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Electrolytes, Acid/base disturbances, endocrinology > Endocrine Emergencies > Flashcards

Endocrine Emergencies Flashcards

1
Q

Acute Adrenal Insufficiency?

A

aka Addisonian Crisis

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2
Q

what are the key clinical features of an addisonian crisis?

A

Hypotension, acute pain (abdomen, low back), hypovolemic shock Vomiting, Diarrhea, dehydration, and altered mental status.

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3
Q

is acute adrenal insufficiency fatal?

A

yes!!! if left untreated

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4
Q

what can cause adrenal crisis?

A

infection, trauma, surgery, stress, lymphoma, metastic cancer, amyloidosis, sclerodema, hemochromatosis, or cessation of corticosteroid medications, anything that may cause severe physiologic stress, high dose of corticosteroids,

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5
Q

what is the most important hormone in adrenal crisis?

A

cortisol

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6
Q

what are the functions of cortisol?

A
  • permissive for the action of Epi and NE on muscles and VB
  • Maintainer of glucose- adequate cellular concentrations of the enzymes need to produce glucose btw meals
  • decreaser of inflammation- changes of capillary permeability and production of prostoglandings
  • fetal development
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7
Q

more things that cortisol does

A
  • increases catabolism in bone and muscle
  • breakdown of adipose
  • inhibits the immune system, growth, reproduction
  • activates protective mechanisms (increases: WBC, Glucose, plasma volume
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8
Q

how does adrenal insuff. cause hypotension?

A

decrease in aldosterone creates imbalance of Na, K and H20!
causes Na to be lost and K to increase!

hypotension and arrhythmias!

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9
Q

what organisms are associated with adrenal crisis?

A

H. Flu, S. aureus, Strept. pnu, fungi

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10
Q

medications that can cause adrenal insuffi?

A

ketoconazole, phenytoin, rimfampin, mitotane, septic shock

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11
Q

laboratory work up for adrenal crisis?

A

hyponatremia, hyperkalemia, Met Acid, hyopglycemia

serum cortisoll: less than 20 mcg/dL in severe stress or after ACTH stimulation

CBC: anemia, lymphocytosis, eosinophilia (highly suggestive)

TSH

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12
Q

what is diagnostic for adrenal insuff?

A

ACTH test: determine baseling serum cortisol, then give ACTH 250 mch IVP, then draw a serum cortisol 30 and 60 mins later

increase of less than 9 mch/dL is considered diagnostic

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13
Q

how do you treat acutre adrenal insufficience?

A

glucocorticoids: dexamethasone

agressive fluid replacement w/ 5-10% IV dextrose and saline solutions

tx of hyperkalemia!!!

fresh frozen plasma

pressors (epi or NE) to combat hypotension

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14
Q

Thyroid storm

A

extreme hyperthyroidism

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15
Q

what can precipitate a thyroid storm?

A

illness, sepsis, trauma, surgery, RAI (radioactive iodine), pregnancy

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16
Q

Clinical features of thyroid storm?

A

high fever, tachycardia, agitation, sweating, tremor, instability, delirium, V, D

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17
Q

what is the treatment for Thyroid storm?

A

PTU, but monitor for liver dysfxn

IV Na-iodid, iV hydrocortisone, Lugol solution (iodine),

propanolol to alleviate signs and sx

long term- PTU or MMI

18
Q

what is contraindicated in a thyroid storm?

A

IV dextrose or oral carbs

19
Q

what electrolyte disorder is seen with a thyroid storm?

