DM):
If the patient presents with ketones, then insulin therapy is most likely warranted
a) The general rule of thumb is, to begin
with ____ u/ kg/day giving 2/3 of the
dose in the morning and remaining 1/3 in
the evening

A

a) 0.5 u/ kg/day

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11
Q
DM type 1:
a) \_\_\_\_ \_\_\_\_ \_\_\_\_\_ \_\_\_\_\_\_
    1) Morning dose of insulin 2/3 NPH and 
       1/3 Regular 
   2) Evening dose 1/2 NPH 1/2 Regular
A

a) Conventional Split Dose Mixtures

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12
Q

DM type 1:
b) ______ ______
1) Reduced or omit the p.m. dose and add
a portion at bedtime

A

Intensive Therapy

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13
Q

DM type 1:

1) _____ (Novolog)
2) Gargine (Lantas)- prolonged duration
3) Lispro (Humalog)- rapid onset

A

1) Aspart

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14
Q

DM Type ____:

Same as for type 1 DM except for ___ ketones in blood/ urine

A

no

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15
Q

DM type _____

a) Obtain baseline data as outlined for type 1 DM
b) Therapy should begin with weight control for obese patients
c) Dietary treatment with guidelines
d) exercise
e) Consider early use of oral anti-diabetics
f) Insulin therapy may be needed in future years of treatment

A

2

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16
Q

Oral Antidiabetic choices ( 5 classes):
_______: Most widely prescribed; stimulate the pancreas to release more insulting
– 2nd generation: Glipizide (Glucotrol). Glyburide (DiaBeta, Micronase), Glimepiride (Amaryl)

A

Sulfonylureas

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17
Q

_____: Good adjunct to sulfonylureas but can be used alone, especially for obese patients
– Metformin (Glucophage): Standard of care upon the diagnosis of Type 2 DM; lactic acidosis is a potential side effect

A

Biguanides

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18
Q

____ ____ ____: Bind to disaccharidases more readily than sucrose so less glucose is absorbed by the gut
– Acarbose (Precose), Miglitol (Glyset)

A

Alpha-glucosidase inhibitors

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19
Q

__________ “ Glitazones”; decrease gluconeogensesis

    • Rosiglitazone maleate (Avandia)
    • Pioglitazone hydrochloride (Actos)
A

Thiazolidinediones

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20
Q

_______ ____ ____ _____: Rapidly absorbed for the intestine and mimics the effect of rapidly acting insulin.

    • Repaglinide (Prandin)
  • -Nateglinide (Starlix)
A

Non- sulfonylurea Insulin Release Stimulators

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21
Q

Management continued: Diabetes Mellitus type 2:
a) ______ (Byetta): Injectable that mimics the effects of incretins (signals pancreas to increase insulin secretion and the liver to spot producing glucagon): may cause significant nausea, vomiting, and diarrhea

A

Exenatide

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22
Q

Management continued: Diabetes Mellitus type 2:

________ (Januvia): Dipeptidyl peptidase -4 (DPP4 inhibitor); DPP4 breakds down incretins

A

Sitagliptin

23
Q

Management continued: Diabetes Mellitus type 2:
________ (Symlin): Injectable for Type 1 and 2 DM; resemble human amylin slow absorption of glucose and inhibits the action of glucagons; promotes weight loss while decreasing blood glucose levels

A

Pramlintide

24
Q

______ ____: Nocturnal hypoglycemia develops stimulating a surge of counter-regulatory hormone (____ ____) which raise blood sugar. Note that the patient is hypoglycemic at 0300 but rebounds with elevated blood glucose at 0700

A

Somogyi Effects

25
Q

Treatment for Somogyi Effect include:

A

Reduce or omit the at bedtime does of insulin

26
Q

____ _____ Results when the tissue becomes desensitized to insulin nocturnal; Note that the blood glucose become progressively elevated throughout the night, resulting in elevated level at 0700

A

Dawn Phenomenon

27
Q

Treatment of the Dawn Phenomenon is:

A

Add or increase the at bedtime dose of insulin

28
Q

a) Stat of intracellular dehydration as a result of elevated blood glucose levels
b) Often, an acute complication of type 1 DM
c) Maybe the presenting sign of DM

A

Diabetic Ketoacidosis (DKA)

29
Q

Signs and symptoms of this are:

a) polyuria, including nocturia
b) polydipsia
c) weakness/ fatigue, nausea, and vomiting
d) Kussmaul’s breathing
e) Altered LOC
f) fruity breath
g) Hypotension and tachycardia
h) Poor skin turgor

A

Diabetic Ketoacidosis (DKA)

30
Q

Lab/ diagnostics: Diabetic Ketoacidosis (DKA)
a) protect airway: administer O2
b) Refer for:
a) fluid resuscitation: _____ fluids (NS),
then 1/2 NS, followed by D51/2 NS
b) 0.10 U/kg regular insulin IV bolus
followed by 0.1 kg/hr
c) Supportive care

