Endocrine Flashcards

1
Q

What is DKA

A

Condition from no insulin in body so serum glucose > 500mg/dL causes body to use fat for energy causing too much ketones which spill over to urine production, and causes acidotic pH (metabolic acidosis) and leading to azotemia (^ BUN)

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2
Q

Causes of DKA

A

Infection, stress, non-compliance by pts with insulin regimen or a new onset type 1 diabetes diagnosis

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3
Q

S&S of DKA

A
Tachypnea-> kusssmaul respirations
Hypotension
Tachycardia
Dry mucous membranes r/t dehydration
Decreased LOC
Hyperkalemia (increased serum potassium)
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4
Q

Treatment of DKA

A

Insulin drip
Fluid replacement start with 0.9% saline then to D5W
Continue until metabolic acidosis resolved then subq insulin
Can give sodium bicarbonate for severe acidosis
**Do not try to reduce K+!!! It will correct as acidosis is corrected

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5
Q

What is Hyper-osmolar hyperglycemic noketonic syndrome/coma (HHS/HHNK)

A

Primarily in type 2 diabetics (there is still insulin production)
A state of SEVERE hyperglycemia that creates a hyper-osmolar state in which no ketones are produced –therefore there’s no acidosis

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6
Q

Causes of HHS/HHNK

A

Infection, stress, however less rapid than DKA
Pts w/non-compliance with diet/meds/insulin regimen, steroids, pancreatitis, TPN use,
(Overal more rare than DKA)

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7
Q

Criteria for HHNK

A
Serum glucose > 800mg/dL
High osmolality (>than 350)
NO ketones in urine
pH > 7.3
Azotemia (increased BUN)
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8
Q

S&S of HHS/HHNK

A

Tachypnea -> rapid+shallow respirations
Profound hypotension
Tachycardia(beta-blockers might mask this)
Dry mucous membranes r/t severe dehydration
Hyperkalemia but may not be as significant as w/DKA

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9
Q

Treat HHNK

A

Insulin drip

Fluid replacement 0.9% NS

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10
Q
What is
Diabetic Insipidus (DI)?
A

Not enough anti-diuretic hormone (ADH) or ADH is present however the kidneys aren’t able to respond which causes abnormal water regulation in the body by the kidneys

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11
Q

S&S of DI

A
Fluid-deficit dehydration -> polydipsia
Polyuria
Hypotension, even hypovolemic shock
Low urine specific gravity < 1.005 (dilute urine)
Low urine osmolality <250
Hypernatremia (hi serum sodium levels)
Increased serum osmolality> 295
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12
Q

DI causes 2 categories

A

1) Neurogenic DI or Central: head; trauma, hypoxia, ischemic, tumors, surgery, autoimmune
- —> lack of ADH production from alterations in the ability of posterior pituitary gland or hypothalamus

  1. ) Nephrogenic DI: kidney; drugs/meds (osmotic agents), osmotic states, decreased osmotic pressure, kidney failure (called high output renal failure, pregnancy (homone-related)
    - —> the kidneys are not abe to respond, thus kidneys cannot retain or reabsorb water
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13
Q

Treatment for DI

A

Nephrogenic– give thiazide diuretic (may help block sodium reabsorption thus correcting Na levels and therefore osmolality abnormalities reducing osmotic diuresis of nephrogenic DI

Neurogenic or Central DI-> replace ADH (vasopressin, DDAVP: desmopressin)

Monitor urine output and specific gravity

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14
Q

What is SIADH symptom of inappropriate anti-diuretic hormone?

A

Too much ADH (too much anti-diuretic hormone) causing water retention in the kidneys -> causes drop in serum sodium and thus serum osmolality
* Referred to dilutional hyponatremia or water intoxication

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15
Q

S&S of SIADH

A

Excess ADH
Hyponatremia (dilutional) can cause seizures
Decreased serum osmolality
Decreased urinary output
Increased urine specific gravity> 1.030 (concentrated urine)
Weight gain
Edema

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16
Q

Causes of SIADH

A

Most common causes: bronchogenic carcinoma (oat cell carcinoma) viral pneumonia, and etiologies from the head: trauma, surgery, tumor, meningitis ect

Other causes: cancer of pancreas, thymus, prostate, lymphatic cancer drugs such as thiazide diuretics (more common in elderly)

17
Q

Treatment for SIADH

A
  • treat underlying cause
  • Fluid restriction
  • Replace sodium with normal or hypertonic saline
  • Give diuretics
  • Monitor Na level-do not correct too fast (pt could develop osmotic demyelination syndrome (ODS) also called central pontine myelinolysis (CPM)
18
Q

Examples of rapid acting insulin

How fast it works, peak, and how long it lasts

A

Aspart
Lispro
Glulisine

SQ
*Preferred for diabetic ketoacidosis
Works 5-15 min
Peak 1 hr, lasts 3-4 hrs

19
Q

Regular insulin
How fast it begins to work
Peak effect & duration

A
*short acting
Only type can be given SQ or IV
Remains stable in body
Begins to work 30 min after admin
Peak 2- 4 hrs
Duration 5-8 hrs 

**Can be used for hyperkalemia

20
Q

Examples of regular (short acting) insulin

A

Humulin R

Novolin R

21
Q

Intermediate-acting insulin (NPH insulin)

A
Less soluble in blood
Works 1-2 hrs after admin 
Peak at 4 hrs
Duration 16-24 hrs 
*Used as a basal insulin 

Examples humulin N

22
Q

Long acting insulin

A

Glargine:slowly and steadily releases into bloodstream. Lasts 24 hrs
Detemir: has a fatty acid side chain binds to albumin before activation. Lasts 20 hrs

Work within 1-2 hrs

No peak effect to either medication

23
Q

Ultra long acting insulin

A
Degludec
By depo injection (beneath skin)
Works 1-3 hrs after admin
NO peak 
Duration 48hrs
24
Q

Effects of regular IV insulin

A

Hypoglycemia

Hypokalemia : K shifts into cell

25
Q

What causes an increase in aldosterone secretion

A

Low CVP (decreased extracellular volume)
HYPERkalemia
Decrease stretch of Right atrium

26
Q

Insulin dose and amount of 25% dextrose for hyperkalemia

A

Dextrose 25% 1ml/kg

Insulin 0.1 units/kg