AM Report 02/07/2017 Posterior STEMI

How do you recognize a Posterior STEMI?

-FIRST, you need to suspect it!
-Only 10 % occur as isolated Posterior STEMI, most occur WITH inferior or lateral STEMI

What do you look for on an EKG?

-Remember that the EKG leads look at the anterior heart so the mirror image must be true for a Posterior STEMI in leads V1-v3

-Instead of ST elevations, you see ST Depressions
-Instead of Q waves, you see tall R waves
-Instead of flipped T waves, you see upright T waves

Example

classic-posterior-stemi

How can you look at the posterior leads on an EKG?

Place 3 leads (V7,V8,V9) below the right scapula (see picture) and look for ST elevations, Q waves and T wave inversions!

posterior-leads

What coronary vessel is often implicated?

Posterior Descending Artery of the Right Coronary Artery (right dominant circulation)

350px-Coronary_arteries.png

How do you recognize a right ventricular infarction on an EKG?

-Often see ST elevations in V1, and in Lead III>Lead II
ST elevations in the right sided leads (especially V4R)-see picture below
Get that Right sided EKG if you suspect RV infarct!

right-sided-leads

Why is it important to recognize?

-Up to 40% of inferior STEMI can be associated with a RV infarction
-These patients are PRELOAD sensitive, so their blood pressures will tank if you give them nitrates or other preload reducers-they need FLUID RESUSCITATION

References

LITFL (Life in the Fast Lane)- an excellent resource for ECGs amongst others

 

AM Report 2/14/17: Aortic Stenosis

Main etiologies of Aortic Stenosis

-Calcific/atherosclerotic: usually in patients >70, RF include HTN, Elevated TG, ESRD
Congenital: etiology in 50 % of patients <70, usually bicuspid AV
Rheumatic heart disease-usually associated with MV disease as well

TRIAD of Aortic Stenosis (not commonly seen)

-Heart Failure
-Syncope (usually with exertion when systemic vasodilation in the presence of a fixed SV causes BP to drop)
-Angina

The most common presenting symptom is DOE followed by decreased exercise tolerance, and pre-syncope.

What to look for on echocardiography if you suspect AS

-Maximum instantaneous velocity across valve (Peak Velocity)
-Mean aortic valve gradient
Aortic Valve Area (AVA)

When is it considered SEVERE aortic stenosis?

-Mean gradient >40, Max Jet Velocity >4 m/s
AVA <1 cm2, or < 0.5 cm2/m2 BSA

When should you replace the valve (surgical replacement vs. TAVR)

-Anyone with SYMPTOMS (usually only in severe AS and can be subtle like decreased exercise tolerance)
Asymptomatic patients with severe AS with decrease in EF (EF<50 %)
-Asymptomatic patients with severe AS who are undergoing other cardiac surgery (eg: CABG)

Note that asymptomatic patients with severe AS do NOT need routinely need surgery.


What if AVA<1 but mean gradient is <40 and peak velocity <4?

This could be due to LOW FLOW-LOW GRADIENT Aortic Stenosis.

Diagnose it with a Dobutamine Echo

If TRUE Aortic Stenosis-Measured AVA will not change but the mean pressure gradient and transvalvular gradient will increase-these patients will benefit from replacement of the valve
If PSEUDO-severe stenosis, low cardiac output is due to myocardial dysfunction, and AVA will increase with dobutamine with minimal change in the gradient-likely will NOT benefit from replacement of the valve.

Medical treatment

-There is NO good medical treatment for severe Aortic Valve stenosis!
-Patients with severe AS can be considered to have a fixed afterload and pre-load dependent, so caution with use of diuretics, afterload reducers, and negative inotropes (CCB/BB) or you can cause them to syncopize!

AM Report 2/15/17: Toxoplasmosis

 

Infection CD4 Count Prophylaxis
PCP pneumonia < 200 TMP-SMX
Toxoplasmosis < 100 TMP-SMX
MAC < 50 Azithromycin

Toxoplasmosis:

Presumptive Diagnosis: *usually made to avoid brain biopsy

  1. CD4 < 100
  2. Lack of effective prophylaxis
  3. Clinical syndrome (headache, neuro symptoms, fever, etc.)
  4. + T. gondii IgG antibody
  5. Imaging consistent with disease (multiple ring-enhancing lesions)

* If present >90% probably of TE.

