Did you know that unique experiences help you remember information better? Pairing holiday characters with their ailments is the perfect way to make information stick in your brain! Plus, we paired them with board pearls for you to remember better on exam day. You'll see all of the high-yield board relevant facts highlighted, just like we do in the Internal Medicine Core.
So, let's say you've decided to open your practice to famous winter characters. Here are the cases you can expect to see.
Patient Case 1:
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Rudolph comes into your office for a check up and you notice that his red nose seems to be spreading to his cheeks! You determine that Rudolph has an atypical case of rosacea.
Rosacea is a lifelong condition that typically affects fair-skinned, middle-aged patients and presents with erythema, telangiectasias, and acne-like lesions on the central face. It occurs more frequently in women but is more severe in men.
It includes 4 main subtypes:
1) Erythematotelangiectatic (vascular): flushing, facial erythema, telangiectasias, and skin sensitivity
2) Papulopustular: facial erythema with transient papules/pustules
3) Phymatous: thickened skin, nodules, prominent pores, rhinophyma (bulbous nose)
4) Ocular: watery/bloodshot appearance, dry/gritty sensation, lid/periocular erythema, chalazia, and hordeola
Patients with rosacea can have a flushing reaction to various stimuli (e.g., alcohol, stress, spicy foods) even before the lesions appear. Once the rosacea manifests, the flush can become permanent. Trigger avoidance is recommended.
You let Rudolph know that perhaps the spiked eggnog or the stress of being "the most famous reindeer of all" might be making his rosacea more apparent. You look at the treatment options: topical metronidazole, azelaic acid, ivermectin, sulfur/sulfacetamide preparations, or oral tetracycline antibiotics. Tetracycline is particularly helpful for the papulopustular and ocular subtypes. Telangiectasias can be treated with laser therapy or brimonidine topical gel (Mirvaso). Those with ocular involvement can be treated with topical erythromycin or metronidazole, but refer to an ophthalmologist.
Patient Case 2:
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Frosty presents to the ED obtunded with multisystem failure and hypothermia. First, you quiz his relatives for previous signs and symptoms of thyroid dysfunction.
Frosty has a history of progressive hypothyroid symptoms, and now presents with decreased mentation, bradycardia, and hypothermia (his body temperature is down to 74° F [23.3° C]!) Other signs indicate a generalized slowing of his systemic processes: hypoventilation, hypoglycemia, and hypotension.
Myxedema coma is 1 of 2 thyroid emergencies (the other being thyroid storm). Mortality is 30–40% and is higher in the elderly and in those with heart disease (which thankfully does not apply to Frosty.) It is a clinical and not a biochemical diagnosis, so the diagnosis depends on recognition of the classic signs and symptoms—not on the absolute value of T4 or TSH.
Any cause of hypothyroidism can lead to myxedema coma. Undiagnosed, long-standing hypothyroidism can progress to myxedema coma. In patients with known but inadequately treated hypothyroidism, myxedema coma can be precipitated by infection, exacerbation of heart disease, opiates, or cold temperature.
You must treat Frosty's myxedema coma with thyroid hormone and need to decide between the following treatments:
Combined T3 and T4 (preferred by most experts) using a loading dose and a smaller daily dose thereafter, or
T3 (advantages: rapid onset and decreased conversion of T4 to T3 during acute illness), or intravenous T4 (due to reduced absorption with oral).
Give empiric stress-dose glucocorticoids until adrenal insufficiency is excluded by ACTH stimulation testing.
Give empiric broad-spectrum antibiotics until infection is excluded. Pay particular attention to gradually warming the body temperature, maintaining adequate blood pressure with IVF and/or vasopressors, and normalizing the serum Na+.
Know that the mortality of myxedema coma is directly related to the degree of hypothermia and that passive rewarming (i.e., with blankets) is one of the most important elements of supportive care. Active rewarming can worsen hypotension (due to vasodilation) and should be avoided.
Patient Case 3:
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You're not surprised by this visit at all. According to common knowledge, Santa's BMI has probably been in the obese range for hundred of years. He indulges in cookies that children set out for him each year, not to mention Mrs. Clause's fabulous cooking. You believe that Santa's lifestyle choices are beginning to catch up with him and that he is experiencing symptoms of T2DM.
More than 90% of diabetes cases are due to T2DM. Obesity increases insulin resistance, and ~ 80% of patients with T2DM are obese. T2DM patients with central obesity, HTN, and dyslipidemia are said to have metabolic syndrome.