A

hypokalemia! this will response to propanolol

20
Q

DKA precipiating factors

A

the 5 I’s:

insulin deficiency
infxn
ischemia
intra-abdominal process
intoxication
21
Q

presentation DKA

A

Polydipsia and polyuria
Weakness, dizziness
Anorexia
Visual disturbances
Tachycardia
Hypotension
Warm, dry skin, sunken eyes, dry mucous membranes (more with HHS)
Weight loss (more with HHS)
Tachypnea (more with DKA)
GI symptoms: N/V/D
Decreased mentation, lethargy, confusion and/or delirium
Focal neurological signs such as hemisensory deficits, hemiparesis that mimic CVA, aphasia and seizures.
Fruity odor breath (only with DKA) (bc of ketone)

22
Q

DKA definition

A

> 200 mg/dL and
acidosis (pH < 7.3 and/or bicarb < 15)

categories:
Mild: pH < 7.30, bicarbonate < 15 mmol/L
Mod: pH < 7.20, bicarbonate < 10 mmol/L
Severe: pH < 7.10, bicarbonate < 5 mmol/L

23
Q

pathophysiology of DKA

A

cells are starving bc not getting glucose (no insulin on board) signals to body that nutrients are needed

-liver makes more glucose and breaks down glycogen so amount of glucose keeps increasing

24
Q

what does the body start to do when the cells are starving?

A

use other sources of nutrients
-breaks down proteins and fats (lipolysis) and results in the production of ketoacids

and dehydration and poor perfusion leads to lactic acidosis!

25
Q

Kussmaul respirations

A

deep sighing that helps increase the bodys way of compensating for metabolic acidosis- decreases CO2

26
Q

PE findings of someone in DKA

A

kussmaul, dehydration, tachycardia, delayed cap refil, abdominal tenderness

27
Q

what do DKA pts get dehydrated?

A

osmotic diuresis- kidnesy are overwhelmed by excess glucose that keeps water in renal tubules that leads to increased urination and dehydration

Vomiting!

28
Q

what electrolyte imbalances are associated with DKA?

A

hyponatremia and hypokalemai bc the ketoacids bind to Na and K

29
Q

treatment of DKA

A

correct dehydration, correct acidosis and reverse ketosis

-correct electrolyte imbalance

give insulin

30
Q

step 1 of tx of DK

A

IV hydration!

NS bolus of LR bolus 20 ml/kg over 1 hours (wathc for cerebral edema)

then at maintainence IV fluid rate

31
Q

why must you be careful when correcting dehydration of DKA pts?

A

must go slow to avoid rapid shift of water from extracellular to intracellular– cell swelling or cereral edema

32
Q

step 2 tx of DKA

A

insulin infusion!

no bolus in kids bc may increase risk of cerebral edema
and switch to D5ND when glucose is < 300 mg/dL

33
Q

cerebral edema and DKA pts

A

watch out for in kids!!! (AMS, dilated pupils, decreased HR w/ increased BP)
Reduce rate of IVF infusion
Mannitol 0.5-1 g/kg over 20 min
3% saline 5-10 ml/kg over 30 min (hypertonic saline)
Consider intubation if cannot protect airway

34
Q

fasting hypoglycemia

A

occurs secondayr to some endocrine disorders (addison, myxedema), liver malfxn, acute alcoholism, ESRD

35
Q

what is primary hypoglycemia caused by?

A

hyperinsulinism, extrapancreatic tumors (insulinoma) or B cell tumors

36
Q

what is postprandial or reactive hypoglycemia?

A

early (2-3 hours after eting) vs late (3-5 hours after eating)

  • GI surgery (espeically postgastrectomy w/ dumping syndrome or roux-en-Y gastric bypass) can be alcohol related, factictious, immunopahtologic, or drug induced
37
Q

CF of hypoglyceia?

A

sx begin at plasma glucose levels of 60 mg/dl

-cognitive impariement at 50

38
Q

what does fasting hypoglycemia occur with?

A

neuroglycopenia

39
Q

what does postprandial hypoglycemia look like?

A

sweating, palpiations, anxiety, and tremulousness

40
Q

what is he Whipple triad?

A

hx of hypoglycemic sx, fasting BG of 45 or less, and immediate recovery when given glucose

Electrolytes, Acid/base disturbances, endocrinology (7 decks)

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