Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

EMed Exam 2 > Endocrine Emergencies > Flashcards

Endocrine Emergencies Flashcards

1
Q

Hypoglycemia sx

A 
irritability
diaphoresis
tachycardia
blurry vision
weak/confused
hx of Type 1 DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Labs for hypoglycemia

A

finger stick glucose - <70 mg/dl
UA - protein
Urine preganncy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cut off for hypoglycemia

A

<70 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causes of hypoglycemia

A

delay in eating
poor caloric intake (diet, vomiting)
increased/unusual physical exertion
increased stress (infection, trauma, emotional upset)
Impaired counter-regulatory hormone axis (glucagon/epi/cortisol don’t kick in)
Altered regiment
Accidental exessive dose of exogenous
Variable absorption @ injection site
excessive insulin release caused by SULFONYLUREA!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypoglycemia more common in

A

Type 1 DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Management of asymptomatic hypoglycemia

A

“defensive actions”

  • repeat measurement soon
  • avoid critical tasks
  • ingest carbs
  • adjust tx regiment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of symptomatic hypoglycemia (awake)

A

15-20 g oral carbs

  • 3-5 glucose tablets/candies; 1/2 c. juice/soda
  • followed by long acting carb to prevent recurrence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Management of severe hypoglycemia w/ AMS

A

can’t swallow glucose
- SC or IM injection of 0.5-1.0 mg of glucagon (works in 15 min)

more quickly

  • 25 g of 50% glucose (dextrose) IV (“1 amp of D50)
  • followed by continues glucose infusion or food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SE of glucagon

A

N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How to know blood sugar normalizes

A

AMS normalizes
no tachy/diaphoresis
focal neuro exam normalizes (stroke-like sx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

F/u after treatment of hypoglycemia

A

monitor w/ serial blood sugars to avoid recurrence

if due to sulfonylurea- ADMIT!!!!! - likely to recur (long 1/2 life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When to admit for hypoglycemia

A

caused by sulfonyruea (worse w/ renal disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sx of ketoacidosis

A 
severe abdominal pain (TTP)
vomiting
confusion
frequent urination
tachycardia
tachypneic
hypotensive
\+/- dehydration
"fruity" breath!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

labs for ketoacidosis

A 
CBC (elevated) - infection
CMP (metabolic acidosis)
- Na: decreased
- bicarb: decreased
- BUN/Cr: increased
- Glucose: increased
EKG- sinus tachy, no ischemia
UA: + ketones, + protein
ABG: metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Anion gap equation

A

Anion gap = Na - (CL + HCO3)

  • normal < 10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of anion gap

A 
(MUDPILES)
Methanol
Uremia (renal failure)
Diabetic, alcoholic, starvation ketoacidosis
Paracetamol; propylene glycol, paregoric
Inborn erros of metabolism; iron; ibuprofen; isoniazid
Lactic acid
Ethylene glycol
Salicylates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hyperosmolar hyperglycemic state (HHS)

A

hyperosmolar nonketotic “Coma” (no ketones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

DKA and HHS both precipitated by

A

infection (UTI/pneumonia)
Trauma/surgery
MI, stroke
Insulin omission!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

DKA more common in

A

Type 1 DM (due to insulin insufficiency in the setting of a precipitant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sx of DKA

A

abdominal pain/n/v
Hyperventilation (Kussmaul- fast & deep)
Hypotension/shock/dehydration
metabolic acidosis w/ increased anion gap
Elevated glucose
elevated serum ketones
polyruria, polydipsia, weight loss

  • develops over hours/days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Presenting sign of 25% of T1 DM

A

DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Normal HCO3

A

22-26

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

normal CO2

A

35-45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diagnostic studies for DKA

A

glucose (350-500 mg/dL)
Ketones (UA & serum positive)
Potassium: high, low or normal
- usually low
- elevated @ presentation, as both insulin deficiency and hyperosmolality result in K+ movement out of cells
- K+ tends to fail w/ treatment … watch K+ closely and be prepared to supplement
Na (low) - can be falesly low (fall 2 for each 100 increase in glucose)
Cl: low in anion gap
Bicarb: low
Bun/Cr: elevated
Anion gap: elevated
Serum osmolarity: elevated (not as much as in HHS)
CBC (elevated WBC)
ABG: acidosis
UA/CXR (infection)
EKG: MI, electrolyte abnormalities, arrhythmias
Heat CT (stroke)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Monitor in DKA

A

K+ levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Goals of DKA therapy

A 
dx &amp; ABCs
restore circulatory volume
correct serum osmolarity
clear serum ketones!
correct electrolytes/anion gap
treat underlying cause
reduce blood glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tx for DKA

A

ABCs
Isotonic saline
Correct electrolytes disorders: replete K+ (monitor), follow Na, replete phosphate if severely defict
Control blood glucose
Reverse acidosis/keotgenesis: INSULIN BOLUS IV (not always givin); IV INSULIN INFUSION!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How to treat acidosis/ketogenesis

