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ENDOCRINE Flashcards

1
Q

Normal range of serum osmolality:

A

275-295 mOs/L

mOs/L = number of osmoles of solute per liter of solution

“If osmos’s high, you’re likely dry.”

If it’s low, maybe blood is diluted.

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2
Q

Two ways to calculate serum osmolality:

A
  1. (2 x Na+) + BG/18 + BUN/2.8

or, if the BG is normal:
2. 2(Na+) This is a ballpark method, not super accurate.

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3
Q

Types of IV fluids and their affects:

  1. Isotonic
  2. Hypotonic
  3. Hypertonic
  4. Colloids
A
  1. Isotonic: Tend to stay in the intravascular space (unless there’s another dz-state causing capillary leakage).
  2. Hypotonic: Will go out to the cells for cellular hydration
  3. Hypertonic: Pulls fluid from the tissues/cells into the vasculature.

4.

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4
Q

What are the osmolalities of the following isotonic IVFs?

  1. NS
  2. LR
  3. Plasmalyte-a
A
  1. 308 Some evidence is showing that prolonged NS infusion (chloride) can lead to AKI
  2. 273
  3. 312

Plasmalyte is more expensive

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5
Q

Osmolalities of the following hypertonic solutions:

  1. D5 0.2 NS
  2. D5 1/2 NS
  3. D5LR
  4. Dextrose 10%
  5. 2% Saline
  6. 3% Saline
  7. 5% Saline
  8. 23.4% Saline
A
  1. D5 0.2 NS = 321
  2. D5 1/2 NS = 406
  3. D5LR = 525
  4. Dextrose 10% = 505
  5. 2% Saline = ?
  6. 3% Saline = 1030
  7. 5% Saline = 1710
  8. 23.4% Saline = ?
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6
Q

How is diabetes mellitus diagnosed?

A

DM = metabolic syndrome w/fasting BG greater or equal to 126 mg/dL (done twice) or fasting >126 AND A1C > or = to 6.5%

DM is either defect in insulin secretion, action of insulin or both.

Should not dx on A1C alone.

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7
Q

4 categories of diabetes:

A
  1. Type 1: Autoimmune response resulting in Beta cell destruction = absolute insulin deficiency
  2. Type 2: Insulin secretory defect. RESISTANCE resulting in RELATIVE insulin deficiency
  3. “Other”: d/t other causes; genetic/medication/?
  4. Gestation DM from pregnancy.
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8
Q

Is D5W isotonic or hypotonic?

A

It’s isotonic in the bag but hypotonic once administered because the body quickly metabolizes the glucose.

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9
Q

Beta Blockers and hypoglycemia. What is the connection?

A

Beta blockers can block the symptoms of hypoglycemia (increased HR, tremors) bc they block the effects of norepinephrine and sympathetic nervous system

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10
Q

What are beta blockers primarily prescribed for?

A

Angina, HTN

CHF, CAD, MI

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11
Q

How do beta blockers work?

A

Blocking the release of the catecholimine hormones epinephrine [adrenaline] and norepinephrine lowers stress on the heart and reduces the force of the contractions of the heart muscle. In turn, it also takes pressure off the blood vessels in the heart, the brain, and the rest of the body.

Beta-blockers also obstruct the production of angiotensin II, which is a hormone that the kidneys produce. This relaxes and widens the blood vessels, easing the flow of blood through them.

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12
Q

Which catecholimine has more an effect on your heart: epinephrine or norepinephrine?

A

Epinephrine affects the heart more
Norepi has more of an affect on your vessels.

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13
Q

Why is metabolic syndrome significant? What does it put ppl at a higher risk for?

A

Cardiovascular dz and stroke.

It’s estimated that 25% of American population have metabolic syndrome. This increases to 40% over the age of 60!

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14
Q

How are African American’s different in r/t other populations in relation to sugar?

A

They have a greater glycation; higher A1C.

