EM- metabolic emergencies Flashcards

1
Q

what is “ketosis”?

A

Ketosis is a metabolic process that occurs when the body begins to burn fat for energy because it does not have enough carbohydrates to burn. During this process, the liver produces chemicals called ketones

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2
Q

3 causes of hypoglycemia? ketosis

A

fasting
malabsorption, GE
increased utilization: exertion

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3
Q

3 causes of hypoglycemia? non-ketosis

A

hyperinsulinism
adrenal insufficiency
congenital disorders
*also drugs, sepsis, hepatic failure

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4
Q

hypoglycemia: S+S, PE

A

S+S: AMS; anxiety, shakiness, nausea, sweating
PE: confusion, diaphoresis, tremor
tachycardia, incr BP
obtundation, seizures

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5
Q

what labs dx hypoglycemia?

A

glucose <50 mg/dL

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6
Q

txt for hypoglycemia?

A

orange juice, snickers

IV D50: 1amp then 100 cal/hr for 2 hrs

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7
Q

what is the pathophys if DKA?

A

liver has increased glucose production but peripheral tissues have decr. glucose uptake = hyperglycemia
–> osmotic diuresis and vol. depletion
liver rapidly increases ketogenesis (body NEEDs fuel) and Adipose releases free fatty acids = ketoacidosis
–> decreased alkali reserve and metabolic acidosis

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8
Q

symptoms of DKA

A

Polydipsia, polyuria, weakness, nausea/vomiting, abdominal pain, weight loss

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9
Q

PE findings for DKA: temp, HR, GI etc.

A
Hypothermia (hyper if infectious etio), tachycardia, tachypnea/hyperpnea (Kussmaul resps), ileus, maybe altered MS. 
acetone breath (fruity)
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10
Q

4 Dx labs for DKA

A

Glucose >250 mg/dL
+ serum acetone
pH≤ 7.3
Anion gap >12

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11
Q

what things can cause DKA?

A

increased cortisol
insulin omission (can’t use glucose)
inflammation; infection ; ischemia

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12
Q

what things 5 can cause DKA?

A

increased cortisol
insulin omission (can’t use glucose)
inflammation; infection ; ischemia

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13
Q

4 goals of DKA mgmt?

A
  1. Volume resuscitate!!! 2L NaCl (for hypoperfused organs)
  2. Correct AG acidosis
  3. Target glucose: 150-200 mg/dL
  4. Correct K+ and Mg2+
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14
Q

if you give insulin to drive glucose into the cells, what electrolyte imbalance can you cause?

A

hypokalemia? so supplement with K+ if they might already be low in K+
(rather be high in K+ than low)

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15
Q

how do you give fluids for DKA? (kinda weeds?)

A
  1. 2L normal Saline for the 1st hour
  2. Replace 50% of estimated TBW deficit over 8 hours
    CHANGE to D5 ½ NS @ 150 mL/hr when glucose <250 mg/dL
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16
Q

DKA: If K _____ mEq/L, hold insulin until actively correcting K. what is your K+ goal?

A

< 3.3 mEq/L

Goal K+ = 4 - 5 mEq/L

17
Q

how often do you check glucose when resuscitating for DKA?

A

finger stick every hour
*Initial Goal: decr. Glucose by 50 - 75/hour
If glucose not decreasing by ≥ 50 mg/dL in 1st hour - double IV insulin rate

18
Q

do you give bicarb supplement for DKA?

A

only if pH <7

19
Q

what is the normal level of K+? what level is life threatening?

A

normal: 3.5- 5

life threatening: >7.5

20
Q

ekg findings of hyperkalemia?

A

peak T waves = hyperkalemia

BUT even if they have a normal EKG, if they have high K+ - still need to treat them

21
Q

what are the 3 mechanisms to hyperkalemia?

A
  1. Excessive cellular release: rhabdo, burns, tumor lysis syndrome, crush injury, if theyve had a tourniquette on a long time
  2. Excessive intake: KCL supplements
  3. Insufficient excretion: AKI, CKD
22
Q

4 clinical causes of hyperkalemia?

A
  1. renal insufficiency : DIALYSIS!!!
  2. Meds (interferes w/excretion): ACEIs, ARBs, spironolactone, NSAIDs,
  3. Mineralocorticoid deficiency: e.g. Addison’s
  4. DKA (but you only wanna txt this with insulin)
23
Q

what is the most common cause of a hyperkalemia finding in lab results?

A

hemolysis from poor labs. Redo the lab sample if K+ >7 but no S+S

24
Q

K+ >7 causes what? what about >9?

A

> 7: conduction abnormalities and bradycardia

>9: Cardiac arrest due to… asystole, Vfib, PEA w/ bizarre wide complex rhythm

25
Q

3 part txt of hyperK+

A
#1 - Stabilize cardiac myocyte membranes
#2 - Drive the K back into the cells
#3 - Get rid of the excess
26
Q

what are 5 ways we drive K+ back into the cells?

A
  1. 50g glucose (D50 ) w/ insulin (10 g) (5:1 ratio)
  2. Beta agonists: Albuterol
  3. bicarbonate - exchanges H+ inside the cell for K+ outside the cell (only if acidodic)
  4. volume (saline) - if dialysis- careful
  5. Mg + - drives K+ into the cell .
27
Q

what two ways do we get rid of the excess K+ ?

A

kayexelate (binds K+ into stool) and hemodialysis

28
Q

what do we do to stabilize the cardiac membrane?

A

give Ca+

29
Q

what level is considered hypoKalemia? severely low?

A

K+ < 3.5

severe if <2.5

30
Q

when are symptoms of Hypokalemia most likely present?

A

when there is a RAPID drop in K+ and it goes below 2.5

31
Q

What are 3 ways someone can get hypokalemia?

A
  1. inadequate potassium intake (alcoholics/malnourished)
  2. excessive loss of potassium
  3. transcellular shift of potassium
32
Q

what is the most common cause of hypokalemia? most common drug-related cause?

A
  • increased loss in the urine: increased urinary flow or delivery of sodium to distal nephron
  • Diuretics
33
Q

GI loss of K+ (in the stool). when does this occur?

A

in pathological states where stool volume increases, as in cases of diarrhea

34
Q

how can transcellular shifts cause hypokalemia?

A

medications that cause transcellular potassium shifts:
stimulating cell membrane Na+/K+-ATPase and promoting K entry into cells
(insulin + glucose, albuterol)

35
Q

what ekg findings may indicate hypokalemia?

A

T flattening and inversion, Uwaves

36
Q

txt for hypokalemia?

A

For many patients, it is unnecessary to bring K+ levels back to normal during their ED stay
(but if you do have to, give K+Cl)
D/c HOME with instructions to eat foods that are high in potassium

37
Q

when would you need cardiac monitoring when repleting K+ via IV?

A

*When infused through a peripheral IV, K+ may be uncomfortable and result in a phlebitis
When the IV repletion rate is faster than 20 mEq/hour