Definitive Diagnosis:

  1. Clinical syndrome (headache, neuro symptoms, fever, etc.)
  2. Identification of ≥ 1 mass lesion by brain imaging
  3. Detection of organism in biopsy specimen

1

Treatment:

  1. Sulfadiazine
  2. Pyrimethamine
  3. Leucovorin – to prevent pyrimethamine induced hematologic toxicity
  • Measure response to treatment with daily neurological exams and repeat neuroimaging after 2-3 weeks
  • 75-80% of patients with TE will show radiographic and/or neurologic improvement
  • Treat for 6 weeks followed by maintenance therapy

ART:

  • 3 drugs from 2 different classes
  • Usually 2 nucleoside RTIs “backbone” and 3rd agent – either  a protease inhibitor or an integrase inhibitor

Post-Exposure Prophylaxis:

  • Started immediately after exposure => continued for 4 weeks
  • Test immediately, 6 weeks, 12 weeks, and 6 months
  • 3 Drug Regimen: Tenofovir-Emtricitabine + Raltegravir

Pre-Exposure Prophylaxis:

  • Recommended for certain high-risk populations: heterosexual partners of infected patients, MSM, IVDU
  • 2 Drug Regimen: Tenofovir-Emtricitabine

 

AM Report 2/8/17: Guillain-Barré Syndrome

GBS Variants:

-AIDP (Acute inflammatory demyelinating polyneuropathy)- 85-95 % of GBS
-Miller Fisher Variant (5 % US but up to 25 % in Japan)
-AMAN (Acute motor axonal neuropathy)
-AMSAN (Acute sensorimotor axonal neuropathy)

Timing:

Acute (<4 weeks)

Pathophysiology:

Due to molecular mimicry from immune response to preceding infection that cross reacts with components of the peripheral nerve.

Diagnostic Criteria:

  1. Progressive weakness of ≥ 2 limbs due to neuropathy
  2. Areflexia
  3. Disease course < 4 weeks
  4. Exclusion of other causes

Supportive criteria:

  1. Symmetric weakness
  2. Mild sensory involvement
  3. Absence of fever
  4. Typical CSF profile
  5. EMG evidence of demylination

Most common infectious triggers:
-Campylobacter Jejuni (most common), CMV, EBV, HIV, VZV, Mycoplasma, and even Zika virus

Most sensitive physical exam findings in GBS

-Absent/Depressed DTR (90 %)
-Ascending extremity weakness (90 %)
-Paresthesias (80 %)
-Dysautonomia (70 %)
-Facial weakness or bulbar signs (55 %)
-Back/extremity pain, respiratory failure, oculomotor weakness

What do you see on LP?

Albumino-cytologic dissociation (normal WBC with high protein)

Miller Fisher variant TRIAD:

-Ophthalmoplegia
-Ataxia
-Areflexia
Antibodies against GQ1b (anti-ganglioside) present in 85-90 % of patients

Treatment

-Supportive treatment
-IVIG
-Plasma Exchange

Remember that steroids are not effective!

AM Report 1/23/17: Endocrinology Board Review

Surreptitious Insulin Use:
– Exogenous insulin intake is associated with increased insulin and low C-peptide levels

Whipple’s Triad:
1.Symptoms consistent with hypoglycemia
2.Documented low plasma glucose when symptoms are present
3.Relief of symptoms following resolution of hypoglycemia

– Consider a psychiatric evaluation in patient’s suspected of intentional exogenous insulin use

Picture1.png
– Endogenous insulin is formed as two insulin chains (A&B) linked by C-peptide.  Measurement of C-peptide can help distinguish from endogenous versus exogenous insulin

Insulinoma:
Diagnosis:
– Clinical + measurement of insulin (normal or elevated), proinsulin (normal or elevated), and C-peptide (normal or elevated)
– Localization of tumor with imaging; start with CT of the abdomen

Glucose Insulin Proinsulin C-peptide BHB
Exogenous Insulin
Insulinoma, NIPHS, PGHS ↑/NL ↑/NL ↑/NL
Sulfonylurea Ingestion

