Mixed 5 Flashcards by Maggie Musso

What is Ludwig angina?

Rapidly progressive cellulitis of the submandibular and sublingual spaces.

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Most cases of Ludwig angina arise from contiguous (rather than lymphatic) spread of polymicrobial dental infections in the ___.

Mandibular molars

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What causes acute airway obstruction in Ludwig angina?

As the submandibular area becomes tender and indurated, the floor of the mouth becomes elevated and displaces the tongue posteriorly

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Infections originating in the ___ space can spread to the infratemporal space and orbit and progress to cavernous sinus thrombosis.

Maxillary

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Complications of drowning are a result of ___.

Hypoxemia from fluid aspiration; the aspirated liquid washes out alveolar surfactant, causing pulmonary edema, respiratory insufficiency, and ARDS, which can develop insidiously over the next 72 hours

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Indications for intrapartum prophylaxis against GBS?

GBS bacteriuria or GBS UTI in current pregnancy (regardless of treatment)
GBS+ rectovaginal culture in current pregnancy
Unknown GBS status PLUS any of the following: <37 weeks, intrapartum fever, rupture of membranes for 18+ hours
Prior infant with early-onset neonatal sepsis or GBS infection

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Intrapartum prophylaxis for GBS?

IV pencillin

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Presentation - relapsing-remitting fevers associated with endometritis

Septic pelvic thrombophlebitis

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What is uterine incarceration?

Rare disorder that occurs during pregnancy as a retroverted uterus enlarges and the fundus becomes entrapped under the sacral promontory; patients have pelvic pain and urinary retention due to bladder obstruction

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DDx - flaccid paralysis?

Infant botulism
Foodborne botulism
Guillain-Barre syndrome

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Compare the pathogenesis of the 3 main causes of flaccid paralysis.

Infant botulism - ingestion of C. botulinum spores from environmental dust

Foodborne botulism - ingestion of preformed C. botulinum toxin

GBS - autoimmune peripheral nerve demyeliation

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Compare the presentation of the 3 main causes of flaccid paralysis.

Infant and foodborne botulism: descending flaccid paralysis

GBS - ascending flaccid paralysis

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Compare the Rx of the 3 main causes of flaccid paralysis.

Infant botulism - human-derived botulism immune globulin

Foodborne botulism - equine-derived botulism anti-toxin

GBS - pooled human immune globulin

Administer as soon as possible, even before diagnostic confirmation

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The incidence of C. botulinum is highest in what three states (greatest concentration of soil botulism spores)?

California
Pennsylvania
Utah

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Effect of botulinum toxin?

Blocks ACh release at presynaptic neuromuscular junctions

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Congenital myasthenia gravis is a rare neuromuscular condition - how can it be distinguished from botulism?

Lack of autonomic symptoms (constipation, drooling); fluctuating generalized hypotonia

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Characteristic features of spinal muscular atrophy?

Generalized symmetric proximal muscle weakness and hyporeflexia; does not affect the pupils, weakness is greater in the lower extremities than the upper

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What are the two types of diabetes insipidus and how do they differ?

Central - 2/2 decreased production of ADH by the pituitary (trauma, hemorrhage, infection, tumors)
Nephrogenic - 2/2 renal ADH resistance (hypercalcemia, severe hypokalemia, tubulointerstitial renal disease, meds)

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Common medications causing nephrogenic DI?

Lithium
Demeclocycline
Foscarnet
Cidofovir
Amphotericin

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Presentation of DI (labs)?

Euvolemic hypernatremia
Urine Osm <300 (complete) or 300-600 (partial) -> elevated in both types
Increased serum Osm

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Describe the development of a left ventricular aneurysm after an MI.

Late complication that can occur up to several months following a transmural (STEMI); delayed coronary reperfusion increases the risk.

The healing process results in replacement of necrosed myocardium with fibrous scar tissue, which in the case of a large MI can result in convexity of a large portion of the left ventricular

Aneurysm is dyskinetic with the remaining healthy wall, resulting in impaired ejection fraction

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Possible presentations of left ventricular aneurysm?

Heart failure (most common)
Angina (increased oxygen demand 2/2 elevated wall stress)
Ventricular arrhythmia
Systemic embolization (mural thrombus)

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EKG findings of a left ventricular aneurysm?

Persistent ST-segment elevation
Deep Q waves

Found in the leads corresponding to the previous MI

Echo findings of a left ventricular aneurysm?

Thinned and dyskinetic myocardial wall

Presentation of right ventricular infarct?

Hypotension Elevated JVP Clear lung fields ECG findings of ST-segment elevation in the inferior leads (II, III, aVF)

List 5 mechanical complications of acute MI.

