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Flashcards in Endocrine Emergencies Deck (57):
1

Pathophysiology of DKA

Body's response to cellular starvation
Relative insulin deficiency
Counterregulatory excess (glucagon)

2

Why does one become acidotic in DKA?

Relative insulin deficiency
Cellular starvation
Lipolysis with subsequent fatty acid transport to hepatocytes
Formation of ketoacids
Ketonuria
Anion gap metabolic acidosis with capensatory tachypnea
Vomiting

3

Why does one become dehydrated in DKA?

Relative insulin deficiency
Hyperglycemia increases osmotic load and leads to glycosuria
Water drawn out of cells via oncotic pressure
Impaired consciousness
Shock

4

Presentation of DKA

Hyperglycemia
Acidosis from ketoacids
Volume loss

5

Presentation of Hyperglycemia

Polydipsia
Polyuria

6

Presentation of Acidosis from Ketoacids

Tachypnea
Fruity odor of breath

7

Signs of Dehydration

Dry membranes
Poor skin turgor
Delayed capillary refill
Mental confusion

8

Management of DKA

Aggressive fluid therapy (NS)
Place monitor
2 large bore IVs
Bedside glucose, urine dipstick, EKG
CBC, CMP, phosphate, and magnesium
ABGs
Blood cultures/other labs as indicated

9

Fundamentals of Treatment of DKA

Volume repletion
Reversal of metabolic consequences of insulin insufficiency
Correction of electrolyte and acid-base imbalances
Treatment of precipitating cause
Avoid complications

10

Why does fluid administration help with a decrease in blood glucose and ketone concentration?

Increases GFR
Allows for glucose and ketones to be excreted

11

Insulin Therapy in DKA

0.1 units/kg/hr after fluid bolus
Use infusion pump for less complications, flexibility in adjusting dose
AVOID IM and subQ doses

12

What is the most life-threatening electrolyte derangement during treatment of DKA?

Hypokalemia

13

Goals of Potassium Therapy in DKA

Maintain normal extracellular K during acute phase
Replace intracellular K over several days

14

Hypokalemia in DKA due to Therapy

Cardiac arrhythmias
Respiratory paralysis
Paralytic ileus
Rhabdomyolysis

15

Complications of DKA

Hypoglycemia
Cerebral edema
Hypokalemia
Hypophosphatemia
Adult respiratory distress syndrome

16

Reasons for DKA in NOT a New Onset Diabetic

Compliance issues
Discontinuation of insulin
Insults to the body such as infection, MI, PE

17

What condition occurs in patients with poorly controlled or undiagnosed type II DM?

Hyperosmolar hyperglycemic state

18

Define Hyperosmolar Hyperglycemic State

Serum glucose: 600+ mg/dL
Plasma osmolality: 315+ mOsm/kg
Bicarbonate: 15+
Arterial pH: 7.3+
Serum ketones negative

19

Shared Symptoms of DKA and Hyperosmolar Hyperglycemic State

Hyperglycemia
Hyperosmolality
Severe volume depletion
Electrolyte imbalances
Acidosis??

20

Mortality Rates in DKA and Hyperosmolar Hyperglycemic State

DKA: 5%
HHS: 15-30%

21

Risk Factors of Hyperosmolar Hyperglycemic State

Inability to access water
Non-ambulatory patients

22

Presentation of Hyperosmolar Hyperglycemic State

Elderly
Abnormalities in vitals or mental status
Precipitated by acute illness
+/- baseline cognitive impairment
Weakness
Anorexia
Fatigue
Cough
Dyspnea
Abdominal pain

23

Treatment of Hyperosmolar Hyperglycemic State

Volume repletion
Correction of electrolyte abnormalities
Treat precipitating cause
Correction of hyperglycemia
Judicious management of concurrent illness

24

Neurogenic (Increased ANS Activity) Hypoglycemia Signs and Symptoms

Sweating
Pallor
Tachycardia
Palpitations
Tremor/shaking
Nervousness/anxiety
Tingling, paresthesias

25

Neuroglycopenic (Lack of Sugar to Brain) Hypoglycemia Signs and Symptoms

Headache
Drowsiness
Lightheadedness or syncope
Mental dullness or confusion
Amnesia
Seizure
Coma

26

At what glucose level do neurogenic symptoms appear?

Approximately less than 54 mg/dL

27

At what glucose level do neuroglycopenic symptoms appear?