– Use a urine sulfonylurea toxicity screen to distinguish insulinoma from sulfonylurea ingestion

Pheochromocytoma:

– always think about pheo when the clinical case includes episodes of hypertension and headache

– Pheochromocytomas are tumors composed of chromaffin cells of the adrenal gland

– Pheochromocytomas almost always realease catecholamines

Classic Triad:

– Diaphoresis

– Headache

– Tachycardia

Genetic disorder associated with pheochromocytoma:

– MEN 2A and 2B

– Neurofibromatosis type 1

– Von Hippel-Lindau syndrome

Diagnosis: – Plasma / Urine catecholamines

– plasma high sensitivity (96-100%), but lower specificity (85-89%); 24 hour urine sensitivity/specificity (91-98%)

– Plasma will exclude a pheo when negative, but need to confirm if positive

– Following biochemical diagnosis – radiographic localization is needed

Preoperative management:

– Alpha-blocker – typically with phenoxybenzamine – is first-line therapy; followed by B-blockers (metoprolol, propranolol) to treat reflex tachycardia

MEN 1, 2A, and 2B disorders:

MEN 1: Pituitary adenoma, Parathyroid hyperplasia, Pancreatic tumors

MEN 2A: Medullary thyroid cancer, Parathyroid hyperplasia, Pheochromcytoma

MEN 2B: Medullary thyroid cancer, Marfanoid habitus/Mucosal neuroma, Pheochromocytoma

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Cushing Syndrome:
– Bright purple abdominal striae always, always, always are associated with Cushing syndrome – striae larger than 1 cm in width are highly specific for hypercortisolism
picture5
Other classic stigmata:
– cervicodorsal fat pad aka “buffalo hump,” acne, hirsutism, moon facies, plethora, easy bruising, hypertension, insulin resistance, hypokalemic metabolic alkalosis, osteoporosis

Picture4.png
Cause:
– Elevated cortisol
– Most common cause is exogenous glucocorticoid therapy for another cause

3 biochemical testing options for CS:
– 1 mg (low dose) dexamethasone suppression test – failure to suppress AM cortisol indicates true Cushing syndrome
– 24 hour urine free cortisol (UFC) – excludes CS when not elevated
– Late-night salivary cortisol
Never measure a random cortisol as part of the work up

After confirming CS biochemically, measure ACTH to establish etiology
– differentiate between ACTH-dependent/Cushing Disease (usually > 20 pg/mL) and ACTH-independent (usually < 5 pg/mL)

If ACTH-dependent CS: order pituitary MRI
If ACTH-independent CS: adrenal gland imaging (either CT or MRI)

ACTH-secreting pituitary adenoma is known as Cushing disease
Pearl: pituitary adenomas do not suppress with low-dose dex, but do suppress with high dose

Other possible ACTH-secreting tumors (but very rare):
– An ectopic ACTH-secreting tumor
– Usually these are primary lung cancers or a carcinoid tumor
– The clinical presentation of an ectopic lung tumor usually is less cushingoid (presenting with only HTN and metabolic abnormalities) due to the rapid growth of these tumors


			

AM Report 1/9/17: Infectious Disease

Pneumocystis jiroveci pneumonia (PJP):
– opportunistic infections are the most common etiologies of infection in patients 1-6 months after solid organ transplant.
Common signs/symptoms of PJP:
– Progressive exertional dyspnea (95%)
– Fever (90%)
– Non-productive cough (90%)
Pearl: walk patients with suspected PCP to reveal hypoxemia!