A

IV insulin infusion (maybe bolus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Fluid management in DKA

A

aggressive
15-20 mL/kg lean body weight per hour (max 50 in 4 hours; after 2-3 hours depends on hydration state)
Monitor output

Add dextrose to saline when blood glucose 200-250 (reverse ketogenesis, not attain normoglycemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Normal urine output

A

0.5-1 mL/kg/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When do you add dextrose to saline

A

glucose 200-250

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Why do you add dextrose to saline

A

reverse ketogenesis, not attain normoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why can’t bicarb be used in DKA

A

complications:

  • hypernatremia
  • hypokalemia
  • paradoxical CSF acidosis
  • residual serum alkalosis
  • slow rate of recovery of ketosis
  • can accelerate ketogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Physiology behind paradoxical CSF acidosis

A

bicarb in blood –> reduces hyperventilatory drive –> raises blood pCO2 –> reuptake of CO2 by cells –> intracellular cerebral acidosis –> paradoxical fall in cerebral pH –> neuro deterioration (cerebral edema –> brain damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When can you administer bicarb?

A

Significant hyperkalemia (pushes K+ into cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Tx of acidosis

A

fluid + insulin

presence of insulin stops lipolysis

37
Q

When to stop insulin infusion

A

until there is no anion gap and glucose normalizes

38
Q

HHS usually seen in

A

T2 DM (NIDDM)

39
Q

Cause of HHS

A

infections, MI, other stressors (older nursing home patients)

40
Q

S/sx of HHS

A 
insidious (days to weeks)
altered state of consciousness (more likely that DKA)
Weakness (generalized &amp; FOCAL)
Polydipsia/polyuria
dehydration
No kussmaul or abdominal pain
41
Q

Pathophys behind HSS

A

hyperglycemia –> glycosuria –> dehydration –> hemoconcentration (leads to worsening hyperglycemia: 500+)

42
Q

Labs for HHS

A

glucose: 500+
plasma osmolality >320 (dehydration: 5-10 L deficient)
Relative insulin deficiency - not enough to prevent hyperglycemia, but enough to prevent ketosis
NO KETONES/ACIDOSIS

43
Q

Tx for HHS

A

Fluid/electrolytes (same as DKA)
Insulin IV (if fluid is inadequate)
Treat underlying problem!

44
Q

Hyperthyroidism sx

A 
fever/palpitations
tachycardic, RR high
diarrhea
hypervigilant/agitated
prominent eyes
tremor
hyperreflexia
BS increased 
Confusion
PE: prominent, tender thyroid
45
Q

Labs for hyperthyroidism

A

TSH: low/undetectable
FT4: high
FT3: high
EKG - a. fib

46
Q

A. fib

A

irregularly irregular rhythm w/ tachycardia

47
Q

Rare/potentiall fatal complication of hyperthyroidism

A

thyroid storm – occurs in those w/ untreated or partially treated thyrotoxicosis

48
Q

Thyrotoxicosis

A

excessive amount of circulating thyroid hormone (in blood)

49
Q

Hyperthyroidism

A

inappropriate exogenous thyroid hormone (overworking)

50
Q

Dx of thyroid storm

A

severe/life-threatening sx in patient w/ biochemical evidence of hyperthyroidism

  • hyperpyrexia, CV dysfunction, AMS
  • elevated free T4/T3
  • low TSH

Critera categories: thermoregulatory dysfunction, AMS, GI dysfunction, CV dysfunction, HF, precipitant hx

51
Q

Who gets thyroid storm?

A
  • long standing untreated/undertreated hyperthyroidism (Graves, TMG, solitary toxic adenoma)
  • event (more common): thyroid or non-thyroid surgery, trauma, infection, acute iodine load, post-partum
52
Q

Thyroid storm sx

A

hyperthyroid sx PLUS:
- hypermetabolism (weightloss/diarrhea)
- excessive adrenergic response
+/- hyperpyrexia, a. fib, goiter, exopthalmos, tremor, moist-skin, shock, confusion/agitation/coma, death

53
Q

Tx of thyroid storm

A 
ICU- ABCs- SUPPORT!
cooling (antipyretic, cooling blanket)
IVF resuscitation
Electrolyte replacement
Nutritional support
Thyroid specific therapy (prevent TH release)
Tx precipitating condition
54
Q

Tx of thyroid storm vs. thyrotoxicosis

A

same but higher doses and more frequent in storm

55
Q

Meds for thyroid storm

A

Propranolol (lower HR & inhibits type 1 deiodinase reducing T3)
Thionamides - PTU/methimazole
Iodine solution (lugol’s solution or SSKI)
Glucocorticoids (hydrocortisone)
Bile acid sequestrants (cholestyramine)