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15
Q

What are the “Deadly Quartet?”
r/t metabolic syndrome

A

If you have 2 of the 4 = metabolic syndrome:

  1. Dyslipidemia
    • Triglycerides > 150 mg/dL
    • HDL < 40 (males), 50 (females)
  2. HTN
    • SBP > 130 or DBP > 85
  3. Hyperglycemia
    • Fasting BG > 100, or dx DM2
  4. Abdominal obesity
    • Waistline > 40 in men, > 35 in women
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16
Q

What do the pancreatic Alpha cells produce?

A

Glucagon.

Glucagon is a hormone that works with other hormones and bodily functions to control glucose levels in the blood.

They are released during hypoglycemia. They stimulate gluconeogenesis and glycogenolysis in the liver and release of glucose to plasma. Raising glucose levels.

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17
Q

What do the pancreatic Beta cells produce?

A

Insulin.

Big transporter… Drives glucose, water, potassium into the cells.

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18
Q

What do the pancreatic Delta cells produce?

A

Somatostatin.

This inhibits the release of glucagon and insulin.

Somatostatin produces predominantly neuroendocrine inhibitory effects across multiple systems. It is known to inhibit GI, endocrine, exocrine, pancreatic, and pituitary secretions, as well as modify neurotransmission and memory formation in the CNS.

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19
Q

Time of onset of action for Humalog (Lispro)?

A

5-15 min. Rapid-acting.

Peak 1-3 hours

Effects last 4-6 hours

Other rapid acting: Novolog, Apidra

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20
Q

Time of onset of action for Regular insulin (Humulin R)?

A

30 minute onset. Short-acting.

Peak 1-3 hours

Effects last 6-8 hours

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21
Q

Time of onset for NPH?

A

Onset 1.5-4 hours. Intermediate-acting.

Peak 4-12 hours

Duration up to 24 hours

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22
Q

Time of onset for Lantus?

A

Onset 0.8-4 hours

Peak is minimal

Duration is up to 24 hours

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23
Q

What # is considered hypoglycemic?

A

< 70 mg/dL

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24
Q

Why are the following causes of hypoglycemia?

Nausea/Vomiting
Strenuous exercise/Stress
Excessive ETOH
Adrenal insufficiency
Severe liver disease

A

N/V - not consuming food/sugar

Strenuous exercise/Stress from increased metabolic needs

ETOH causes an increase in insulin secretion 2/2 to nitric oxide and vagus causing redistribution of blood flow from exocrine to endocrine. (Also chronic alcoholics have difficulty converting glycogen to glucagon, and their pancreatic alpha cells may not be producing well)

Adrenal insufficiency bc depleted cortisol increases insulin sensitivity.

Liver dz bc this is where glycogen is stored - the polysaccharide of sugar - the main form for storage.

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25
Q

What are the following symptoms r/t?

Palpitations
Tachycardia
Diaphoresis
Pallor
Cool skin
Piloerection
Irritability

A

Hypoglycemia

Cardiovascular signs may be noticed first bc of the stimulation of the sympathetic nervous system (palpitations/gitteriness)

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26
Q

Concerns when glucose is < 50 mg/dL?

A

Seizures

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27
Q

Concerns when glucose is < 20 mg/dL?

A

Coma

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28
Q

What are the following neurologic symptoms r/t?
- blurred vision
- slurred speech
- weakness
- HA
- Diplopia
- Anxiety
- Tremors
- Staggering gate

A

Hypoglycemia

also:
difficulty concentrating, confusion, and/or fatigue

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29
Q

Hypoglycemia treatment if conscious?

A
  • 4 oz of juice
  • 10-15 grams of carbs
  • Glucose tablets/gel
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30
Q

Hypoglycemia treatment if unconscious with an IV?

A
  • 0.5 to 1 amp of D50
  • Consider 5 - 10% DW infusion
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31
Q

Hypoglycemia treatment if unconscious w/out IV access?

A

Glucagon 0.5 - 1 mg IM

Then provide longer acting carbohydrate once stabilized.

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32
Q

With ANY neuro change, what test should you get?

