Endocrine CIS Flashcards
Deep rapid respirations associated with acidosis
Kussmaul respirations
Calculation of anion gap
Na - (Cl + HCO3)
MUDPILES mnemonic for HAGMA
Methanol Uremia (kidney failure) Diabetic ketoacidosis Paraldehyde/propylene glycol Infection/iron/isoniazid Lactic acidosis Ethylene glycol Salycylates
GOLDMARK mnemonic for HAGMA
Glycols (ethylene, propylene) Oxoproline (metabolite of paracetamol) Lactate/lactic acidosis D-lactate (GI disorders) Methanol Aspirin Renal failure Ketoacidosis (starvation/ETOH/DKA)
DDx for diffuse abdominal pain — GI considerations
GERD +/- hiatal hernia
Gastritis
PUD
Small or large bowel obstruction
Inflammaton (ileitis, colitis, appendicitis, pancreatitis, cholecystitis)
Infectious: viral, bacterial, fungal, parasitic
Vascular, mesenteric thrombosis
DDx for diffuse abdominal pain — GU considerations
Renal lithiasis
Blocked or torsed ureter, testicular torsion
DDx for diffuse abdominal pain — toxic causes
Black widow spider bite
Snake bite
DDx for diffuse abdominal pain — metabolic considerations
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)
Most common cause of hypoglycemia
Medications — exogenous insulin, sulfonylurea and meglatinides, alcohol
Besides medications, what are some causes of hypoglycemia to include in the DDx?
Critical illness — organ failure (hepatic, cardiac, renal); sepsis (hypermetabolic state)
Rarely hormone deficiency (cortisol, glucagon, epinephrine); endogenous hyperinsulinism (insulinoma, functional beta-cell disorder, etc)
Where should you admit a pt with DKA or hypoglycemia?
ICU — where they will get one-on-one nursing, continuous cardiac monitoring, and frequent lab evaluation
What is the most important treatment for DKA?
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
Besides administering high volume IV fluids, what are other important points of treatment for DKA?
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
Overall goal of treatment for DKA
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
When can you end DKA treatment protocol?
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)
Symptoms of hypoglycemia
Weakness or shakiness
Sweating
Altered mental status
Seizure
Treatment of hypoglycemia if pt is awake and alert
Fast acting carbs such as oral glucose tablet, hard candy etc.
Treatment of hypoglycemia if pt exhibits decreased level of consciousness or seizure
IV D50, glucagon IM
Anterior chapmans point for pancreas
R 7th ICS
Sympathetics and parasympathetics associated with pancreas
Sympathetics: T5-10
Parasympathetics: OA, AA
Sympathetics and parasympathetics associated with kidneys
Sympathetics: T10-L2
Parasympathetics: OA, AA
Anterior kidney chapmans points
1” superior and 1” lateral to umbilicus
Lymphatic OMT considerations for DKA pt
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
______________ drains right head and neck, right UE, all lung lobes except upper left
Right lymphatic duct
Treatment order for lymphatics
Thoracic inlet Thoracic area Abdominal area UE or LE Head and neck Thoracic inlet
VINDICATE mnemonic for coming up with a DDx
Vascular Infection, inflammation Neoplasm Drugs (toxins) Iatrogenic, idiopathic Congenital Autoimmune, allergic Trauma Endocrine/metabolic/environmental
What is Whipples triad?
- Symptoms potentially explained by hypoglycemia
- Low blood glucose during symptoms
- Relief of symptoms with administration of glucose or glucagon
Effects of regular IV insulin on DKA in terms of hepatic glucose output, glucose utilization, and lipogenesis
Decreased hepatic glucose output
Increased glucose utilization (increased GLUT4 cell membrane translocation in muscle and adipose)
Increased lipogenesis (decreases ketonemia, blood pH normalization)
Second generation sulfonylurea that blocks K(ATP) channel and is not considered a euglycemic drug
Glyburide
Drug interaction of glyburide + naproxen
Enhanced hypoglycemia — both glyburide and naproxen are highly plasma albumin bound (over 99%); adding naproxen will increase free glyburide levels
Drug interaction of glyburide + alcohol
Enhanced hypoglycemia — ethanol enhances the effect of glyburide on K(ATP) channel; ethanol suppresses gluconeogenesis by depleting gluconeogenic substrates, pyruvate and oxaloacetate
2 options for treating glyburide-induced hypoglycemia
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]
