Myocardial Perfusion Imaging: Mechanism

Functions on the premise of mismatch in coronary perfusion after a vasodilator (e.g dipyridamole) is administered. 

HOW? The coronary vessels with disease burden are already maximally dilated, hence after the addition of the vasodilator, perfusion mismatch occurs as the healthier vessels dilate further.

False NEGATIVES:

  • Caffeine or theophylline can interact with dipyridamole.
  • Severe flow limiting triple vessel disease or LEFT main diseae (may both cause a balanced defect). 

CONTRAINDICATIONS:

  • Severe airway disease (COPD or Asthma)

BONUS: reversal agent to dipyridamole is amiophylline.

REFERENCES

  1. Driessen, Roel S et al. “Myocardial perfusion imaging with PET.” The international journal of cardiovascular imaging vol. 33,7 (2017): 1021-1031. doi:10.1007/s10554-017-1084-4
  2. Burrell S, MacDonald A. Artifacts and pitfalls in myocardial perfusion imaging. J Nucl Med Technol. 2006 Dec;34(4):193-211; quiz 212-4.

 

Hepatopulmonary syndrome vs. Portopulmonary hypertension

Often confused as the same syndrome, Hepatopulmonary syndrome and Portopulmonary hypertension are two distinct disease processes. Both are characterized as pulmonary vascular abnormalities in the context of liver disease.

 

Hepatopulmonary Syndrome (HPS): triad of vasodilatation (Intrapulmonary vascular dilatations), abnormal oxygenation (an elevated alveolar-arterial oxygen gradient) and liver disease (any degree of liver disease). *LOOK FOR: digital clubbing, cyanosis and spider angiomas.

 

Portopulmonary hypertension (POPH): vascular obstruction secondary to portal hypertension (varices, splenomegaly, thrombocytopenia, portal vein abnormalities) with concomitant pulmonary arterial hypertension (mean pulmonary artery pressure >25 mmHg at rest, mean pulmonary capillary wedge pressure <15 mmHg, and pulmonary vascular resistance (PVR) >3 Wood units.

 

REFERENCES:

1. Porres-Aguilar M, Altamirano JT, Torre-Delgadillo A, Charlton MR, Duarte-Rojo A. Portopulmonary hypertension and hepatopulmonary syndrome: a clinician-oriented overview. Eur Respir Rev. 2012 Sep 1;21(125):223-33. doi: 10.1183/09059180.00007211.

2. Gupta S, Krowka M J. Hepatopulmonary syndrome. CMAJ Feb 2018, 190 (8) E223; DOI: 10.1503/cmaj.170253

7 I’s of DKA: Causes Mnemonic

When a patient presents with DKA, it is important to try to elucidate the cause. An easy way to remember those causes are the 7 I’s of DKA:

  1. Infection: Look for potential infectious foci (pneumonia, bacteremia, UTI etc.).
  2. Ischemia: Such as ACS, critical limb ischemia or ischemic bowel.
  3. Intoxication: ETOH, MDMA, Cocaine, Methamphetamine etc. 
  4. Infraction/ Intolerance: Patient not taking their insulin. 
  5. Iatrogenic: Secondary to medications (i.e steroids) or surgeries.
  6. Initial Presentation: First time presentation typically in young children. 
  7. Impregnation: Increased metabolic demands of pregnancy make precipitate an episode of DKA.

*NOTE: These causes are also precipitants for Hyperosmolar Hyperglycemic State (HHS).

REFERENCES

  1. Umpierrez GE, Kitabchi AE. Diabetic ketoacidosis: risk factors and management strategies. Treat Endocrinol. 2003;2(2):95-108.

Alpha 1 Anti Trypsin: Pi*MM, Pi*MZ, Pi*ZZ, Pi*null

Alpha1 antitrypsin (α1 AT) deficiency is the only known genetic abnormality that leads to COPD; it accounts for less than 1% of COPD in the United States.

Typically:

  • Basilar-predominant hyperlucency on chest imaging -> early-onset emphysema (eg, before age 55).
  • Occurrence of emphysema in a non- or trivial-smoker, or a family history of liver or lung disease.

WHY? Unimpeded neutrophil elastase contributes to the alveolar destruction of emphysema.

NAMING (disease is inherited co-dominant)

Pi*MM– Normal

Pi*S (essentially normal; leading to a mild decrease in circulating A1-PI)

Pi*null– They do NOT make any alpha-1 antitrypsin. The rare null variants that are characterized by complete absence of AAT synthesis; does not cause liver disease.

Pi*MZ– heterozygous. Heterozygotes are not deemed to be at significant risk of developing emphysema.

PI*ZZ– Homozygotes for the severe deficiency allele Z. Most* but not all severely deficient individuals develop emphysema, risk for which is markedly increased by smoking. For liver disease, the lifetime risk is estimated to be approximately 40%.

Copyright: Craig TJ 2015.

*More than 95% of persons in the severely deficient category are homozygous for the Z allele, designated PiZZ.

REFERENCES

  1. Craig TJ. Suspecting and Testing for Alpha-1 Antitrypsin Deficiency-An Allergist’s and/or Immunologist’s Perspective. J Allergy Clin Immunol Pract. 2015 Jul-Aug;3(4):506-11. doi: 10.1016/j.jaip.2015.04.005. Epub 2015 May 29.
  2. Stoller JK, Aboussouan LS. A review of α1-antitrypsin deficiency. Am J Respir Crit Care Med. 2012;185:246–59.
  3. de Serres F, Blanco I. Role of alpha-1 antitrypsin in human health and disease. J Intern Med. 2014;276:311–35.