Diagnosis:
– Direct fluorescent antibody stain (DFA stain)
– Gomori methenamine silver stain (GMS stain)
*Must visualize the cystic/trophic forms directly
picture1

Treatment: TMP/SMX for 21 days
Add steroids for pO2 ≤ 70 or A-a gradient ≥ 35

Toxic Shock Syndrome:
– expect a TSS board question to present as overwhelming sepsis in the context of a menstruating female or a post-surgical wound infection
– toxins (called super antigens) stimulate cytokine production, resulting in systemic signs of shock

Triad of TSS:
Shock
Fever
Rash – diffuse macular rash with subsequent desquamation, especially on the palms and soles
*Along with involvement of at least 3 organ systems
picture2

Organisms often involved:
– S. aureus
– S. pyogenes

Treatment:
S. pyogenes: penicillin plus clindamycin
MSSA: Nafcillin or oxcillin plus clindamycin
MRSA: Vancomycin plus clindamycin
* add clindamycin to suppress protein synthesis and, therefore, toxin production

Scarlet Fever:
Key features:
– “circumoral pallor” – pale area around mouth
– “Pastia lines” – petechial lines in the skin creases
– desquemation

Most common organism: Group A Streptococcus

5 “S'” of Scarlet Fever:
– Streptococci (causative organism)
– Sorethorat
– Swollen tonsils
– Strawberry tongue
– Sandpaper rash

Treatment: Oral penicillin V; amoxicillin, 1st generation cephalosporins, and IM PCN G are alternatives


Lyme Disease:

– Erythema migrans is the associated rash
picture3
– Borelia burgdorferi is the causitive organism and Ixodes tick is the vector
– > 95% of cases occur in regions where the Ixodes tick is abundant
picture4
Other infections spread by Ixodes tick:
– Babesiosis
– Anaplasmosis

Signs/Symptoms of different stages of Lyme disease:
Localized: erythema migrans (target lesion at site of tick attachment ~ 60-80%), fever/other systemic symptoms are rarely present
Early disseminated: erythema migrans at multiple sites, febrile illness with constitutional symptoms (myalgia, arthralgia, and headache)
Cardiac: asymptomatic PR prolongation → complete heart block
Neurologic: facial nerve palsy (most common) either unilateral or bilateral
Late disseminated: oligoarticular inflammatory arthritis involving large joints (i.e. knee)

Rocky Mountain Spotted Fever:
Look for a history of exposure to ticks in endemic areas (southeast / south central US) and features of:
– Pancytopenia (esp thrombocytopenia)
– Hyponatremia
– No evidence of DIC (normal PT/PTT)
– ↑ transaminases

picture6
Rash of RMSF:
– >85% of patients by 1 week
– May lag behind other symptoms (~50% by day 3)
– Typically starts at the distal extremities and progress centrally; involves the palms/soles in >30% and typicially spares the face

Treatment:
– Doxycycline; choloramphenicol is an alternative option in pregnancy

Ehrlichiosis:
Think of Ehrlichia as “Rocky Moutain spotless fever”
– presents similarly to Anaplasmosis
– endemic to the southcentral and southeastern US
– spread via the Lone Star tick

Symptoms in order of frequency:
Fever (~90%) > headache > myalgia > arthralgia > meningismus

– Blood smear can help with visualization of intracytoplasmic inclusions in WBCs; only present in ~30%

Treatment:
– Doxycycline

Coccidioides Infection (Valley Fever):
– Clues to be aware of: Arizona/New Mexico and erythema nodosum
– Endemic to SW US (Arizona, New Mexico, Texas, and central valley of California)
– Route of infection: inhalation of fungal particles found in the sand
– Arthralgia of multiple joints “desert rheumatism” is common.
picture7
Diagnosis confirmed on fungal stains
– Thick walled spherules (10-80 uM) with endospores are seen in tissue
picture8
No treatment for mild disease; use itraconazole or fluconazole for severe illness

Histoplasmosis:
Exposure history is key here; think of histo with any of the following exposures in the SE/SC US:
– Bats (or guano)
– “Spelunking” (cave exposure)
– Farm buildings / bird-roosting locations
picture9
Most infections are subclinical (~95%); can see mucocutaneous lesions
Antigen detection in urine great for disseminated infections (>85%)

Blastomycosis:
– Endemic to Ohio and Mississippi/ River valleys
picture10
– Primarily a pulmonary infection, may disseminate to the skin and bone
– Well demarcated skin lesion is most common manifestation of disseminated disease
picture11
– Appears as a broad based budding pattern at 37 C
picture12

