Endocrine Disorders Flashcards

1
Q

What is metabolic syndrome?

A
  • Waist circumference: >40 inches/101.6cm in men, >35 inches/88.9cm in women
  • BP > or = 130/85
  • Triglycerides > 150
  • FBG > 100
  • HDL: <40 in men and <50 in women
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2
Q

What are some distinguishing factors of DM 1?

A
  • ketonuria and ketonemia
  • acute onset
  • HLA/pancreatic islet cell antibody production
  • Treatment/management is insulin
  • nocturnal enuresis
  • weight loss
  • weakness/fatigue
  • p/p/p
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3
Q

What are some distinguishing factors of DM 2?

A

-insidious onset
-circulating insulin exists enough to prevent ketoacidosis,
but is inadequate to meed pt’s insulin needs
-in females, often the first symptom is recurrent vaginitis;
chronic skin infections
-mostly managed with oral anti-diabetics; also with
weight reduction and dietary treatment
-peripheral neuropathy
-blurred vision
-polyuria/polydipsia

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4
Q

What is the recommended intake of carbs, fats, fiber, and protein?

A

Carbs: 50-60% total caloric intake
Fat: 20-30%
Fiber: 25g/1000 calories
Protein: 10-20%

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5
Q

What do sulfonylureas do?
Examples?
Any specific drug class-associated precautions?

A

-Stimulate pancreas to release insulin/enhances insulin
release

  • glipizide
  • glyburide
  • glimepiride
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6
Q

What do biguanides do?
Example?
Any specific drug class-associated precautions?

A

-Good adjunct to sulofonylureas, but can be used alone,
especially in obese patients

-Reduces hepatic glucose production and intestinal
glucose absorption + insulin sensitizer via increased
peripheral glucose uptake and use

Metformin

**Monitor Cr
**lactic acidosis is a possible side effect
(presents as muscle pain)

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7
Q

What do alpha-glucosidase inhibitors do?
Example?
Any specific drug class-associated precautions?

A

Binds to disaccharidases so less glucose is absorbed by
the gut/delays intestinal carbohydrate absorption–>
helpful in managing post-prandial hyperglycemia

  • acarbose (Precose)
  • miglitol (Glyset)

-Monitor for GI side effects; take with 1st bite of meal

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8
Q

What do thiazolidinediones do?
Example?
Any specific drug class-associated precautions?

A

-Decreases gluconeogenesis; insulin sensitizer

  • rosiglitazone (Avandia)
  • pioglitazone (Actos)

Monitor ALT; may take up to 12 weeks for therapeutic
effect

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9
Q

What do non-sulfonylurea insulin release stimulators do?
Example?
Any specific drug class-associated precautions?

A
  • Rapidly absorbed from the intestine and mimics the
    effect of rapidly acting insulin
  • repaglinide (Prandin)
  • nateglinide (Starlix)

Take within 30 mins prior to meal

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10
Q

What does exenatide (Byetta) do?

Any specific drug class-associated precautions?

A

-Mimics the effects of incretins - signals the pancreas to
increase insulin secretion and the liver to stop
producing glucagon

Injectable

N/V, D

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11
Q

What do DD-4 inhibitors do?
Example?
Any specific drug class-associated precautions?

A

-Breaks down incretins so that the level increases which
stimulates release of insulin

-sitagliptin (Januvia)

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12
Q

What do amylin analogues do?
Example?
Any specific drug class-associated precautions?

A

-Slows absorption of glucose and inhibits the action of
glucoagons

  • pramlinitide (Symlin)
  • Promotes weight loss while decreasing blood glucose
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13
Q

What is the Somogyi effect and how do you manage it?

A

-When you get early morning hyperglycemia (peaking
around 7am; is hypoglycemic at 3am) as a result of
nighttime hypoglycemia. Counter regulatory hormones
surge, raising blood sugar.

-Decrease or omit night-time dose of insulin

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14
Q

What is the Dawn phenomenon and how do you manage it?

A

-Gradually elevating glucose levels through the night that
result in morning hyperglycemia due to tissues
becoming desensitized to insulin nocturnally

-Increase or add bedtime insulin dose

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15
Q

What is Cushing’s Syndrome?

A
-Caused by the overproduction/hypersecretion of 
    adrenocorticoid hormone (ACTH) by the pituitary gland

-Increase in cortisol

-Can be caused by chronic use of glucocorticoids or
adrenal tumors

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16
Q

What are key signs/symptoms of Cushing’s Syndrome?

A
Moon face and buffalo hump
Weakness (so much so it is hard to walk up stairs)
HTN
Labile mood
Hirsutism/acne/purple striae
Frequent infections
Hyperglycemia, Hypernatremia, and Hypokalemia
Elevated plasma cortisol in the AM
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17
Q

How do you treat Cushing’s Syndrome?

A

Depends on cause: DC medications inducing symptoms;
surgery for removal of adrenal tumors

Electrolyte balance

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18
Q

What is Addison’s Disease?

A

A deficiency of cortisol, aldosterone, and androgens

Results from an autoimmune destruction of adrenal gland

Pituitary failure resulting in decreased ACTH

19
Q

What are key signs/symptoms of Addison’s Disease?