A

b) a) Isotonic fluids

31
Q

Patho:

1) State of greatly elevated serum glucose, hyperosmolality, and severe dehydration without ketone production
2) Usually occurs as a complication of type 2 DM
3) Patients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion
4) Mortality rate around 30 to 50 %

A

Hyperosmolar Hyperglycemic Non-ketosis (HHNK)

32
Q

Signs and symptoms: Hyperosmolar Hyperglycemic Non-ketosis (HHNK)

1) Polyuria
2) Weakness
3) Altered LOC
4) __________
5) Tachycardia
6) Poor skin turgor
7) Other signs of dehydration

A

4) Hypotension

33
Q

Lab/ diagnostics: Hyperosmolar Hyperglycemia Non- Ketosis (HHNK)

1) Greatly elevated serum glucose ( > 600 mg/dL; commonly > 1000 mg/dL)
2) Hyperosmolality (> _____ mOsm/L)
3) Elevated BUN and Cr
4) Elevated Hgb A1c
5) Relatively normal pH
6) Normal anion gap

A

2) 310 mOsm/L

34
Q

Management: HHNK
1) Protect airway; administer O2
2) Refer for:
a) Normal saline IV massive fluid
replacement (overall fluid deficit maybe
6 to 10 liters), then 1/2 NS, followed by
D5 1/2 NS
b) ____ Units regular insulin IV followed by
10 to 15 Units subcutaneous (immediately)
c) Additional insulin depends on the
the severity of condition and response-
may not be necessary
d) Supportive care

A

2) b) 15 units

35
Q

a) Hypothalamus
- –> —-> —->
b) Thyroid releasing hormone
- –> —> —->
c) ______ _____
- –> —> —->
d) Thyroid Stimulating Hormone
- –> —> —->
e) Thyroid Gland

A

Anterior pituitary

36
Q

Causes/Etiology:
A) _________:
1) More common in women (8:1 ratio) •
2) Onset most commonly between 20 and 40 years of age
3) Grave’s disease is the most common presentation
4) Other causes of hyperthyroidism include toxic adenoma, subacute thyroiditis, TSH secreting tumor of the pituitary, high dose, amiodarone

A

Hyperthyroidism •

37
Q

Signs and symptoms: Hyperthyroidism

1) Nervousness
2) Anxiety
3) Increased sweating
4) _______
5) Emotional lability
6) Fine tremors
7) Hyperreflexia of DTRs
8) Increased appetite
9) ___ ____
10) Smooth, warm, moist velvety skin •
11) Fine/thin hair•
12) Exophthalmos•
13) Lid lag•
14) Tachycardia
15) Heat intolerance
16) Others•
17) Increases incidence of atrial fibrillation

A

4) Fatigue

9) Weight loss

38
Q

Hypothyroidism Signs/Symptoms:

1) Primary disease of the thyroid gland •
2) Pituitary deficiency of TSH •
3) Hypothalamic deficiency of TRH •
4) _____ ______
5) Hashimoto’sthyroiditis •
6) Idiopathic causes
7) Damage to the gland

A

4) Iodine deficiency

39
Q

Hypothyroidism:

1) Extreme weakness •
2) Muscle fatigue •
3) Arthralgias
4) Cramps
5) Cold intolerance •
6) Constipation
7) ____ ____
8) Dry skin
9) Hair loss
10) Brittle nails
11) Puffy eyes
12) Edema of the hands and face •
13) _______
14) Slowed DTRs •
15) _______ bowel sounds

A

7) Weight gain
13) Bradycardia •
15) Hypoactive bowel sounds

40
Q

Laboratory/ Diagnosis:

Management: Hyperthyroidism
1) TSH assay is the most sensitive test and is
low in most cases
2) Serum T3, T4, thyroid resin uptake, and
free thyroxine index increased Sometimes
T4 is normal, but T3 elevated (_____
ng/dL)
3) Serum ANA usually elevated without
evidence of lupus or other collagen
diseases
4) Thyroid radioactive iodine uptake and
scan usually performed to establish
etiology of hyperthyroidism
- A high iodine uptake is consistent with Grave’s disease
- A low uptake is consistent with subacute thyroiditis
5) MRI of the orbits is tile preferred choice for visualizing Grave’s ophthalmopathy

A

2) 80-230 ng/ dL

41
Q

Management: Hyperthyroidism
1) Specialist referral as needed, especially with
patients who have co-morbidities •
2) ________ (Inderal) for symptomatic relief:
Begin dosing with 10 mg p.o., may go to
80 mg four times daily •
3) Thiourea drugs for patients with mild
cases, small goiters or fear of isotopes
-Methimazole (Tapazole) 30-60 mg every
day in 3 divided doses
- Propylthiouracil 1300-600 mg daily in 4
divided doses
4) Radioactive iodine ____ used to destroy goiters
5) Thyroid surgery (must be euthyroid prop)
6) Lugol’s solution 2-3 gtts p.o, everyday X 10
days to reduce the vascularity of the gland 7) Patients with subacute thyroiditis are best
treated symptomatically with Propranolol