AM Report 2/6/17: Neurology Board Review

Normal Pressure Hydrocephalus:
Crude mnemonic: Wet (incontinence), Wobbly (ataxia), and Wacky (dementia)
Abnormal gait typically develops first!
Magnetic gait” – is the characteristic gait of NPH – the patient’s walk appears as if his/her feet are stuck to the floor.
The gait is wide based, with slow, small steps, and reduced foot-to-floor clearance

Visualize hydrocephalus on CT/MRI – specifically ventriculomegaly that is disproportionate to corticol atrophy
picture1

LP: Normal (or slighty elevated) opening pressure and cell count

Standard of care: Ventriculoperitoneal (VP) shut – can perform large volume (30-50 mL) LP prior to placement to verify benefit

picture2

Cluster Headache:
Presentation: Shorter duration (usually < 3 hours), ipsilateral congestion and lacrimation with headache, nocturnal attacks
Epidemiology: Young or middle aged, male sex, history of cigarette smoking
Common trigger: Alcohol

First-line therapy: Inhalation of 100% oxygen and/or SQ or intranasal sumatriptans
Prevention medication: Verapamil

Transverse Myelitis:
TM is thought to be due to an autoimmune inflammation
~50% of the time it is preceded by an infection

Diagnosis requires:
– Presence of clinical features
– Evidence of inflammation (either leukocytosis in CSF or contrast enhancement on MRI)
– Exclusion of other potential causes

Treatment: IV methylprednisolone; plasmapheresis or cyclophosphamide for refractory disease

Alzheimer Disease:
Presentation: >60 years old, decline is insidious and progressive, definite impairment in 2 or more domains of cognition that impacts daily living

Treatment options:
– Cholinesterase inhibitors: Donepezil, Rivastigmine, Galantamine
– N-methyl-D-asapartate receptor antagonists: Memantine
*mild improvements in measured cognition and performance of some activities; no clinically significant outcome

Frontotemproal Dementia:
– 3rd most common type of neurodegenerative disorder (2nd in those < 65 years old); average age of onset is 50-60
– Social behavior / personality changes are variable
– Genetics of FTD are heterogenous ~40% of patients with FTD have at least one family member with a neurodegenerative disorder

Difference with Lewy Body Dementia – Lack of significant psychosis – especially visual hallucinations

Parkinson Disease:
4 main features:
Tremor: “pill-rolling” and always gets better with action
Bradykinesia
Rigidity
Gait/Postural impairment: “festinating gait” – meaning hurried small shuffles, often on tippy toes
* diagnostic criteria require the presence of bradykinesia with at least one other cardinal feature
* MRI is recommended to rule out vascular lesions and hydrocephalus when suspected

Treatment options:
– Non-pharmacologic: rigorous daily exercise
– Pharmacologic: Dopamine substrate (levodopa), Decarboxylase inhibitors (carbidopa), Dopamine agonists (Ropinirole, Bromocriptine, Pergolide), Catechol-O-methyltransferase inhibitors (Entacapone, Tolcapone), Monoamine oxidase type B inhibitors (Selegiline, Rasagiline), Glutamate antagonist (Amatadine), Anticholinergic agents (Benztropine)
– Surgical: Deep brain stimulation (DBS) – consider in patients who have sustained motor benefit from medication, but are limited by adverse effect of medications

Myasthenia Gravis:
Cause: autoimmune disease directed against post-synaptic NM junction
Labs:
Anti-acetylchoine receptor antibodies (~90% sensitive)
– Anti-muscle-specific kinase (MuSK) antibodies
EMG: repetitive nerve stimulation shows decremental response
Imaging: CT or MRI of mediastinum to screen for thymoma (~15% present, 85% hyperplasia)

Treatment:
– Cholinesterase inhibitors: pyridostigmine
– Glucocorticoids
– Immunosuppressive agents: azathioprine, cyclosporine, etc.

Crisis Treatment:
– Plasmapheresis or IVIG

Lambert-Eaton Syndrome:
Cause: autoantibodies against voltage-gated calcium channels located at the presynaptic NM junction
Associations: small cell lung cancer – can occur before tumor has been discovered; found in as many as 60% of patients

Differentiate from MG:
Repetitive contraction IMPROVES muscle strength
– Hyporeflexia and dysautonomia are also present

Treatment:
– Remove the malignancy
– IVIG +/- immunomodulators