A

Hyperpigmentation of mucous membranes, palms, and
knuckles

Orthostasis and hypotension

Hypoglycemia, Hyponatremia, and HYPERkalemia

Plasma cortisol low in AM

20
Q

How do you treat Addison’s Disease?

A

Glucocorticoid (hydrocortisone) and mineralcorticoid
(fludrocortisone) replacement

Referral to endocrinology

21
Q

When you hear HYPERthyroidism, what do you think?

A
  • less common than hypothyroid
  • Grave’s disease
  • Low TSH and High T3 (80-230)
  • Tachycardia, exopthalmos, nervousness/anxiety, heat intolerance, fine hair, weight loss, increased appetite
  • Treament: Propanolol (start with 10mg, titrate to as high as 80mg QID) for tremors/tachycardia; PTU or methimazole; Radioactive iodine 131-I used to destroy goiters
  • Adverse outcomes: Thyroid crisis
22
Q

When you hear HYPOthyroidism, what do you think?

A

Hashimoto’s thyroiditis most common cause

Everything slows down

Elevated TSH, Low T4, hyponatremia, hypoglycemia
Treatment: Levothyroxine 50-100mcg/day, may titrate
dose by 25mcg every 1-2 weeks until symptoms
stabilize

Draw levels after 2 months of consistent therapy
Adverse outcome: myxedema coma

23
Q

What are the normal values for BUN and Cr?

A

BUN: 10-20 (dehydration most common cause for elevation)
Cr: 0.5-1.5 (most sensitive indicator for renal function/failure)

24
Q

What is normal blood glucose?

A

60-99

25
Q

What is the goal level for HgbA1c?

A

6

26
Q

What is the role of Lantus?

A
  • Onset of action is 1 hour

- Lasts 24 hrs (no peak)

27
Q

How does Humalog/Lispro work?

A
  • Onset of action is 15-30 mins
  • It should be given within 15 mins or right after eating
  • Peaks in 30 mins to 2.5 hrs
  • Lasts 3-6.5 hrs
28
Q

How does Regular insulin work?

A
  • Onset of action 0.5-1 hr
  • Peaks in 2-3 hrs
  • Lasts 4-6 hrs
29
Q

What is the role of NPH?

A
  • Onset of action 1-2 hrs
  • Peaks in 6-14 hrs
  • Lasts 16-24 hrs
30
Q

DM Labs

All the same except…

A

-random plasma glucose ≥200 with polyuria, polydipsia,
and WL
-Serum FBS ≥126 on 2 separate occasions (8 hr fast)
-FBG may be elevated secondary to corticosteroids, beta
blockers, thiazide diuretics, or statins
-Ketonuria, ketonemia or both (Not in DM 2)
-Elevated BUN/Cr
-Oral GTT ≥200
-Hgb A1c

31
Q

Meds that may cause elevated FBG

A

Corticosteroids
Beta Blockers
Thiazide Diuretics
Statins

32
Q

Impaired glucose tolerance lab levels

A

FBG ≥100 and ≤125

33
Q

When does insulin need to be initiated?

A

When there is presence of ketones
ketonuria
ketonemia

34
Q

Starting insulin dose is calculated how?

A

Begin with 0.5 u/kg/day giving 2/3 in the morning and 1/3
in the evening

Morning dose is 2/3 NPH and 1/3 Regular

Evening dose is 1/2 NPH and 1/2 Regular

For intensive therapy, reduce or omit the PM dose and
add a portion at bedtime

35
Q

Insulin agents

A

aspart (NovoLog)

glargine (Lantus)

lispro (Humalog)

36
Q

DKA pathology

A

-State of intracellular dehydration as a result of elevated
blood glucose levels
-Often an acute complication of DM 1
-May be presenting sign of DM

37
Q

DKA S/S

A
  • *Diabetic in Shock**
  • Polyuria, including nocturia
  • Polydipsia
  • Weakness, fatigue, N/V
  • Kussmaul’s breathing
  • Altered LOC
  • Fruity breath
  • Hypotension and tachycardia
  • Poor skin turger
38
Q

DKA Labs/Diagnostics

A
-Hyperglycemia (serum glucose >250 and frequently 
    >300)
-Ketonemia and/or ketonuria
-Marked glycosuria
-Acidosis (pH <7.3): Metabolic
-Elevated Hct, BUN, Cr
-Hyperkalemia
39
Q

DKA Management

A
  • Protect airway
  • Administer O2
  • Hospital
40
Q

HHNK pathology

A

-State of greatly elevated serum glucose, hyperosmolality,
and severe dehydration without ketone production
-Usually occurs as a complication of DM 2
-Pt’s cannot produce enough insulin to prevent severe
hyperglycemia, osmotic diuresis and extracellular fluid
depletion
-Mortality rates 30-50%

41
Q

HHNK S/S

A
  • Polyuria
  • Weakness
  • Altered LOC
  • Hypotension
  • Tachycardia
  • Poor skin turgor
  • Other signs of dehydration
42
Q

HHNK Labs/Diagnostics

A
-Greatly elevated serum glucose (>600, commonly 
    >1000)
-Hyperosmolality
-Elevated BUN, Cr
-Elevated Hbg A1c
-Relatively normal pH
-Normal anion gap
43
Q

HHNK Managment

A
  • Protect airway
  • Administer O2
  • Hospital