Approximately less than 47 mg/dL

28

Define Hypoglycemia Unawareness

Development of low serum sugar values without physiologic ability to react

29

Patients at Greatest Risk for Hypoglycemia Unawareness

Extremes of age
Co-morbidities
Medications

30

Outpatient Recommendations for Treatment of Hypoglycemia

15-20 g of glucose
Retest glucose in 15 minutes
Prescribed glucagon
Alter insulin or dosage adjustment of oral medication

31

ED Management of Hypoglycemia

1 g/kg body weight dextrose
Retest glucose q30 for 2 hours
Oral replacement (300g)
Glucagon 1 mg IM/IV
Octreotide

32

Other Considerations for Hypoglycemia in Non-Diabetic Patients

ETOH
SEpsis

33

What does the adrenal medulla secrete?

Epinephrine
Norepinephrine

34

What does the adrenal cortex secrete?

Mineralocorticoids (aldosterone)
Glucocorticoids (cortisol)
Sex hormones

35

Function of Adrenocorticotropic Hormone (ACTH)

Stimulate synthesis and secretion of adrenocortical hormones

36

Define Adrenal Insufficiency

Failure of adrenal glands to produce essential BASAL secretion of steroids

37

Symptoms of Insidious Wasting Disease in Adrenal Insufficiency

Weight loss
Fatigue
Lack of ambition
Hypotension
Hyper-melanoma

38

Define Adrenal Crisis

Failure to RESPOND to the increased demands caused by stress or SUDDEN INABILITY to secrete essential steroids

39

Define Primary Adrenal Insufficiency

Results from destruction or dysfunction of the adrenal cortex

40

Define Secondary Adrenal Insufficiency

Results from inadequate stimulation of adrenal cortex by ACTH

41

Where is adrenal crisis seen?

Undiagnosed primary adrenal insufficiency subjected to major stress
Known adrenal insufficiency who doesn't take extra steroids during major stress
After bilateral adrenal infarction or hemorrhage

42

Presentation of Adrenal Crisis

Marked hypotension
Abdominal and flank pain

43

Treatment of Adrenal Crisis

IV glucocorticoids
D5NS: correct hypovolemia and hypoglycemia

44

Signs and Symptoms of a Pheochromocytoma

Episodic or sustained
Palpitations
Sweating
Headaches
Fainting spells
HTN emergencies

45

Key History of Pheochromocytoma

Episodes of HTN, headache, palpitation, and sweating

46

Diagnosing a Pheochromocytoma

Demonstrating elevated urinary excretion of catecholamines or metabolites DURING a hypertension period

47

Lab Levels in Hypothyroidism

TSH: high
T4, T3: low

48

When does myxedema occur?

In individuals with long-standing preexisting hypothyroidism presents with life-threatening decompensation

49

Most Common Patient Population

Geriatric patients

50

Presentation of Myxedema

Alteration in mental status
Hypothermia
Bradycardia
Hypotension
Hypoventilation
Cardiovascular collapse
Decreased drug clearance
History of primary hypothyroidism, previous thyroid surgery, or hypercholesterolemia

51

What is myxedema coma generally preceded by?

Medication non-compliance
Cold exposure
Severe infection
Addition of new medications

52

Laboratory Findings in Myxedema Coma

Anemia
Hyponatremia
Hypoglycemia
Elevated transaminases
Elevated CPK
Elevated lactate dehydrogenase
Hypercholesterolemia
Decreased PO2
Increased PCO2

53

Treatment of Myxedema Coma

Stabilization
Correction of hypothermia (passive external rewarming)
IV levothyroxine
Routine administration of glucocorticoid
Gentle fluid restriction

54

Hyperthyroidism Symptoms

Heat intolerance
Palpitations
Weight loss
Sweating
Tremor
Nervousness
Weakness
Fatigue

55

What is a thyroid storm potentially preceded by?

Infection
Trauma
DKA
MI
CVA
Thromboembolic disease
Surgery
Withdrawal of thyroid medications
Iodine administration

56

Symptoms Seen in Thyroid Storm but not Hyperthyroidism

Fever
Arrhythmias
CHF
CNS dysfunction: agitation, confusion, delirium, stupor, coma, seizure

57

Treatment of Thyroid Storm

Stabilization
Beta-blockers: severe adrenergic symptoms
Antithyroid agents
Iodine: decrease preformed thyroid hormone