56
Q

Sequence of tx for thyroid storm

A
  1. ) beta blocker (propranolol)
  2. ) thionamide
  3. ) 1 hour after thionamide – give iodine solution (prevent it being used as substrate)
57
Q

PTU MOA

A

decreases TH synthesis &

blocks conversion of T4 to T3

58
Q

Methimazole MOA

A

decreases TH synthesis

59
Q

Lower T3 levels

A

w/ PTU

60
Q

DOC for severe, but non-life-threatening hyperthyroidism

A

Methimazole

  • longer 1/2 life
  • lower risk of hepatic toxicity
  • restores euthyroidism
61
Q

Pts treated w/ PTU for outpatient

A

transition to methimazole before d/c

62
Q

hepatotoxic

A

metimazole

63
Q

Glucocorticoids MOA

A

reduce T4 to T3 conversion
promote vasomotor stability
treat adrenal insufficiency

64
Q

Cholestyramine use

A

decrease enterohepatic recycling of thyroid hormones

65
Q

Tx for those allergic to thionamides or refractory

A

thyroidectomy!

66
Q

Sx of myxedema coma

A 
cool to touch 
hx of thyroidectomy
low BP, HR, temp, RR
slowed speech
hyporeflexia
generalized muscle weakness
67
Q

Labs for hypothyroidism

A

Elevated TSH

Markedly depressed T4

68
Q

Severe form of hypothyroidism

A

myxedema coma (complication of hypothyrodiism)

69
Q

What is myxedema coma

A

severe deficiency in thyroid hormone leads

to encephalopathy

70
Q

Cause of myxedema coma

A

untreated hypothyroidism

precipitant (opiods, infection, MI, cold exposure)

71
Q

Hallmark features of myxedema coma

A

hypothermia
CNS depression/coma

other common: Hypotension, bradycardia, hyponatremia, hypoglycemia, and hypoventilation

Myxedema: puffiness of hands/face, thick nose, swollen lips, enlarged tongue (nonpitting edema)

72
Q

Most common to get myxedema

A

elderly (women)

73
Q

What causes myxedema

A

abnormal deposits of mucin in skin leading to non-pitting edema

74
Q

Pretibial myxedema

A

Grave’s disease (hyperthyroidism)

75
Q

Labs for myxedema coma

A 
CMP: hypoglycemia/hyponatremia
CT: normal unless stroke
CXR: PE/pneumo r/o
EKG: bradycardia, flat/inverted T waves
ABG: hypercarbia/hypoexmia
TSH: HIGH (primary) or low (if secondary)
FT4/3: low/undectable
76
Q

Management of myxedema coma

A 
ABCs
Thyroid hormones
Hydrocortisone - given until adrenal insufficiency is r/o
IVF
Correct electrolytes
Warming blankets
SLOW RECOVERY
77
Q

Thyroid hormone administration

A

T4 IV

T3: controversial/faster acting (can precipitate MI or arrhythmias) - start w/ low dose

78
Q

What is adrenal insufficiency

A

Potentially life-threatening condition that occurs when there is a lack of cortisol, produced by the adrenal glands

79
Q

Primary adrenal insufficiency (ADDISON’S DISEASE)

A

adrenal gland is damaged/not functioning and can’t produce glucocorticoids or mineral corticoids

80
Q

Secondary adrenal insufficiency

A

defect of pituitary gland inhibiting proper release of ACTH (may occur w/ panhypopituitarism)

81
Q

Tertiary adrenal insufficeincy

A

suppression of HPA function

82
Q

Most common cause of tertiary adrenal insufficiency

A

abrupt withdrawal of chronic administration of high doses of glucocorticoids (COPD and chronic prednisone)

mineral corticoid secretion is nearly normal – function depends mainly on renin-angiotensin rather than ACTH

83
Q

What is acute adrenal crisis?

A

acute exacerbation of chronic insufficiency, usually caused by sepsis or surgical stress (primary adrenal insufficiency)

84
Q

Causes of acute adrenal crisis

A 
Stress/sepsis
adrenal hemorrhage
adrenal infarction
anticoagulation complications
congenital abnormalities
85
Q

Presentation of acute adrenal crisis

A

n/v/d, abdominal pain
confusion, coma, fever, hyponatremic, hypoglycemic,
weight loss
PROFOUND HYPOTENSION

86
Q

Waterhouse-Friderichsen syndrome

A

adrenal infarction due to meningococcemia; think w/ fevere, AMS, purpura

87
Q

Tx for adrenal crisis

A 
ABCs
IVF
electrolytes
Hydrocortisone!!!!
Mineralcorticod (Florinef) - not as important as steroid
88
Q

When to think of adrenal cirsis

A

shock (hypotension) w/ unexplained & inadequately responsive to vasopressors & volume replacement

EMed Exam 2 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions