Endocrine Disorders Flashcards

(43 cards)

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

25
What is the goal level for HgbA1c?
6
26
What is the role of Lantus?
- Onset of action is 1 hour | - Lasts 24 hrs (no peak)
27
How does Humalog/Lispro work?
- 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
How does Regular insulin work?
- Onset of action 0.5-1 hr - Peaks in 2-3 hrs - Lasts 4-6 hrs
29
What is the role of NPH?
- Onset of action 1-2 hrs - Peaks in 6-14 hrs - Lasts 16-24 hrs
30
DM Labs | All the same except...
-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
Meds that may cause elevated FBG
Corticosteroids Beta Blockers Thiazide Diuretics Statins
32
Impaired glucose tolerance lab levels
FBG ≥100 and ≤125
33
When does insulin need to be initiated?
When there is presence of ketones ketonuria ketonemia
34
Starting insulin dose is calculated how?
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
Insulin agents
aspart (NovoLog) glargine (Lantus) lispro (Humalog)
36
DKA pathology
-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
DKA S/S
* *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
DKA Labs/Diagnostics
``` -Hyperglycemia (serum glucose >250 and frequently >300) -Ketonemia and/or ketonuria -Marked glycosuria -Acidosis (pH <7.3): Metabolic -Elevated Hct, BUN, Cr -Hyperkalemia ```
39
DKA Management
- Protect airway - Administer O2 - Hospital
40
HHNK pathology
-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
HHNK S/S
- Polyuria - Weakness - Altered LOC - Hypotension - Tachycardia - Poor skin turgor - Other signs of dehydration
42
HHNK Labs/Diagnostics
``` -Greatly elevated serum glucose (>600, commonly >1000) -Hyperosmolality -Elevated BUN, Cr -Elevated Hbg A1c -Relatively normal pH -Normal anion gap ```
43
HHNK Managment
- Protect airway - Administer O2 - Hospital