A

Glucose

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33
Q

An 18 yof w/DM1 comes in w/540 BG and K of 6.5, what’s priority tx?

  1. Correcting BG
  2. Lowering K
  3. Correcting her fluid deficit
  4. Restarting home SQ insulin
A
  1. Correcting her fluid deficit.

Provider should use algorithm to calculate their deficit (most have at least a 5L+ deficit)

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34
Q

Where do the ketones come from in DKA?

A

Body not able to utilize the glucose = breakdown of fatty acids which lead to metabolic waste of ketones

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35
Q

What are the 3 P’s for DKA??

A
  1. Polyuria - early; oliguria is late
  2. Polydipsia - excessive thirst r/t polyuria
  3. Polyphagia - excessive hunger r/t the cells starving
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36
Q

What do we call the deep DKA breathing?

A

Kussmaul.

Acetone/Fruity.

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37
Q

When do we want to replace phosphate? (In DKA pt)

A

When it’s below 1.

Replacement has little impact on the outcome of DKA.

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38
Q

In DKA, it is not recommended to replace this unless the patient’s pH is < 6.9

A

Bicarb

Lots of trans-cellular shifting as fluid resuscitation is going on.

Stomach, pancreas and kidneys produce bicarbonate. Lungs and kidneys regulate acid base balance by removing excess acid.

American Diabetes Association recommends 100 mmol sodium bicarbonate in 400 mL sterile water with 20 mEq of KCl until it’s above 7.00

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39
Q

What does MUD PILES stand for?

A

Causes of metabolic acidosis:

M- methanol (methanol is metabolized by alcohol dehydrogenase in the liver to formic acid = acidosis)

U- uremia (in end-stage renal failure in which glomerular filtration rate falls below 10-20 mL/min, acids from protein metabolism are not excreted and accumulate in blood).

D- DKA (incomplete oxidation of fatty acids causes a build up of beta-hydroxybutyric and acetoactic acids [ketoacids]).

P- propylene glycol / Paraldehyde

I- isoniazid (abx for TB) or Ischemia (bowel ischemia, trauma, inflammatory issues, etc.) or Iron (low iron = hypoperfusion = ischemia)

L- lactic acidosis (Lactic acid is mainly produced in muscles and RBCs, caused by hypoxia/ ischemia/ hypotension/ sepsis. The end product of anaerobic glycolysis, isn’t oxidized to CO2 & H2O via the Tricarboylic Acid Cycle).

E- ethylene glycol (From antifreeze. Ethylene is metabolized by alcohol dehydrogenase to oxalic acid in the liver. usu there’s a coexisting lactic acidosis)

S- salicylates (ASA, aspirin)

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40
Q

Normal anion gap?

A

< 11

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41
Q

What IS an anion gap?

A

The anion gap measures the difference—or gap—between the negatively charged and positively charged electrolytes in your blood. If the anion gap is too high, your blood is more acidic than normal. If the anion gap is too low, your blood isn’t acidic enough.

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42
Q

What type of fluids should be given to DKA and when?

A

First NS/ LR/ Plasmalyte
- ( 1-3 L the first hour, 1 L 2nd hr, 1 L following 2 hrs )
When BG <250 then something with dextrose.
Then hypotonic for cellular hydration (250-500 mL/hr)

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43
Q

If your facility doesn’t have DKA algorithm, then you want to infuse insulin at 0.1 units/ kg/ hr

A

Don’t drop BG more than 50-100 mg/dL an hr.

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44
Q

How many hours should you overlap from insulin infusion to SQ?

A

There should be a 2 hour overlap time. Super important.
Otherwise they can go back into DKA.

45
Q

What is the relationship (inverse/direct) between pH and potassium?

A

Inverse relationship.

For every 0.1 drop in pH = 0.6 increase in serum K+

Ex:
pH 7.1 —> K+ 5.8
pH 7.0 —> K+ 6.4
pH 6.9 —> K+ 7.0

46
Q

Can DM1 develop HHS (Hyperosmolar Hyperglycemic Syndrome)?

A

Yes, not as common. Usually DM2 develop this HHS.

47
Q

What is the biggest difference between HHS and DKA?

A

No ketones.

This is bc they have enough endogenous insulin to prevent fat-burning (that causes byproduct of ketones)

48
Q

HHS glucose levels can be crazy high (> 600 to in the thousands)

A

Received a text showing someone w/BG of 3200!

Takes days to weeks to develop.

Massive osmotic diuresis, osmo’s in the 300’s. With significant polyuria.

49
Q

Cardinal sign of HHS =

A

Markedly elevated BG and altered mental status.

altered mental status R/T extreme dehydration
They can be > 10 L negative

50
Q

HHS labs. What will they look like… high or low?

pH

Na

K+

Mg

Phosphate

Hgb/Hct

Urine glucose

A

pH: normal to mild acidosis

Na: High r/t extreme dehydration

K+: Low (if you have to start insulin = need replacement!)

Mg: K and Mg go together, so this will also be Low

Phos: Low

Hgb/Hct: High r/t extreme dehydration (blood concentrated)

Urine glucose: High. Spill = sticky!

51
Q

Who has higher mortality rate, HHS or DKA?

A

HHS.

DKA 1%
HHS 5-10%

probably bc they have other co-morbidities, whereas DKA may only have DM1 as their only ailment.

52
Q

What is ADH’s purpose?

Where is it synthesized?

A

Anti-Diuretic Hormone… Causes the kidneys to release LESS water, decreasing urine production (a LOW level of ADH = more urine production).

Forms in the hypothalamus, released from posterior pituitary, and has vasopressor qualities (tighten blood vessels and increase BP).

53
Q

What is SIADH?

A

Syndrome of Inappropriate Anti-Diuretic Hormone.

“Swimming In ADH” = too much ADH… leads to water intoxication and often diluting Na.

54
Q

What labs represent signs of SIADH?
What will you expect to see in:
Na
Serum osmolality
Urine osmolality
Urine output

A
  • Severe dilutional hyponatremia: < 120-130 mEq/L.
  • Decreased serum osmolality: < 280 Osm/L (d/t dilution)
  • Urine osmolality increases: > 100 Osm/L (concentrated)
  • Decreased urine output
55
Q

Causes of SIADH?

A
  1. Infection
  2. Any pulmonary cause - pna, COPD, PE
  3. CNS insults - CVA, ICH, head trauma
  4. Variety of carcinomas/tumors (vasopressin is being produced outside the hypothalamus/pituitary; over stimulation of pituitary, etc.)
  5. Recent surgery (stress)

Most common causes are the pulm and neuro insults.

56
Q

Another name for ADH?

A

Vasopressin.

57
Q

Complications of SIADH?

(Think about the sodium issue)

A

Since they are in the setting of severe dilution hyponatremia this will lead to CEREBRAL EDEMA.

Possible seizure activity. Falls.

58
Q

Treatment of SIADH?

A
  1. Fluid restriction.

Remedy the problem…
- hypertonic saline: 2-3%
- assess for fluid overload: diuretic (loop, like lasix)
- sodium correction: SLOW
Do not exceed plasma Na of 130 mEq/L w/ replacement

59
Q

What can happen if you raise serum sodium levels up too quickly?

A

De-mylenation syndrome. Permanent nerve damage.

“High to low, the brain will blow.
Low to high, the brain will die.”

60
Q

What is the sodium replacement maximum rate per hour and per day?

A

Per hour: Do not exceed 0.5 mEq/L per hour

Per day: Do not exceed raising 12 mEq/L per DAY
8-12 mEq/L per day is a normal rate.

61
Q

Diabetes Insipidus (DI)
What kind of patients are at risk for this?

A

Neurogenic patients are majority
- TBI

  • Hypoxic-Ischemic encephalopathy (such as after a code)
  • Meningitis
  • Brain death
  • Dilantin (Phenytoin - antiepileptic)
  • Tumors
  • Can also see nephrogenic causes: d/t impaired renal tube unable to respond to vasopressin.
62
Q

What do you expect to see in the labs of a person with DI?
1. Urine specific gravity

  1. Urine osmolality
  2. Serum osmolality
  3. Serum Na
  4. BUN
  5. Serum ADH
A
  • Polyuria
    1. Urine specific gravity < 1.005 (dilute)
    2. Urine osmolality < 200 mOsm/L (dilute, 50-200)
    3. Serum osmolality elevated, > 295 mmol/L
    4. Serum Na elevated, > 145 mEq/L (d/t H20 loss)
    5. BUN elevated, d/t dehydration (cardiovascularly)
    6. Low serum ADH levels
  • Extreme Polydipsia
63
Q

What is the range for a normal urine specific gravity?

A

1.005 to 1.030

Easy to remember “Ten Ten” 1.010 as a ball park method

64
Q

What mnemonic helps remembering what Diabetes Insipidus is about?

A

“Sip and piss” from In SIP idus

Polyuria and polydipsia

65
Q

How is DI treated?

A

TREAT THE CAUSE

  1. Given ADH! via IV, IM, SQ or intranasal
  2. Desmopressin (DDAVP) is first line. Vasopressin is also an option but has vascular constriction effects.
    • Desmopressin: FYI dosages
      – IV/SQ: 2-4 mcg/day
      – PO: 0.05 mg Q 12hr
      – Intranasal: 10-40 mcg/day
  3. Fluid replacement
    • Calculate and replace the free water deficit
    • Correct slowly over 2-3 days. This will limit the risk of
      cerebral edema from occurring.
66
Q
  1. What is a messenger system comprising feedback loops of the hormones released by internal glands of an organism directly into the circulatory system, regulating distant target organs? 2. What is the neural “control center?”
A
  1. Endocrine system. The endocrine system is a complex network of glands and organs. It uses hormones to control and coordinate your body’s metabolism, energy level, reproduction, growth and development, and response to injury, stress, and mood.
  2. Hypothalamus is the main control center. The region of the forebrain below the thalamus which coordinates both the autonomic nervous system and the activity of the pituitary, controlling body temperature, thirst, hunger, and other homeostatic systems, and involved in sleep and emotional activity.
67
Q

Which butterfly-shaped gland is located at the base of the front of your neck, just below your Adam’s apple?

A

THYROID. Negative feedback loop.

Hormones produced by the thyroid gland — triiodothyronine (T3) and thyroxine (T4) — have an enormous impact on your health, affecting all aspects of your metabolism.

68
Q

What does the ANTERIOR PITUITARY do if the T3 and T4 levels are low?

A

Increases TSH production.

Thyroid stimulating hormone. To stimulate it to make more T3 and T4. The opposite happens when the T3/T4 levels are high. Genius.

69
Q

Thyroid storms are scary. Why? What is another known name of this?

A

They get REALLY sick.

Aka Thyrotoxic crisis. Result in HYPERthyroidism. Body goes into “overdrive.”

Rapid HR
HIGH BP
Fever

70
Q

What “control center” and pea-sized endocrine gland are KEY in maintaining thyroid balance?

A

Hypothalamus and pituitary gland.

Hypothalamus detects low levels of thyroid hormones (T3/4) and lets the anterior pituitary gland know that it needs to make more stimulant to get the thyroid back on track.

71
Q
  1. What labs are assessed to determine thyroid function?
  2. Which one is the most RELIABLE diagnostic tool?
A
  1. T3, T4, and TSH
  2. TSH

T3/4 are mostly bound to plasma proteins! (>99%)

< 1% are in free form and active!

72
Q
  1. Normal TSH level?
  2. At what time of the day are the levels highest?
  3. Lowest?
A

1) 0.3 - 4.5 mU/dL

2) At bedtime

3) Late afternoon

73
Q

What 2 clinical settings can depress the anterior pituitary from producing enough TSH?

A
  1. Sepsis
  2. Steroid therapy
74
Q

When will TSH and T4 have an INVERSE relationship?

A

During PRIMARY thyroid disorders.

TSH and T4 will be opposite.

75
Q

When will TSH and T4 have a one to one relationship?

A

In SECONDARY thyroid disorders.

TSH and T4 will trend in the same direction.

76
Q
  1. Which hormone is the MAIN secreted by thyroid, T3 or T4?
  2. What is the normal Free range of this hormone?
A
  1. T4.
  2. Normal T4: 0.8 - 1.8 ng/dL

T4 is measured more frequently d/t the availability of the test.

77
Q

In which condition are these 3 symptoms commonly seen in? Tachycardia, palpitations, heat intolerance

A

Hyperthyroidism

78
Q

Which condition of hyperthyroidism is d/t the overproduction of thyroxine hormone?

A

Thyrotoxicosis.

T3/4 are elevated.
TSH decreased… opposite = primary disorder

  • Increased metabolism
  • Worst form is thyroid storm.
79
Q

Causes of hyperthyroidism?

A
  1. Grave’s dz:
    • Autoimmune
    • B-Cells produce antibodies against thyroid proteins
    • Imitate TSH
  2. Toxic nodular goiter
  3. Hyper-functioning Thyroid Adenoma
    • Benign tumor makes excess thyroid hormone
80
Q

What do the following symptoms make you think may be happening?
- Agitation
- Heat intolerance / diaphoresis
- Tachycardia / Afib / palpitations
- Weight loss
- Anxiety/ Insomnia

A

Hyperthyroidism.

  • Hyperexia/ Fever - thyroid storm
  • Whites of eyes are more pronounced from the sympathetic overstimulation of muscles around the eyes, & that control eye movement.

Chronic states of hyperthyroidism:
- High CO heart failure
- Osteoporosis

Its a sudden release of thyroid hormones that cause the body to go into severe hypermetabolism

81
Q

First line therapy for hyperthyroidism?

A

First line: BETA BLOCKER is key. Most common is Propranolol - Blocks conversion of T4 to T3

Radio Iodine therapy - Blocks secretion of T4 by partially or completely halting thyroid function

Methimazole - Blocks T4 synthesis
of

82
Q

What medication is preferred over PTU for thyrotoxicosis?

A

Methimazole

(PTU is Propylthiouracil)

83
Q

Which medication is preferred (the “go-to” med) for use during a thyroid storm?

A

PTU: Propylthiouracil

Blocks the synthesis of T4 and conversion of T4 to T3

84
Q

Which medication is used for adrenal insufficiency in a thyroid storm?

A

Hydrocortisone.

85
Q

Surgical treatment for severe cases of hyperthyroidism?

A

Thyroidectomy.

86
Q

Clinical signs of hyperthyroidism:

A

Tachycardia
Palpitations
Diaphoresis
SOB
Chest Pain
HTN with wide pulse pressure (high systolic, low diastolic)

Trembling
Confusion
Diarrhea
Hyperexia temp > 100 - 106

87
Q

What are “The 5 B’s” of Thyroid Storm?

A
  1. Block synthesis: anti-thyroid Rx (PTU and methimazole)
  2. Block release: Iodine
  3. Block T4 to T3 conversion: (a) High dose PTU (b) propranolol (c) corticosteroid (d) amiodarone - rarely used
  4. Beta Blocker: to treat immediate symptoms
  5. Block enterohepatic circulation
88
Q

Causes of hypothyroidism?

A
  1. Hashimoto’s thyroiditis
    – autoimmune inflammation of thyroid
  2. Treatment of hyperthyroidism
  3. Thyroidectomy
  4. Amiodarone long term (has iodine in it)
  5. Lithium - inhibits thyroidal iodine uptake
  6. Secondary causes - pituitary gland tumor
89
Q

What do the following symptoms make you think of?