Know the mechanisms that lead to T2DM:
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- Insulin resistance in muscle and fat tissues
- Gradual reduction in insulin secretion by the pancreas
- Dysregulated hepatic gluconeogenesis and glucagon secretion
- Reduction in gastrointestinal incretins (glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide)
You suggest that it is time for Santa to change his lifestyle. (TLC; i.e., diet and exercise, weight loss). You suspect he will ignore your medical advice!
Patient Case 4:
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One of Santa's elves comes in to see you. His deadlines at work are quickly approaching and his excessive worry that the toys will not be done in time is interfering with his daily function.
Several years ago he was diagnosed with Generalized Anxiety Disorder (GAD), characterized by persistent and excessive worry about events or activities. GAD affects 3–4% of individuals, and females are affected 2× > males. Although it starts gradually and can begin at any age, it typically starts between childhood and middle age, with median age of onset of 30 years of age (later than other anxiety disorders). Individuals of European descent and more developed countries experience GAD more frequently than others. In some cultures, somatic symptoms predominate, while in others, cognitive symptoms predominate.
GAD also can co-occur with conditions associated with stress, which in turn can lead to gastrointestinal or cardiovascular sequelae. Worrying impairs scholastic and employment progress. Risk factors include parental overprotectiveness, anxiety, sensitivity, and genetics. GAD is 30–50% comorbid with other anxiety disorders, depression, and Cluster C personality disorders. Patients are at risk for alcohol or sedative-hypnotic use disorders. Associated features of GAD include:
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- Headaches
- Upset stomach, vomiting, diarrhea
- Numbness in hands and feet
- Hot flashes, sweating
- Difficulty breathing or swallowing
- Difficulty concentrating
Cognitive Behavioral Therapy (CBT) and serotonergic antidepressants (e.g., SSRIs, SNRIs), alone or in combination, are the treatment for GAD. Antidepressants are effective medications to manage anxiety disorders in the long run; however, antianxiety medications (e.g., buspirone, hydroxyzine) are also effective in resolving anxiety symptoms and are commonly used. Long-term use of benzodiazepines can worsen anxiety.
Patient Case 5:
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Dasher and Prancer come in to see you directly after a test flight with the sleigh getting ready for Christmas Eve. They are both complaining of shortness of breath and headaches. You suspect they are experiencing hypoxemia from high altitude. Hypoxemia (low oxygen tension) has 6 causes: high altitude, ventilation/perfusion (V/Q) mismatch, right-to-left (R-to-L) shunting, decreased alveolar ventilation, low mixed venous O2, and decreased diffusion.
High altitude (low FiO2) results in a reduced PAO2 which results in a reduced PaO2. The A-a gradient is normal unless lung disease is present. Dasher and Prancer both have a normal A-a gradient. The alveolar-arterial gradient (A-a gradient, A-a O2, or DA-aO2) is the difference between the partial pressure of oxygen in the alveoli (A) and that in arterial blood (a): DA-aO2 = PAO2 – PaO2.
Only 2 situations are associated with hypoxemia and a normal A-a gradient: Breathing air that has a reduced concentration of oxygen (such as at high altitudes) and hypoventilating. This is why the A-a gradient assessment is so important. The normal A-a gradient tells you that no disease is present in the alveoli to disrupt diffusion of gases between the capillaries and the airways.
Patient Case 6:
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You've diagnosed The Grinch with Major depressive disorder (MDD). According to the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), major depressive episodes are characterized as ≥ 5 of the following symptoms within the same 2-week period, and 1 of the symptoms must be either a depressed mood or anhedonia (the loss of pleasure or interest in nearly all activities):
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- Depressed mood
- Anhedonia
- Significant weight loss or gain or significant loss or increase in appetite
- Hypersomnia or insomnia
- Psychomotor retardation or agitation
- Loss of energy or fatigue
- Feelings of worthlessness or excessive guilt
- Decreased concentration ability or marked indecisiveness
- Preoccupation with death or suicide; patient has planned or attempted suicide.
- ≥ 1 major depressive episodes do not occur with mania or hypomania, and symptoms are not due to another medical condition, substances, or another mental disorder.
Remember the mnemonic SIG E CAPS:
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- Sleep disturbance (insomnia or hypersomnia)
- Interest diminished
- Guilt
- Energy loss or fatigue
- Concentration diminished
- Appetite changes
- Psychomotor retardation (or agitation)
- Suicidal thoughts
Adjustment disorder with depressed mood occurs within 3 months of a stressful event (e.g., divorce, or around the holidays in his case). There is no change in appetite, sleep patterns, or cognition.
MDD typically starts during puberty and peaks in the 20s. It is a recurrent illness, with a 50% relapse after 1 episode and 80% relapse after 3 episodes. The duration of each episode is ~ 3 months. In 6 months, about 60% of individuals have recovered, and in 2 years, 80% have recovered with proper treatment. Treatment includes a combination of cognitive behavioral therapy (CBT) and medications (e.g., selective serotonin reuptake inhibitors [SSRIs], serotonin- norepinephrine reuptake inhibitors [SNRIs]) for mild-to-moderate cases. Many medications can cause weight gain and sexual dysfunction. Antipsychotics and electroconvulsive therapy (ECT) can be added for psychotic depression and treatment-resistant depression, respectively. The stigma of ECT prevents its use in many patients who might benefit. An adequate trial of an antidepressant medication is 4–12 weeks. Treatment-resistant depression (failure to respond to 2 antidepressants) occurs in 10–30% of patients. Consult a psychiatrist if there is a suspicion of hypomania, mania (see Bipolar Disorder), psychosis, or treatment-resistant depression. Transfer individuals to emergency care for suicidal ideation.
Patient Case 7:
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You must see this patient outside, as he was not able to fit into the exam room. He complains that his hands and feet are getting larger and that his voice is getting deeper. During the exam you see that he is excessively sweating and has body odor.
You know that growth hormone (GH) is required for normal growth. GH production is suppressed by hyperglycemia, somatostatin, and chronic corticosteroid use and is stimulated by hypoglycemia. But, when excess GH presents in childhood before growth plates are closed, it is termed gigantism. When it occurs in adulthood, it is termed acromegaly because the growth plates are closed; there is not excessive linear growth, but there is acral growth (i.e., hands, feet).
> 99% of acromegaly cases are due to a benign, well-defined adenoma, which is recognized on CT or MRI.
Affected patients typically become symptomatic in their late 30s to mid-40s. Signs and symptoms of acromegaly include:
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- Enlarging hands and feet
- Coarsening of the facial features
- Deepening of the voice
- Carpal tunnel syndrome, often bilateral
- Acanthosis nigricans
- Skin tags
- Pronounced jaw growth (which leads to multiple dental problems)
- Excessive sweating, body odor
Acromegaly has an insidious onset associated with an increased mortality when untreated. The most important long-term problem associated with acromegaly is cardiovascular disease due to accelerated atherosclerosis. Patients have increased risk of:
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- Ischemic heart disease
- Cardiomyopathy
- Diastolic dysfunction
- Hypertension
- Left ventricular hypertrophy
- Stroke
Acromegaly is also associated with obstructive sleep apnea, insulin resistance/diabetes mellitus, colon polyps, and colorectal cancer.
Screen for acromegaly by checking an IGF-1 level. Do not order a random GH level because a single value of GH is not useful in diagnosing acromegaly; its secretion is pulsatile, and levels in the blood can vary greatly in a healthy individual. IGF-1 is produced by the liver and mediates the growth-promoting effect of GH. Unlike GH, IGF-1 levels are stable throughout the day. A normal age-adjusted IGF-1 level almost always excludes the diagnosis of acromegaly. If the IGF-1 level is elevated, confirm the diagnosis by demonstrating a failure of GH to suppress after a 75-g oral glucose load (via an oral glucose tolerance test [OGTT]). A post-OGTT GH level > 1 ng/mL (1 μg/L) is diagnostic of acromegaly. Also check prolactin levels (elevated due to cosecretion in 25% of GH tumors). If the tumor is > 1 cm, check for visual field deficits and for other hormonal deficiencies.
Order a screening colonoscopy and echocardiogram on all patients diagnosed with acromegaly, regardless of age.
Treat all patients with transsphenoidal surgery, even if they are asymptomatic. Some experts recommend medical therapy with somatostatin analogs as initial therapy prior to surgery for a better chance for a cure and possibly safer intubation.
Radiation is used as initial therapy only in poor surgical candidates.
Medical treatment may be used as adjuvant therapy in patients with residual tumor after surgical resection and in poor surgical candidates. Options include somatostatin analogs (e.g., octreotide) +/– dopamine agonists (e.g., cabergoline or bromocriptine), and GH receptor antagonists (i.e., pegvisomant).
Episodic memory, which is the source of all semantic memory, is event-based. The importance attached to elements of an event is derived from previous experience and from hard-coded, brain-based processing. So, we hope that if you see any of these ailments on your exam that you will remember these mythical holiday characters and immediately know the answer! Download StudyWise to discover more about this and other evidence-based brain-hacking techniques.
Can you think of any other ailments that winter characters may have? Let us know!
