Lecture 8 - Endocrine Flashcards

1
Q

DKA

A

hyperglycemia –> ketosis –> metabolic acidosis

most common acute life threatening complication of diabetes
MC in type 1 than type 2

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2
Q

What is the pathophysiology behind DKA?

A

decreased insulin –> decreased glucose utilization –> body in starvation mode
starvation –> promote gluconeogensis and glycogenolysis –> increase glucose leves
(convert adipose to free fatty acids)
fatty acids make blood highly osmotic
fatty acids oxidized to ketones –> metabolic acidosis

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3
Q

What causes DKA?

A
precipitating event, commonly: 
infection (MC) 
injury/trauma
MI, CVA, TIA 
pancreatitis 
ethanol, drug use 
gastroenteritis 
noncompliance with meds
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4
Q

What are the signs and sxs of DKA?

A
general fatigue/weakness 
abdominal pain, can include N/V
Kussmaul's respiration (deep and fast, trying to compensate for acidosis) 
fruity breath
polyuria, polydipsia, polyphagia 
AMS
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5
Q

What lab findings do you see in a pt with DKA?

A
serum glucose >250 
serum ketones 
serum bicarb <15 
arterial pH <7.3
anion gap 
BUN elevated

always be sure to check serum potassium (this needs to be corrected before you give insulin)

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6
Q

Why do you need to correct potassium before giving insulin in a pt with DKA?

A

acidosis drive K out of the cell, raising serum K+

when insulin is given, it drives K into the cells, causing HYPOkalemia –can lead to lethal arrhythmia

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7
Q

What is the treatment for DKA?

A

1) Fluids
2) Potassium
3) Insulin

ABCs
monitor glucose hourly
monitor VBG every 2 hours
determine underlying cause of DKA

Fluids - expand extracellular volume and stabilize cardiovascular status
If shock: give isotonic saline bolus
if NO shock: give IV isotonic saline 15-20ml/kg/hour

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8
Q

If a pt is not in shock but is in DKA< what is the rate of NS we give?

A

15-20ml/kg/hour

after volume restored:
five 1/2NS at 4-14ml/kg/h

when serum glucose reaches approx 200, add dextrose

potassium replacement:
<3.3: HOLD insulin, KCL 20-40 mEq/h
>3.4 - <5.3: start IV and PO KCL at 20-30 mEq/L
>5.3: no K, monitor K every 2 hours

insulin:
Bolus 0.1 units/kg IV then start continuous IV infusion fo 0.1units/kg/hr

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9
Q

HHS

A

hyperglycemic hyperosmolar non-ketone syndrome

dehydration! you have enough glucose

unlike DKA, HHS have sufficient insulin to prevent lipolysis and ketogenesis
HHS results from gradual diuresis causing significant dehydration, leading to electrolyte deficiencies and ultimately mental status changes
HHS caused by physiological stressors like DKA (infections, MIs, CVA, trauma, decreased PO intake or medications)

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10
Q

Who gets HHS?

A

> 65, chronic care facility, dementia
change in DM medications, new medications (especially steroids)
infection hx

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11
Q

What are the signs and sxs of HHS?

A

polydipsia, polyphagia, polyuria
generalized weakness
AMS
dry mucus membrane

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12
Q

What labs do you expect see for someone in HHS?

A

fluid deficit (9L vs 3–5L in DKA)

serum glucose >600 mg/dl

glycosuria is prominent
serum osmolality is 320-380 mOsm/kg
serum bicarb usually >15mEg/L, pH is usually >7.3, usually no anion gap

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13
Q

What is the treatment for HHS?

A

1) Fluids
2) Potassium
3) Insulin

FLUIDS
usually 1-1.5 L of NS over the first hour, then
correct 1/2 fluid deficit in first 8 hours and then the other 1/2 over the next 24 hours
if sodium is high: use 1/2NS at rate of 250mml/h after initial bolus
if sodium is normal or low: continue NS
once serum glucose reaches 250mg/dl 5% dextrose in 1/2NS at rate 250ml/h if sodium is high, if normal sodium or low sodium 5% NS

potassium (same as DKA, basically correct potassium before insulin)

insulin IV only
goal: decrease glucose by 50-70mg/dl/hr

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14
Q

Hypoglycemia

A

serum glucose less than 50mg/dL

severe hypoglycemia is <30mg/dl

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15
Q

What are the most common causes of hypoglycemia?

A

exogenous insulin

others:
pancreatic B cell tumor
EtOH

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16
Q

What are the signs and symptoms of hypoglycemia?

A
initially: increased catecholamine release: tachycardia, irritable, diaphoresis, paresthesia's, hunger, and decreased concentration 
AMS 
visual disturbances 
hallucinations 
seizures
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17
Q

What is the treatment for hypoglycemia?

A

give 50cc of 50% dextrose (amp of D50)

remember to give thiamine 100mg IV /IM in alcoholics to prevent Wernicke’s encephalopathy

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18
Q

What is the most common cause of hyperthyroidism?

A

grave’s disease
autoimmune disorder resulting from thyroid stimulating hormone receptor antibodies that stimulate thyroid gland growth and thyroid hormone synthesis and release

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19
Q

What are the signs and sxs of hyperthyroidism?

A

“high/fast”

changes in vision, dry eyes, increased neck size, palpitations, heat intolerance, tremor, moist skin, weight loss, diarrhea, fatigue, anxiety

tachycardia
HTN
anxious/agitated 
tremor 
ophthalmopathy 
pretibial myxedema 
lid lag 
diffuse goiter 
thyroid nodule 
brisk reflexes
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20
Q

How do you dx hyperthryoidism?

A

suppressed serum TSH

elevated T3/T4

21
Q

What is the treatment for hyperthyroidism?

A

supportive
beta blockers (atenolol 25-50mg) for symptom control
long term treatment: antithyroid drugs (thionamides), radioiodine, or surgery
MC thionamides: MMI or PTU

22
Q

Thyroid storm

A
hx of hyperthyroidism 
often thyrotoxic sxs over many months prior 
AMS 
recent thyroid surgery/treatment 
D/c MMI or PTU 

precipitating factors:
infection, trauma, MI, radioiodine, pregnancy

23
Q

What are the signs and sxs of thyroid storms?

A
tachycardia (SVT) 
tachypnea
systolic HTN 
hypotension from cardiac collapse 
FEVER (can be greater than 104, don't let this throw you off your track of endocrine etiology) 
hyperthermia 
AMS 
N?V?D 
dehydration
24
Q

How do you dx thyroid storm?

A
TSH low 
T4 elevated 
hyperglycemia 
leukocytosis 
abnormal LFTs
25
Q

What is the treatment for thyroid storm?

A

FLUIDS @ least 1 L NS in 1 hour
vasopressors if hypotensive (After fluids)
consider phenobarbital for sedation
treat fever aggressively with cool IV fluids, cooling blankets
AVOID: iodine contrast, amiodarone, NSAIDs, aspirin, ketamine

BB (block peripheral effects of excess thyroid hormone)
1st line: PTU 600-1000mg first dose then 200-250mg q4h

steroids: reduce T4 to T3 conversion, promote vasomotor stability (hydrocortisone 100mg IV q8)

admit to ICU

26
Q

Hypothyroidism signs and sxs

A
fatigue 
weakness
dry skin 
coarse hair 
cold intolerance 
weight gain 
constipation 
"Brain fog" 
depression 
thyroidectomy
abnormal menstrual cycles 

bradycardia
puffy, dry skin
delayed reflexes

27
Q

How is hypothyroidism dx?

A

elevated TSH
depressed free T4
positive TPO antibiotics

28
Q

What is the treatment for hypothyroidism?

A

L-thyroxine or levothyroxine

may not need to treat, but need to refer

29
Q

Myxedema coma

A

rare complication of extreme hypothyroidism with multi-organ failure, AMS, and hypothermia
most often seen in previously untreated/inadequately treated elderly pts
hx of thyroid disease, surgery, or treatment should make you suspicious especially in an unresponsive elderly pt
-look for thyroid surgery scar

hypothermia 
precipitating even: 
infections, PNA
MI, CHF
CVA
30
Q

What are the signs and sxs of myxedema coma?

A

hypothermic
bradycardic
hypotensive
cardiomegaly

generalized puffiness, periorbital edema
anorexia
contipation

31
Q

Myxedema wit

A

inappropriate humor seen in myxedema coma pts

32
Q

How is myxedema coma dx?

