Review: Endocrine CIS

Question 1

Deep rapid respirations associated with acidosis

Answer 1

Kussmaul respirations

Question 2

Calculation of anion gap

Answer 2

Na - (Cl + HCO3)

Question 3

MUDPILES mnemonic for HAGMA

Answer 3

Methanol
Uremia (kidney failure)
Diabetic ketoacidosis
Paraldehyde/propylene glycol
Infection/iron/isoniazid
Lactic acidosis
Ethylene glycol
Salycylates

Question 4

GOLDMARK mnemonic for HAGMA

Answer 4

Glycols (ethylene, propylene)
Oxoproline (metabolite of paracetamol)
Lactate/lactic acidosis
D-lactate (GI disorders)
Methanol
Aspirin
Renal failure
Ketoacidosis (starvation/ETOH/DKA)

Question 5

DDx for diffuse abdominal pain — GI considerations

Answer 5

GERD +/- hiatal hernia

Gastritis

PUD

Small or large bowel obstruction

Inflammaton (ileitis, colitis, appendicitis, pancreatitis, cholecystitis)

Infectious: viral, bacterial, fungal, parasitic

Vascular, mesenteric thrombosis

Question 6

DDx for diffuse abdominal pain — GU considerations

Answer 6

Renal lithiasis

Blocked or torsed ureter, testicular torsion

Question 7

DDx for diffuse abdominal pain — toxic causes

Answer 7

Black widow spider bite

Snake bite

Question 8

DDx for diffuse abdominal pain — metabolic considerations

Answer 8

Uremia

Hyperlipidemia (significantly elevated triglycerides can cause a pancreatitis)

DKA (note kussmaul breathing, unintentional weight loss, polyuria, polydipsia, polyphagia, hyperglycemia, positive ketones in urine and blood, low pH with anion gap)

Question 9

Most common cause of hypoglycemia

Answer 9

Medications — exogenous insulin, sulfonylurea and meglatinides, alcohol

Question 10

Besides medications, what are some causes of hypoglycemia to include in the DDx?

Answer 10

Critical illness — organ failure (hepatic, cardiac, renal); sepsis (hypermetabolic state)

Rarely hormone deficiency (cortisol, glucagon, epinephrine); endogenous hyperinsulinism (insulinoma, functional beta-cell disorder, etc)

Question 11

Where should you admit a pt with DKA or hypoglycemia?

Answer 11

ICU — where they will get one-on-one nursing, continuous cardiac monitoring, and frequent lab evaluation

Question 12

What is the most important treatment for DKA?

Answer 12

DKA requires high volume IV fluids

Initially normal saline, switch to D51/2 NS when pt on insulin gtt when their glucose gets to 250 to prevent hypoglycemia

Question 13

Besides administering high volume IV fluids, what are other important points of treatment for DKA?

Answer 13

Electrolyte replacement (potassium, even if initially elevated — because insulin/IVF pH correction will drive K into cells and they usually become hypokalemic)

Frequent vital and lab monitoring (electrolytes need replacement — K, Mg, Ph-); check if AG is closing

Correct sodium when sugar is high (Na + [(glucose - 100) x 0.016]

Insulin gtt

Question 14

Overall goal of treatment for DKA

Answer 14

Fix acid-base disturbance, NOT to bring sugar to normal level!

They can have a “normal” sugar and still have an anion gap acidosis, they will go right back into DKA if you stop tx too soon

Question 15

When can you end DKA treatment protocol?

Answer 15

When anion gap is closed — then switch to subcutaneous insulin, stop gtt 2 hrs after administration of SQ long acting (they will go right back into DKA if you stop too soon)

Question 16

Symptoms of hypoglycemia

Answer 16

Weakness or shakiness

Sweating

Altered mental status

Seizure

Question 17

Treatment of hypoglycemia if pt is awake and alert

Answer 17

Fast acting carbs such as oral glucose tablet, hard candy etc.

Question 18

Treatment of hypoglycemia if pt exhibits decreased level of consciousness or seizure

Answer 18

IV D50, glucagon IM

Question 19

Anterior chapmans point for pancreas

Answer 19

R 7th ICS

Question 20

Sympathetics and parasympathetics associated with pancreas

Answer 20

Sympathetics: T5-10

Parasympathetics: OA, AA

Question 21

Sympathetics and parasympathetics associated with kidneys

Answer 21

Sympathetics: T10-L2

Parasympathetics: OA, AA

Question 22

Anterior kidney chapmans points

Answer 22

1” superior and 1” lateral to umbilicus

Question 23

Lymphatic OMT considerations for DKA pt

Answer 23

CV4 or condylar decompression to promote lymphatic flow and restore CRI (could be used for pts with complications of cerebral edema s/o DKA)

Pts with DKA may exhibit Kussmaul breathing, which can lead to rib and diaphragmatic dysfunctions — tx diaphragm and ribs

Make sure pt can handle return of fluid from 3rd spacing. If pt has heart failure or kidney problems, do not be as aggressive with treatment. If DKA was the result of infection, avoid lymphatics until infection is controlled

Question 24

______________ drains right head and neck, right UE, all lung lobes except upper left

Answer 24

Right lymphatic duct

Question 25

Treatment order for lymphatics

Answer 25

Thoracic inlet
Thoracic area
Abdominal area
UE or LE
Head and neck
Thoracic inlet

Question 26

VINDICATE mnemonic for coming up with a DDx

Answer 26

Vascular
Infection, inflammation
Neoplasm
Drugs (toxins)
Iatrogenic, idiopathic
Congenital
Autoimmune, allergic
Trauma
Endocrine/metabolic/environmental

Question 27

What is Whipples triad?

Answer 27

1. Symptoms potentially explained by hypoglycemia
2. Low blood glucose during symptoms
3. Relief of symptoms with administration of glucose or glucagon

Question 28

Effects of regular IV insulin on DKA in terms of hepatic glucose output, glucose utilization, and lipogenesis

Answer 28

Decreased hepatic glucose output

Increased glucose utilization (increased GLUT4 cell membrane translocation in muscle and adipose)

Increased lipogenesis (decreases ketonemia, blood pH normalization)

Question 29

Second generation sulfonylurea that blocks K(ATP) channel and is not considered a euglycemic drug

Answer 29

Glyburide

Question 30

Drug interaction of glyburide + naproxen

Answer 30

Enhanced hypoglycemia — both glyburide and naproxen are highly plasma albumin bound (over 99%); adding naproxen will increase free glyburide levels

Question 31

Drug interaction of glyburide + alcohol

Answer 31

Enhanced hypoglycemia — ethanol enhances the effect of glyburide on K(ATP) channel; ethanol suppresses gluconeogenesis by depleting gluconeogenic substrates, pyruvate and oxaloacetate

Question 32

2 options for treating glyburide-induced hypoglycemia

Answer 32

Octreotide (50-150 mcg SC or IM q6-8h x24h) = DRUG OF CHOICE in glyburide-induced hypoglycemia

Glucagon (1 mg SC or IM)

[glucagon may not be a good choice — very short acting, may not be effective in cases of prolonged hypoglycemia when hepatic stores of glycogen are depleted]