Ascites, Ascites Baby
Slow down, grab the wall
This Girl Is on Fire
Listen to Your Heart
I’ve Been Everywhere, Man
100

Name three causes of ascites with a LOW SAAG gradient. 

Low SAAG (<1.1 g/dL) — No Portal Hypertension (high protein in fluid!) 

Common causes include:

  • Peritoneal carcinomatosis / malignancy
  • Tuberculous peritonitis
  • Pancreatic ascites
  • Serositis (e.g., SLE)
  • Bowel perforation / secondary peritonitis
  • Nephrotic syndrome / severe hypoalbuminemia
100

A patient with complete heart block is being transcutaneously paced at 80/min. The monitor shows a pacing spike followed by a wide QRS after every stimulus, yet the patient remains hypotensive. What do you suspect is happening doctor?

Lack of mechanical capture!

Electrical capture ≠ mechanical capture. With TCP, monitor artifact can look convincingly like a paced QRS. You need a corresponding pulse or arterial waveform to confirm mechanical capture.

100

This short-acting medication, used in many rheumatolgical causes of fever, has a half-life of approximately 4–6 hours and may be administered in divided doses such as TID in severe hyperinflammatory disease. It works by competitively inhibiting the receptor shared by IL-1α and IL-1β.

What is anakinra?

It interrupts the cytokine amplification loop rather than broadly suppressing every component of the immune system.

100

This common arrhythmia can substantially increase NT-proBNP independent of heart failure and must be considered when interpreting an elevated value.

What is a fib?

AF increases atrial wall stress and natriuretic peptide release.

100

This African country contains the Ebola River, from which Ebola virus received its name.

What is Democratic Republic of the Congo?

200

This lab value can help distinguish between cardiogenic and cirrhotic causes of ascites.

What is Ascities total protein?

200

A patient with an STEMI develops complete heart block with a narrow-QRS escape rhythm at 45/min. Occlusion of this coronary artery most commonly produces this conduction abnormality.

What is the RCA?

  • In about 85–90% of people, the AV nodal artery arises from the RCA, usually near the crux of the heart.
  • An inferior STEMI is most commonly caused by RCA occlusion, which can produce AV nodal ischemia and therefore second- or third-degree AV block.
  • Because the block is usually at the AV node, the escape rhythm originates from the AV junction/His region → relatively fast escape rate (~40–60/min) and a narrow QRS because ventricular activation still travels through the normal His-Purkinje system.
  • It is often transient and may improve after reperfusion.


200

Approximately what percentage of patients with HLH may have no hemophagocytosis on initial bone marrow examination? 

Give me one percentage estimate!

 ~30–50%

important point: a negative marrow does not rule out HLH, nor is it needed to make the diagnosis of HLH

200

This type of analysis, performed after the data have been examined and often not specified in the original study protocol, carries an increased risk of false-positive findings.


What is a post-hoc analysis?

200

This U.S. state lends its name to the tick-borne Rickettsia infection famous for causing fever, headache, and a centrifugal rash.

Montana

300

These are the two indications for primary SBP prophylaxis.

  • Low ascitic fluid protein (<1.5 g/dL) + high-risk features — renal dysfunction/hyponatremia or advanced liver failure.
  • Acute upper GI bleeding in a patient with cirrhosis — short-term antibiotic prophylaxis (typically ceftriaxone).
300

This treatment of beta blocker toxicity improves chronotropy and inotropy by activating adenylate cyclase and increasing intracellular cAMP. 

What is Glucagon? 

Glucagon binds its own Gs-coupled receptor → activates adenylate cyclase → ↑ cAMP → ↑ intracellular calcium → improved heart rate and contractility, bypassing the blocked β-receptor. 

300

In the HLH-2004 criteria, fasting elevation of this lipid and/or reduction of this coagulation protein constitute a single diagnostic criterion.

Triglycerides and fibrinogen.

High triglycerides: The cytokine storm—particularly TNF-α—suppresses lipoprotein lipase, impairing triglyceride clearance. Liver dysfunction can contribute as well.

Low fibrinogen: Severe macrophage/T-cell activation produces systemic inflammation with coagulation activation, fibrinogen consumption, and increased fibrinolysis. Significant hepatic dysfunction can further reduce fibrinogen production.

300

A 76-year-old with exertional dyspnea has a normal EF and an equivocal NT-proBNP. Name one validated scoring system that can estimate the likelihood of HFpEF.

What is HF2PEF score?

It estimates the probability that unexplained exertional dyspnea is due to HFpEF using six clinical/echocardiographic variables: obesity, ≥2 antihypertensives, atrial fibrillation, pulmonary hypertension, age >60, and elevated E/e′

  • H₂FPEF score — clinical + echocardiographic variables; gives a probability of HFpEF.
  • HFA-PEFF score — evaluates functional, morphological, and biomarker domains. ≥5 supports HFpEF, ≤1 makes it unlikely, and 2–4 is indeterminate and generally prompts functional testing.
300

In 1976, an outbreak of severe pneumonia among attendees of an American Legion convention occurred in this U.S. city, leading to the discovery of Legionella pneumophila.