1. R ventricular failure 2. Papillary muscle rupture 3. Interventricular septum rupture 4. Free wall rupture 5. L ventricular aneurysm

Compare the time course of the 5 mechanical complications of acute MI.

1. R ventricular failure - acute 2. Papillary muscle rupture - acute or within 3-5 days 3. Interventricular septum rupture - acute or within 3-5 days 4. Free wall rupture - within 5 days to 2 weeks 5. L ventricular aneurysm - up to several months

Compare the involved coronary artery of the 5 mechanical complications of acute MI.

R ventricular failure and papillary muscle rupture - RCA Interventricular septum rupture - LAD (apical septal) or RCA (basal septal) Free wall rupture and L ventricular aneurysm - LAD

Clinical and echo findings of R ventricular failure?

Hypotension, clear lungs, Kussmaul sign Hypokinetic RV

Clinical and echo findings of papillary muscle rupture?

Severe MR with flail leaflet

Clinical and echo findings of interventricular septum rupture?

Chest pain, new holosystolic murmur, biventricular failure, shock L->R ventricular shunt, increase in O2 level from RA to RV

Clinical and echo findings of free wall rupture?

Chest pain, shock, distant heart sounds Pericardial effusion with tamponade

Clinical and echo findings of L ventricular aneurysm?

Subacute heart failure, stable angina Thin and dyskinetic myocardial wall

Pertussis is a highly contagious disease and transmission occurs by spread of ___. Recommended first-line treatment? Timing of treatment?

Respiratory droplets Macrolide antibiotic (azithro/clarithro/erythro) Rx during catarrhal stage may help shorten the course; treatment later will not shorten the duration but will reduce transmission

Prophylactic recommendations for close contacts of patients with pertussis?

Recommended for all close contacts despite vaccination status; macrolides are preferred. If <1 month, only azithromycin If not fully immunized, give vaccination according to recommended schedule

Etiology of acute bacterial prostatitis?

Intraprostatic reflux of pathogens in urine | Primarily GN bacilli (75% E. coli)

Manifestations of acute bacterial prostatitis?

Flu-like illness Lower urinary symptoms (dysuria, urine retention, pelvic pain, etc.) Perineal pain

Dx acute bacterial prostatitis?

Digital rectal exam (tender, swollen prostate) | Urine culture

Rx acute bacterial prostatitis

6 weeks TMP-SMX or FQ

Complications of acute bacterial prostatitis?

Bacteremia/systemic spread Prostatic abscess Chronic prostatits

What should be avoided in patients with acute bacterial prostatitis and why?

Cystoscopy and urethral catheterization; passage of instruments through the urethra can cause septic shock due to release of bacteria from the prostate or prostatic rupture

Presentation - headache worse at night, N/V, mental status changes, papilledema, focal neuro deficits

Intracranial hypertension

What is the Cushing reflex?

HTN Bradycardia Respiratory depression

Possible etiologies causing intracranial HTN?

Trauma, space-occupying lesions, hydrocephalus, impaired CNS venous outflow, idiopathic ICH (pseudotumor cerebri)

What maneuvers increase ICP?

Leaning forward Valsalva Cough

Presentation - headache with decreased vision, age >60, conjunctival erythema, mid-dilated pupil poorly reactive to light

Acute angle closure glaucoma

What is a case-control study?

Study used to compare the exposure of the people with the disease (cases) to the exposure of the people without the disease (controls)

What is the main measure of association in a case-control study?

Exposure odds ratio

Why can incidence measures such as relative risk or relative rate not be directly measured in case-control studies?

Because the people being studied are those who have already developed the disease

Bell palsy is a peripheral neuropathy of the ___ nerve characterized by facial weakness involving both the upper and lower face. What causes it?

Facial nerve (CN VII); reactivation of neurotrophic viruses (eg, HSV), resulting in inflammation, edema, and degeneration of the myelin sheath

Presentation of Bell palsy?

Unilateral mouth dropping, loss of nasolabial fold, involvement of the upper face (weakness in closing the eye or raising the eyebrow)

What distinguishes Bell palsy from UMN disorders like stroke?

Upper face involvement in Bell palsy; UMN lesions spare the upper face

Timing of Bell palsy presentation?

Weakness typically develops acutely over a course of hours; often occurs at night. Symptoms progress over 2-3 weeks, gradual improvement over the following 3-6 months

Rx Bell palsy?

Glucocorticoids; some experts recommend adding valacyclovir

The ___ tract carries input from upper motor nuclei and innervates CN V, VII, IX, I, XI, XII.

Corticobulbar

Most of the CNs innervated by the corticobulbar tract receive bilateral input and are unaffected by a unilateral lesion like stroke. What are the exceptions to this?

CN XII (innervates the genioglossus muscle -> tongue) CN VII (innervates the lower face)