Why Prednisolone for Alcoholic Hepatitis?

Patients presenting with severe alcoholic hepatitis (Discriminant Function value ≥32) have high short-term mortality and may benefit from treatment with glucocorticoids.

Prednisolone is used as oppose to prednisone for 28 days (with taper).

 

WHY? Prednisone requires conversion to prednisolone (the active metabolite) in the liver. This process may be impaired in alcoholic hepatitis.

 

REFERENCES

  1.  Ramond MJ, Poynard T, Rueff B, Mathurin P, Theodore C, Chaput JC, Benhamou JP. A randomized trial of prednisolone in patients with severe alcoholic hepatitis. N Engl J Med 1992; 326:507. 
  2. Friedman SL, McQuaid KR, Grendell JH, et al. Current Diagnosis & Treatment in Gastroenterology, 2nd ed, McGraw-Hill Medical 2002.

Factor VIII: DIC vs Liver Disease (Cirrhosis)

Distinguishing between the coagulation abnormalities of liver disease vs. Disseminated intravascular coagulation (DIC) can be difficult as clinical and biochemical findings are similar.

However, Factor VIII levels are usually increased or normal in liver disease. 

Whereas, Factor VIII levels are decreased in DIC.

WHY? Factor VIII is produced in endothelial cells rather than the liver; hence it is not affected by the process of cirrhosis.

REFERENCES

  1. Senzolo M, Burra P, Cholongitas E, Burroughs AK. New insights into the coagulopathy of liver disease and liver transplantation. World J Gastroenterol. 2006;12(48):7725-36.
  2. Mammen EF. Coagulation abnormalities in liver disease. Hematol Oncol Clin North Am. 1992 Dec;6(6):1247-57.

What is Hoover Sign?

Hoover’s sign refers to the paradoxical inspiratory retraction of the rib cage and lower intercostal

interspaces. Normally, the costal margin moves minimally during the regular respiratory cycle. However, if it does, it moves outward and upward.

It is commonly seen in COPD. However, it may also be seen in numerous other conditions (i.e congestive heart failure, asthma, severe pneumonia etc.)

It results from alterations in dynamics of diaphragmatic contraction due to hyperinflation, resulting in traction on the rib margins by the flattened diaphragm.

REFERENCES

  1. Klein M: Hoover sign and peripheral airways obstruction. JPediatr 1992, 120:495-496.
  2. Johnston, Chambless R et al. “The Hoover’s Sign of Pulmonary Disease: Molecular Basis and Clinical Relevance” Clinical and molecular allergy: CMA vol. 6 8. 5 Sep. 2008

Why does the lupus malar rash spare the nasolabial folds?

Malar rash (also known as the “butterfly rash,”) is an acute manifestation of lupus (SLE) seen in over 50% of patients. It is a bilateral, erythematous maculopapular rash which spares the nasolabial folds. The rash will last anywhere from days to weeks, and it can be painful/ itchy. It is a photosensitivity phenomenon.

Suspected Mechanism: the nasolabial folds are a relatively UV protected surface and therefore less affected.

REFERENCES:

  1. Amre Nouh, Jodi Speiser, José Biller. Chapter 3 – Acquired neurocutaneous disorders. Handbook of Clinical Neurology. Volume 132, 2015, Pages 29-73
  2. Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology, 8e. Klaus Wolff, Richard Allen Johnson, Arturo P. Saavedra, Ellen K. Roh. THE SKIN IN IMMUNE, AUTOIMMUNE, AUTOINFLAMMATORY, AND RHEUMATIC DISORDERS.

Why no Nitrates in Right Ventricle Myocardial Infarction (MI)?

Up to 40% of inferior wall Myocardial infarctions have associated right ventricular involvement. Venodilation and medications that decrease RV filling (i.e nitrates, diuretics) should be avoided.

WHY?

The right ventricle contains less myocardial tissue compared to the left ventricle. It is more dependent on adequate preload (Frank-Starling curve) to assure adequate cardiac function (CO). If there is damage to the right ventricle, preload reduction from nitrates/ diuresis could result in significant hypotension.

REFERENCES

  1. Albulushi A., et al. Acute right ventricular myocardial infarction. Expert Rev Cardiovasc Ther. 2018 Jul;16(7):455-464.
  2. Bouhuijzen LJ, Stoel MG. Inferior acute myocardial infarction with anterior ST-segment elevations. Neth Heart J. 2018 Oct;26(10):515-516.

What is Ventricular interdependence?

Ventricular interdependence occurs when there is discordance. This results from the heart ventricles filling out of phase with one another. It is an important physiological manifestation of cardiac tamponade and constrictive pericarditis.

The ventricles experience impaired diastolic relaxation secondary the constrictive pericardium and are unable to fully expand. During inspiration, the right ventricle will fill and shift the interventricular septum to the left reducing its filling capacity. During expiration, the opposite will occur with the interventricular septum moving to the right.
REFERENCES
  1. Santamore WP, Dell’Italia LJ. Ventricular interdependence: significant left ventricular contributions to right ventricular systolic function. Prog Cardiovasc Dis. 1998 Jan-Feb;40(4):289-308.