Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
Monitor in DKA
K+ levels
26
Goals of DKA therapy
``` dx & ABCs restore circulatory volume correct serum osmolarity clear serum ketones! correct electrolytes/anion gap treat underlying cause reduce blood glucose ```
27
Tx for DKA
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!
28
How to treat acidosis/ketogenesis
IV insulin infusion (maybe bolus)
29
Fluid management in DKA
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)
30
Normal urine output
0.5-1 mL/kg/hr
31
When do you add dextrose to saline
glucose 200-250
32
Why do you add dextrose to saline
reverse ketogenesis, not attain normoglycemia
33
Why can't bicarb be used in DKA
complications: - hypernatremia - hypokalemia - paradoxical CSF acidosis - residual serum alkalosis - slow rate of recovery of ketosis - can accelerate ketogenesis
34
Physiology behind paradoxical CSF acidosis
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)
35
When can you administer bicarb?
Significant hyperkalemia (pushes K+ into cells)
36
Tx of acidosis
fluid + insulin | presence of insulin stops lipolysis
37
When to stop insulin infusion
until there is no anion gap and glucose normalizes
38
HHS usually seen in
T2 DM (NIDDM)
39
Cause of HHS
infections, MI, other stressors (older nursing home patients)
40
S/sx of HHS
``` insidious (days to weeks) altered state of consciousness (more likely that DKA) Weakness (generalized & FOCAL) Polydipsia/polyuria dehydration No kussmaul or abdominal pain ```
41
Pathophys behind HSS
hyperglycemia --> glycosuria --> dehydration --> hemoconcentration (leads to worsening hyperglycemia: 500+)
42
Labs for HHS
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
Tx for HHS
Fluid/electrolytes (same as DKA) Insulin IV (if fluid is inadequate) Treat underlying problem!
44
Hyperthyroidism sx
``` fever/palpitations tachycardic, RR high diarrhea hypervigilant/agitated prominent eyes tremor hyperreflexia BS increased Confusion PE: prominent, tender thyroid ```
45
Labs for hyperthyroidism
TSH: low/undetectable FT4: high FT3: high EKG - a. fib
46
A. fib
irregularly irregular rhythm w/ tachycardia
47
Rare/potentiall fatal complication of hyperthyroidism
thyroid storm -- occurs in those w/ untreated or partially treated thyrotoxicosis
48
Thyrotoxicosis
excessive amount of circulating thyroid hormone (in blood)
49
Hyperthyroidism
inappropriate exogenous thyroid hormone (overworking)
50
Dx of thyroid storm
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
Who gets thyroid storm?
- 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
Thyroid storm sx
hyperthyroid sx PLUS: - hypermetabolism (weightloss/diarrhea) - excessive adrenergic response +/- hyperpyrexia, a. fib, goiter, exopthalmos, tremor, moist-skin, shock, confusion/agitation/coma, death
53
Tx of thyroid storm
``` ICU- ABCs- SUPPORT! cooling (antipyretic, cooling blanket) IVF resuscitation Electrolyte replacement Nutritional support Thyroid specific therapy (prevent TH release) Tx precipitating condition ```
54
Tx of thyroid storm vs. thyrotoxicosis
same but higher doses and more frequent in storm
55
Meds for thyroid storm
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
Sequence of tx for thyroid storm
1. ) beta blocker (propranolol) 2. ) thionamide 3. ) 1 hour after thionamide -- give iodine solution (prevent it being used as substrate)
57
PTU MOA
decreases TH synthesis & | blocks conversion of T4 to T3
58
Methimazole MOA
decreases TH synthesis
59
Lower T3 levels
w/ PTU
60
DOC for severe, but non-life-threatening hyperthyroidism
Methimazole - longer 1/2 life - lower risk of hepatic toxicity - restores euthyroidism
61
Pts treated w/ PTU for outpatient
transition to methimazole before d/c
62
hepatotoxic
metimazole
63
Glucocorticoids MOA
reduce T4 to T3 conversion promote vasomotor stability treat adrenal insufficiency
64
Cholestyramine use
decrease enterohepatic recycling of thyroid hormones
65
Tx for those allergic to thionamides or refractory
thyroidectomy!
66
Sx of myxedema coma
``` cool to touch hx of thyroidectomy low BP, HR, temp, RR slowed speech hyporeflexia generalized muscle weakness ```
67
Labs for hypothyroidism
Elevated TSH | Markedly depressed T4
68
Severe form of hypothyroidism
myxedema coma (complication of hypothyrodiism)
69
What is myxedema coma
severe deficiency in thyroid hormone leads | to encephalopathy
70
Cause of myxedema coma
untreated hypothyroidism | precipitant (opiods, infection, MI, cold exposure)
71
Hallmark features of myxedema coma
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
Most common to get myxedema
elderly (women)
73
What causes myxedema
abnormal deposits of mucin in skin leading to non-pitting edema
74
Pretibial myxedema
Grave's disease (hyperthyroidism)
75
Labs for myxedema coma
``` 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
Management of myxedema coma
``` ABCs Thyroid hormones Hydrocortisone - given until adrenal insufficiency is r/o IVF Correct electrolytes Warming blankets SLOW RECOVERY ```
77
Thyroid hormone administration
T4 IV | T3: controversial/faster acting (can precipitate MI or arrhythmias) - start w/ low dose
78
What is adrenal insufficiency
Potentially life-threatening condition that occurs when there is a lack of cortisol, produced by the adrenal glands
79
Primary adrenal insufficiency (ADDISON'S DISEASE)
adrenal gland is damaged/not functioning and can't produce glucocorticoids or mineral corticoids
80
Secondary adrenal insufficiency
defect of pituitary gland inhibiting proper release of ACTH (may occur w/ panhypopituitarism)
81
Tertiary adrenal insufficeincy
suppression of HPA function
82
Most common cause of tertiary adrenal insufficiency
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
What is acute adrenal crisis?
acute exacerbation of chronic insufficiency, usually caused by sepsis or surgical stress (primary adrenal insufficiency)
84
Causes of acute adrenal crisis
``` Stress/sepsis adrenal hemorrhage adrenal infarction anticoagulation complications congenital abnormalities ```
85
Presentation of acute adrenal crisis
n/v/d, abdominal pain confusion, coma, fever, hyponatremic, hypoglycemic, weight loss PROFOUND HYPOTENSION
86
Waterhouse-Friderichsen syndrome
adrenal infarction due to meningococcemia; think w/ fevere, AMS, purpura
87
Tx for adrenal crisis
``` ABCs IVF electrolytes Hydrocortisone!!!! Mineralcorticod (Florinef) - not as important as steroid ```
88
When to think of adrenal cirsis
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.
© 2025 Bold Learning Solutions. Terms and Conditions