Metabolic Emergencies Flashcards

1
Q

2 major causes of hypoglycemia

A

1) excess endogenous/exogenous insulin or hypoglycemic agents (metformin, TZDs, sulfonlyureas)
2) failure of other organs to produce or mediate glucose metabolism (pancreas, liver)

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2
Q

glucose reference range

A

~65-110 mg/dl

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3
Q

when does the body usually stim catecholamine release

A

Glucose 30-50 mg/dL

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4
Q

what are the effects of a catecholamine release

A

Irritability, hunger (“hangry”), trembling
Diaphoresis
Tachycardia

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5
Q

what glucose level are there neuroglycopenic effects

A

less than or equal to 30

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6
Q

Neuroglycopenic effects of low glucose

A

Focal neurologic deficits, headaches, dizziness
Confusion, bizarre behavior, visual disturbances
Hypothermia
Seizure or seizure-like activity

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7
Q

tx of hypoglycemia if IV is not available

A

IM glucagon

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8
Q

how does IM glucagon work

A

trigger liver to convert glycogen to glucose (glucagon is typically release by pancreatic alpha cells in response to hypoglycemia)

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9
Q

tx of hypoglycemia with IV access

A

Glucose
IV D50 (IV dextrose)
Oral glucose gel/tabs
If conscious and responsive with mild
hypoglycemia: OJ, candy, a snack or meal

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10
Q

*what is DKA

A

Profound deficiency of insulin results in hyperglycemia
Results in hyperglycemia
(has glucose but there is no insulin to put it in the cells)

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11
Q

*MC life threatening condition with DM (typically type I)

A

DKA

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12
Q

*lack of insulin in DKA leads to…

A

breakdown of triglycerides/fatty acids for energy with production of ketones

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13
Q

*often initial clinical presentation of Type I DM

A

DKA

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14
Q

*onset of DKA

A

rapid (within days of symptom onset)

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15
Q

*symptoms of DKA

A
Polyuria & polydipsia
Headache
Abdominal pain
Nausea & vomiting
Weakness/lethargy
Kussmaul respiration
             Deep, rapid, sighing; aka air hunger
Depressed mental status
Dehydration
*acidosis (fruity breath)
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16
Q

DKA labs:

  • serum glucose
  • ketones
  • serum bicarb
  • arterial pH
A
Serum Glucose > 250mg/dl
Ketones
         Ketonuria
          Serum ketones
Serum Bicarbonate  < 15mEq/lL 
pH <7.3
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17
Q
*DKA Labs:
Anion Gap 
Serum Sodium 
Serum Phosphate 
Serum Potassium
A

Elevated Anion Gap (see next slide)
Serum Sodium – usually low (osmotic hemodilution)
Serum Phosphate – low (hemodilution and diuresis)
Serum Potassium – often normal to elevated
Paradoxical elevation caused by extracellular shift
of potassium resulting in a relative hyperkalemia

18
Q

what is a normal anion gap, how is it calculated and what is it for

A

Anion Gap = Serum NA+ – (Serum Cl- + HCO3-)
Normal: ~8 +/- 4 mmol/L
Generally accepted > 12 mmol/L = elevated

19
Q

causes of increased anion gap and what is it for

A
MUDPILERS: DKA 
Methanol
Uremia
Diabetic/alcoholic/starvation ketosis
Paraldehyde
Isoniazid/Iron
Lactic acidosis
Ethylene Glycol
Rhabdo, Salicylates
20
Q

*step 1 tx for DKA

A

IV Fluids: Normal Saline @ 500-1000 ml/hr
-DO 1st! Why?? –> when give insulin, the glucose
goes into he cells and the water follow and their BP
can tank
-Once orthostatic hypotension resolves (fluid loss due
to polyuria), decrease to 200-500 cc/hr.

21
Q

*step 2 tx for DKA

A

Insulin 10 U bolus and then 5 U/hr.
-~1hr post IVF
-Follow blood sugar: expect serum glucose to
decrease at 100/hr
-Lower blood glucose, gradually, to <250
-If inadequate fall in blood glucose,  the insulin
and the IVF

22
Q

*step 3 tx for DKA

A

Potassium replacement considered
-Pre-labs:
-If urinating and non-peaked T waves; add 20
mEq to IV
-If urinating and flat/depressed T waves or U
waves; add 40 mEq to IV
-If anuric and peaked T waves – await labs to
determine amount

23
Q

*why do you not want to decrease glucose too quickly in DKA and what should you keep glucose levels at

A

Too rapid of a correction can lead to sequelae such as cerebral edema

150-250 mg/dL

24
Q

*onset of HHS

A

insideous

25
Q

*what is HHS

A

adequate insulin, decreased cell response

26
Q

*HHS is MC in…

A

Type II DM

27
Q

*cause of HHS

A

precipitating event

28
Q

*labs for HHS

A
  • severely elvated glucose (>600)
  • absence of lipolysis/ketogenesis
  • low/absent serum/urine ketones
29
Q

*typical HHS pt

A

Typically ≥ 60 years old
Chronic care facility or nursing home
Change in diabetic regimen or addition of meds that raise glucose levels
Corticosteroids, thiazides, anticonvulsants,
sympathomimetics
Recent or current infection
Dementia

30
Q

*is kussumal signs present in DKA, HHS, or both

A

DKA ONLY

31
Q

*s/sxs HHS

A
  • N/V-abdominal pain
  • sig dehydration
  • depressed mental status
  • Focal neurologic abnormalities
  • NO kussumal signs
32
Q

*t/f-pH is decreased in HHS

A

FALSE, pH is normal in HHS!

DKA has low pH

33
Q

tx for alcholic ketoacidosis

A

*thiamine 100mg IV or IM –> for neuron function

34
Q

what is thyroid storm

A

extreme form of thyrotoxicosis

35
Q

clinical manifestation of thyroid storm

A
Fever – may exceed 104°F
Tachycardia (Sinus, SVT, Atrial arrhythmias, CHF)
Delirium, confusion
N&amp;V and diarrhea, abdominal pain
Agitation, tremor, generalized weakness
36
Q

labs for thyroid storms

A

TSH (low), Free T4 (high)

37
Q

what should you avoid as tx for someone with thyroid storm

A

ASA- displaces t4

38
Q

myxedema coma

A

severe hypothyroidism

39
Q

s/sxs of myxedema coma

A

Hypothermia
Hypoventilation leading to hypoxia and hypercapnia
Hyponatremia
Hypotension
Seizures and abnormal CNS signs may occur including altered mental status.

40
Q

what med is myxedema coma pts very sensitive to

A

opiates- a normal dose can kill them

41
Q

tx for myxedma coma

A

1) loading dose of 500 micrograms of levothyroxine

2) hydrocortisone 100mg IV bolus followed by 25-50 every 8 hrs

42
Q

*adrenal insufficiency dx

A

synthetic ACTH (cosyntropin) stimulation test