A
elevated TSH 
low T4,T3
hyponatremia 
hyoglycemia
increased urine Na
increase CR
increased LDH
EKG changes 
-bradycardia
-non-specific ST changes or T wave inversion 
-low voltage
-long QT interval
33
Q

What is the treatment for myxedema coma?

A
ICU (mortality 30-40%) 
ventilator support 
fluid replacement (treat hyponatremia with 3%NS) 
glucose
sodium replacement
heating 
IV T4 with loading dose of 200 to 500 mcg over 1 hour, then 50-100 mcg/d
T3 loading dose 

broad spectrum ABX for underlying infection
steroids (100mgc/8hr)

34
Q

Addison’s disease

A
fatigue, weakness 
anorexia, weight loos 
irritability, 
myalgias, arthralgias 
amenorrhea
sensory hypersensitivity 
salt craving 

orthostatic hypotension
delayed reflexes
hyperpigmentation

35
Q

How is addison’s disease dx?

A

hard to dx in ER – will most likely be in crisis in ER
hyperkalemia
hyponatremia
hypoglycemia
hypercalcemia
low BUN
low 8am cortisol accompanied by high plasma ACTH

36
Q

What is the treatment for addison’s disease?

A

oral hydrocortisone or prednisone

fludrocortisone if primary disease only

37
Q

Addisonian crisis

A

hx of adrenal insufficiency complicated by infection, trauma, stress, amyloidosis, scleroderma, tumor
often in times of stress
-pts require a stress dose of cortisol

38
Q

What are the signs and sxs of addisonian crisis?

A

shock refractory to fluids and vasopressors

abdominal and/or back pain 
V/D
fatigue, weakness
shock
hypotension
dehydration
AMS
39
Q

How is addisonian crisis dx?

A
hyponatremia and hyperkalemia 
elevated ACTH (primary) 
low serum cortisol 
increased Cr 
hypoglycemia 

test of choice: ACTH stimulation test

abdominal CT to see adrenals

40
Q

What is the treatment for addisonian crisis?

A

IV hydration
hydrocortisone 100mg IV q8h
treat underlying cause

(dexamthasone for never dx pts to prevent effecting the dx exams)

41
Q

What causes catecholamine crisis?

A

pheochromocytoma
MAOIs
intoxication with cocaine

unopposed high circulating levels of catecholamines acting at adrenoreceptors

  • epi and norepi (crap ton of adrenaline)
  • alpha receptors: pressor response, increase in BP
  • beta receptors: cardiac contractions; increased HR
42
Q

Chromaffin cells

A

in the adrenal medulla

location where catecholamine secreting tumors arise

43
Q

What is the classic triad of sxs for pheochromocytoma?

A

episodic HA
sweating
tachycardia

others:
feeling of impending death
palpitations
young person with poorly controlled HTN

44
Q

How is catecholamine crisis dx?

A

24 hour urine collection for free catecholamines and metanephrines
screen with plasma metanephrines
CT or MRI to find tumor

45
Q

What is the treatment for catecholamine crisis?

A

supportive measures: IV, O2, correct electrolyte abnormalities
IV phentolamine (initial 1mg IV every 5 minutes, if no improvement then up dose to 5mg every 5 mins)
OR CCB IV
IV fenoldopam
benzos

46
Q

Diabetes insipidus

A

caused by deficiency (central) or resistance (nephrogenic) to vasopressin (antidiuretic hormone)

Central DI (aka neurogenic) 
-problem with secretion from the pituitary 

Nephrogenic DI

  • normal secretion of ADH but renal resistance to its water-retaining effects
  • often congenital
47
Q

How do pts with DI present?

A

intense thirst, polydipsia, ice craving
large volume polyuria
unremitting enuresis
hypernatremia and dehydration

dry skin
dehydration sxs

48
Q

How is DI dx?

A

serum sodium (high) and urine osmolality (low)

how to tell central vs nephrogenic:
give 1mcg DDAVP (exogenous vasopressin)
if urine osmolality increases and volume decreases its central

49
Q

What is the treatment for DI?

A

hydration with IV fluids

don’t replace too face – can cause cerebral edema

sodium restriction

desmopressin acetate nasal spray