Fatigue - mental fog, depression
Weight gain
Cold intolerance
Constipation (big one)
Fluid retention:
- Edema
- Ascites
- Pleural/pericardial effusions
Hair loss, dry skin
Decreased libido
Goiter and atrophy of thyroid

A

1 cause of goiter - low iodine

Hypothyroidism

90
Q

Anti-Arrhythmic FDA approved for life-threatening V arrhythmias that is also used off-label for SVTs (ex: afib RVR). Also prescribed preventatively for those high risk for V tachy arrhythmias.

A

Amiodarone

91
Q

What do you expect to see on TSH and T4/T3 levels in hypothyroidism?

A

HIGH TSH
low T3/T4

92
Q

When would you see low TSH AND low T3/T4?

A

Pituitary gland tumor

93
Q

How to treat hypothyroidism?

A

PO Levothyroxine (Synthroid): synthetic T4 that metabolizes to T3.

94
Q

What is the name of the condition of adrenal insufficiency (adrenal glands don’t produce enough cortisol hormone (and sometimes aldosterone)?

A

Addisons’s Disease aka hypocortisolism

A decrease in the “3 S’s”: sugar, salt, sex

95
Q

What does the medulla (inner layer) of the adrenal gland secrete?

A

Catecholamines (epi and norepi)

96
Q

What does the cortex (outer layer) of the adrenal gland secrete?

A

Aldosterone - controls salt
Cortisol - controls sugar
Sex steroids - secondary sex characteristics (breasts, voice pitch, facial hair, etc)

97
Q

This hormone controls potassium secretion, and controls sodium/water retention - maintaining BP.

A

Aldosterone

It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon

98
Q

This hormone’s main function is to stimulate gluconeogenesis (BG), as well as Lypolysis, depresses immune response, and decrease inflammation.

A

Cortisol

Lypolysis: fat metabolism

99
Q

What are the “3 S’s” that are decreased in Addison’s Disease?

A
  1. Sugar (cortisol)
  2. Salt (aldosterone)
  3. Sex steroids
100
Q

What are the following symptoms related to?

Fatigue
Weight Loss
Muscle weakness
Abdominal pain
Diarrhea
Hypoglycemia (d/t low cortisol)
Hyperpigmentation
Hypotension (d/t low aldosterone)
Orthostatic hypotension
Salt craving (d/t low aldosterone)

A

Addison’s Disease

Also alopecia
The ONLY thing that will be elevated will be K

101
Q

What labs will you see in Addison’s Disease?

Cortisol
BG

ACTH
Heme

A

Diagnostics:

Cortisol < 3 mg/dL (starting level will be usu less than 3)
– then you perform cortisol stimulation test
– results < 19 mg/dL

BG low

ACTH levels: elevated

Heme: anemia

102
Q

Treatment for Addison’s Dz?

For low aldosterone:

A

Cortisol replacement: Prednisone

Aldosterone: Fludrocortisone 0.05 - 0.1 mg/day
(causes sodium and water retention)

103
Q

What is Adrenal Crisis?

What is the treatment?

A

A sudden severe adrenal insufficiency.
“In ADDison’s you have to ADD”

  1. Adding IV glucocorticoids
  2. Adding IVF Dextrose
104
Q

What is the opposite of Addison’s Disease?

A

Cushing’s Disease. An INCREASE in the 3 S’s.

105
Q

What will you see in cortisol levels in Cushing’s?

How is it diagnosed?

A

Elevated. Amplification of catecholamines.

Diagnosis is a little tricky:
1. Measure 24 hour urine - for free cortisol
2. Dexamethasone suppression test

106
Q

Causes of Cushing’s Dz?

A
  1. Exogenous:
    – Medications such as long term steroid use
  2. Endogenous:
    – Pituitary adenoma (benign) or carcinoma
107
Q

Cushing’s treatment:

A

Control the cause… taper off meds, etc.

Remove tumor.

108
Q

What are the following symptoms of?

High (too much) steroids
High BP
Hypernatremia
Hyperglycemia
Big, round, and hairy (belly, face, buffalo hump, stretch marks)

A

Cushing’s

Everything is high… the only thing LOW will be slow wound healing.

CCRN (11 decks)

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