A

2) Propranolol

4) 131-I

42
Q

Treatment of Thyroid Crisis:

1) ________ 150-250 mg every 6 hours OR
2) Methimazole (Tapazole) 15-25 mg every 6 hours WITH the following in one hour:
a) Lugol’s solution 10 gtts t.i.d. OR -
b) Sodium iodide 1 gm slow IV along with
c) _______ 0.5 - 2 gm IV every 4 hours
or 20 - 120 mg p.o. every 6 hours with
d) Hydrocortisone 50 mg every 6 hours
with rapid reduction as situation
improves
3) Avoid ASA

A

1) Propylthiouracil

2) c) Propranolol

43
Q
Hypothyroidism Labs: •
1) TSH: Elevated
2) T4: \_\_\_\_\_\_\_\_\_\_\_\_\_\_ •
3) Resin T3 uptake: Decreased (T3 is not a 
    reliable test)
4) Hyponatremia
5) Hypoglycemia
A

2) Low or low normal

44
Q

Management of Hypothyroidism:
1) _________ (Synthroid): 50-100
mcg every day, increasing dosage by 25
mcg every 1-2 weeks until symptoms
stabilize; > 60 years of age, decrease the
dosage

A

1) Levothyroxine

45
Q

In-Patient Management of Myxedema Coma: •
1) Protect airway: Mechanical ventilation as needed
2) Fluid replacement, as needed •
___________ (Synthroid) 400 meg IV x 1, then 100 mcg every day •
3) Supporthypotension
4) Slow rewarming with blankets (not hyperthermia blankets): Avoid circulatory collapse
5) Symptomatic care

A

Levothyroxine

46
Q

Cushing’sSyndrome Cause/ etiology:

1) ____ hypersecretion by the pituitary •
2) Adrenal tumors
3) Chronic administration of glucocorticoids

A

1) ACTH

47
Q

Signs/ symptoms of _____ _____:

1) Central obesity •
2) Moon Face with buffalo hump
3) Acne
4) Poor wound healing
5) Purple striae
6) Hirsutism
7) Hypertension
8) Weakness
9) Amenorrhea
10) Impotence
11) Headache
12) Polyuria and thirst
13) Labile mood
14) Frequent infections

A

Cushing’s Syndrome

48
Q

Cause/ etiology of Addison’s Disease:
1) Deficient _____, androgens, and
aldosterone
2) Autoimmune destruction of the adrenal
gland
3) ______cancer
4) Bilateral adrenal hemorrhage (e.g., with
anticoagulant therapy) •
5) Pituitary failure resulting in decreased ACTH

A

1) cortisol

3) Metastatic

49
Q
Laboratory/ Diagnosis: Cushing's Syndrome
1) Hyperglycemia •
2) Hypernatremia •
3) \_\_\_\_\_\_\_\_•
4) Glycosuria •
5) Leukocytosis
6) Elevated plasma cortisol in the a.m.
7) Dexamethasone suppression test to 
    differentiate cause
8) Serum \_\_\_\_\_
A

3) Hypokalemia

8) ACTH

50
Q
Signs and symptoms of Addison's Disease:
1) \_\_\_\_\_\_\_\_ in buccal mucosa and 
    skin creases (especially knuckles, nail 
    beds, nipples, palmar creases, and 
    posterior neck) 
2) Diffuse tanning and freckles •
3) Orthostasis and hypotension •
4) Scant axillary and pubic hair •
5) Rapid worsening of chronic signs and 
    symptoms (acute) •
6) \_\_\_\_ (acute)
7) Changes in the level of consciousness 
    (acute)
A

1) Hyperpigmentation

6) Fever

51
Q

Laboratory/ diagnosis of Addison’s Disease:

1) ____________
2) Hyponatremia •
3) Hyperkalemia •
4) Elevated ____
5) Lymphocytosis
6) Plasma cortisol

A

1) Hypoglycemia •
4) ESR
6) 5

52
Q

Management of Cushing’s Syndrome:
1) Depends on the cause:
a) Discontinue medications inducing
symptoms
b) ___________ resection of a pituitary
adenoma
c) Surgical removal of adrenal tumors -
d)Resection of ACTH secreting tumors •
2) Manageelectrolytebalance

A

1) b) Transsphenoidal

53
Q

Outpatient Management: Addison’s Disease •
1) Specialist referral
2) Glucocorticoid and mineralocorticoid
replacement
a) -
b) - Fludrocortisone acetate (Florinef)

A

a) Hydrocortisone

54
Q

Inpatient Management: Addison’s Disease•
1) _______ (Solu-Cortef): 100-300 mg
IV -initially with NS; replace volume with
D5NS at 500 cc /hr X 4 hours and then
taper per condition
2) Vasopressors usually ineffective •
3) Treat the underlying cause: Often is an
infection

A

1) Hydrocortisone