Philadelphia

400

These three additional paracentesis studies should be checked when you are concerned about secondary peritonitis.




1.Total protein >1 g/dL

2. Glucose <50 mg/dL

3. LDH > the serum upper limit of normal

These are the three additional ascitic fluid studies used in Runyon’s criteria to help distinguish secondary bacterial peritonitis from spontaneous bacterial peritonitis (SBP). 

The physiology is intuitive: higher protein reflects greater inflammatory/peritoneal injury and protein-rich exudate; low glucose reflects consumption by bacteria and inflammatory cells; and high LDH reflects tissue injury and intense inflammation.

400

In atropine-refractory bradycardia, dopamine and epinephrine both increase chronotropy through β₁ stimulation, but only dopamine also increases sympathetic tone through presynaptic release of this endogenous catecholamine.

What is Norepinephrine?

400

**DAILY DOUBLE**

Fever, thrombocytopenia, anasarca, organomegaly, elevated alkaline phosphatase, and renal dysfunction constitute the clinical syndrome abbreviated TAFRO, which is considered a subtype of this disease.

What is Idiopathic multicentric Castleman disease? 

Rare lymphoproliferative inflammatory disorder causing enlarged lymph nodes throughout the body. Driven largely by excessive IL-6 signaling → systemic inflammation/cytokine release.

TAFRO is an acronym for its major features:

  • T — Thrombocytopenia
  • A — Anasarca → edema, ascites, pleural effusions
  • F — Fever → systemic inflammation
  • R — Reticulin fibrosis / Renal dysfunction
  • O — Organomegaly → lymphadenopathy, hepatosplenomegaly
400

The Lyme disease outbreak that led to recognition of the disease occurred near this Connecticut town.

Lyme, Connecticut


500

A patient with acute Budd–Chiari syndrome undergoes diagnostic paracentesis. Predict the SAAG, ascitic total protein, and PMN count you would expect.

SAAG ≥1.1 g/dL, total protein ≥2.5 g/dL, PMNs <250 cells/mm³.

500

This medication can cause clinically significant bradycardia in older adults by reversibly inhibiting acetylcholinesterase, increasing synaptic acetylcholine and enhancing vagal activity at the SA and AV nodes.

What is Donepezil?

Donepezil is an acetylcholinesterase inhibitor used for symptomatic treatment of Alzheimer disease. Increased acetylcholine can produce vagotonic effects, causing sinus bradycardia or AV block, particularly in susceptible older adults or when combined with other negative chronotropes such as beta-blockers. Other cholinergic adverse effects include nausea, diarrhea, increased secretions, and weight loss.

Major medication causes of bradycardia include:

  • β-blockers — metoprolol, carvedilol, propranolol, ophthalmic timolol
  • Non-DHP calcium-channel blockers — verapamil, diltiazem
  • Digoxin
  • Antiarrhythmics — amiodarone, sotalol, flecainide, propafenone
  • Ivabradine — directly inhibits the SA-node If (“funny”) current
  • Cholinesterase inhibitors — donepezil, rivastigmine, galantamine
  • Lithium — can cause sinus-node dysfunction even at therapeutic concentrations
  • Clonidine — central α₂ agonism → reduced sympathetic outflow
  • Dexmedetomidine — central α₂ agonist; sometimes profound bradycardia
  • Opioids — particularly high doses; fentanyl can be notably vagotonic
  • Fingolimod — S1P-receptor modulation; classically first-dose bradycardia/AV block
  • Certain antineoplastics — e.g., paclitaxel can produce transient bradycardia
500

A 29-year-old with recurrent high-spiking fevers and inflammatory polyarthritis develops this transient, nonpruritic eruption on the trunk and proximal extremities that appears during febrile episodes and fades as the temperature normalizes. ANA and RF are negative.


What is adult onset stills disease?

  • High-spiking quotidian fever — often ≥39°C, typically once or twice daily
  • Evanescent salmon-pink rash — usually trunk/proximal extremities, often appears with fever
  • Inflammatory polyarthritis/arthralgias
  • Sore throat — particularly early and surprisingly characteristic
  • Myalgias
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Pleuritis / pleural effusion
  • Pericarditis
  • Abdominal pain
  • Constitutional symptoms — fatigue, weight loss

Approximately 10–15% of patients with adult-onset Still disease develop macrophage activation syndrome (secondary HLH).

500

This U.S. river valley gave its name to a fungal infection caused by Coccidioides, historically called “Valley fever.”

San Joaquin Valley