Review: Endocrine CIS Flashcards

1
Q

Deep rapid respirations associated with acidosis

A

Kussmaul respirations

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2
Q

Calculation of anion gap

A

Na - (Cl + HCO3)

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3
Q

MUDPILES mnemonic for HAGMA

A
Methanol
Uremia (kidney failure)
Diabetic ketoacidosis
Paraldehyde/propylene glycol
Infection/iron/isoniazid
Lactic acidosis
Ethylene glycol
Salycylates
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4
Q

GOLDMARK mnemonic for HAGMA

A
Glycols (ethylene, propylene)
Oxoproline (metabolite of paracetamol)
Lactate/lactic acidosis
D-lactate (GI disorders)
Methanol
Aspirin
Renal failure
Ketoacidosis (starvation/ETOH/DKA)
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5
Q

DDx for diffuse abdominal pain — GI considerations

A

GERD +/- hiatal hernia

Gastritis

PUD

Small or large bowel obstruction

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

Infectious: viral, bacterial, fungal, parasitic

Vascular, mesenteric thrombosis

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6
Q

DDx for diffuse abdominal pain — GU considerations

A

Renal lithiasis

Blocked or torsed ureter, testicular torsion

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7
Q

DDx for diffuse abdominal pain — toxic causes

A

Black widow spider bite

Snake bite

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8
Q

DDx for diffuse abdominal pain — metabolic considerations

A

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)

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9
Q

Most common cause of hypoglycemia

A

Medications — exogenous insulin, sulfonylurea and meglatinides, alcohol

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10
Q

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

A

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

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

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11
Q

Where should you admit a pt with DKA or hypoglycemia?

A

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

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12
Q

What is the most important treatment for DKA?

A

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

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13
Q

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

A

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

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14
Q

Overall goal of treatment for DKA

A

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

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15
Q

When can you end DKA treatment protocol?

A

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)

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16
Q

Symptoms of hypoglycemia

A

Weakness or shakiness

Sweating

Altered mental status

Seizure

17
Q

Treatment of hypoglycemia if pt is awake and alert

A

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

18
Q

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

A

IV D50, glucagon IM

19
Q

Anterior chapmans point for pancreas

20
Q

Sympathetics and parasympathetics associated with pancreas

A

Sympathetics: T5-10

Parasympathetics: OA, AA

21
Q

Sympathetics and parasympathetics associated with kidneys

A

Sympathetics: T10-L2

Parasympathetics: OA, AA

22
Q

Anterior kidney chapmans points

A

1” superior and 1” lateral to umbilicus

23
Q

Lymphatic OMT considerations for DKA pt

A

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

24
Q

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

A

Right lymphatic duct

25
Treatment order for lymphatics
``` Thoracic inlet Thoracic area Abdominal area UE or LE Head and neck Thoracic inlet ```
26
VINDICATE mnemonic for coming up with a DDx
``` Vascular Infection, inflammation Neoplasm Drugs (toxins) Iatrogenic, idiopathic Congenital Autoimmune, allergic Trauma Endocrine/metabolic/environmental ```
27
What is Whipples triad?
1. Symptoms potentially explained by hypoglycemia 2. Low blood glucose during symptoms 3. Relief of symptoms with administration of glucose or glucagon
28
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)
29
Second generation sulfonylurea that blocks K(ATP) channel and is not considered a euglycemic drug
Glyburide
30
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
31
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
32
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]