Random pulmonology notes

Miscellaneous pulmonology notes:

Pleural pearls:

Normal pH of pleural fluid is 7.6 secondary to bicarbonate rich pleural fluid -so if you get a pH of 7.4 that’s actually abnormal

pH and glucose move the same direction- glucose can be falsely elevated or falsely low, rely on the pH
Diagnosis: Urinothorax- if pleural creatinine is greater than two times the serum creatinine
Pleural fluid adenosine deaminase?-high sensitivity for tuberculosis

Cytology will have low sensitivity when you tap midlung field because most of thelymphatics of vasculature are near the diaphragm and so that is why you end up missing it.
Sensitivity of cytology is around 60% but that increases about 10-15% on the second tap
Sensitivity of cytology for a thoracentesis for mesothelioma is around 20%
*Neurovascular bundle in the intercostal is unpredictable within 10 cm of the spine

chylous effusion- lymphoma obstructing the thoracic duct

75% of all pleural effusions?
CHF then pneumonia then malignancy (lung > breast >lymphoma)
CHF the pleural effusion is always transudative

“Never let the sun set on a pleural effusion” as true today as when it was said whenever that was.
CT scan for further evaluating pleural lining.
The parietal pleura secretes most of the effusion.


Miscellaneous neurology notes:

Clinical clue: Classic presentation of neuro invasive West Nile virus
Flaccid paralysis with parkinsonism typically, in the late summer
Post infection fatigue and less up to one year
*yellow fever vaccine can also cause false positive West Nile
**West Nile IgM to be positive in the serum and CSF up to one year


Potent pimpables: Neurological manifestation of Whipple's disease oculomasticatory myodysrhythmia

Transfusion medicine random notes

: Coombs test: elution of cold autoantibody uses anti-complement. elution of warm autoantibodies as antiIgG


Half-life of immunoglobulin G 21 days
Immunoglobulin a monomer in serum but it dimers in secretions

Most likely bacterial contaminant In packed red blood cells Gram-negative rods particularly your Sennea because They like the cold I like iron

Transfusion reaction summary
Hepatitis B 1:220K
Hepatitis C 1:1.8 million
H I V one and 2.3 million


Red blood cell
Intravascular hemolysis: 1:250,000 to 1 in 1 million Mortality is 3.5% Clinical management: Stop transfusion intervenous hydration Maintain renal perfusion Allergic three and 1000 -Only transfusion Reaction where you can restart after pre medication Anaphylaxis one and 17,000 -Most likely etiology anti-immunoglobulin a antibiotic- Don't bother getting an IGA level just get anti-IGA because isotype variation Febrile nonhemolytic: Secondary to anti-granulocyte antibiotics. Stop the transfusion. Dear antipyretics and meperidine for severe rigors


TRALI -transfusion related acute lung injury- One in 5000 presents between three and six hours normally with ARDS picture Most likely etiology of agranulocyte antibodies from the donor-Donor must deferred Platelet Donors are mostly male now because lower risk of leukocyte allo-sensitization

Transfusion associated circulatory overload TACO One 700 presents as dyspnea cough cyanosis chf exacerbation Management is diuresis and supportive

Transfusion related sepsis one and 500,000 for red blood cells 1:12,000 for platelets Red blood cell associated sepsis higher mortality rate

Delayed hemolytic - One in 7000- anamnestic immune response to RBC antigen - Patient will require antigen negative RBC

Graft versus host:- 1:400,000
etiology Lymphocyte contamination Cellular Products the setting of immune compromised host
Presentation is normally between four and 10 days posttransfusion 90% mortality rate
Prevention is with irradiated blood products



Post transfusion Purpura: 1:200k'
Presentation is DIC picture between one and 24 days after transfusion Etiology is antiplatelet antibody Lysis of transfused and autologous platelets Treatment is intravenous immunoglobulin and plasma exchange Patient will require antigen negative platelets or washed products going forward


Iron overload: At least greater than 50 RBC transfusion

GI miscellaneous notes summary

Caudate lobe hypertrophy finding think hepatic vein thrombosis


Ulcerative colitis clinical notes:

Ulcerative colitis flare the max benefit with steroids 40 mg prednisone equivalent not better in 7-10 days?  Not going to get better
Consider steroid enema
   FYI mesalamine makes the diarrhea worse and hold and see what happens
Ulcerative colitis flare did not need to be n.p.o. unless toxic megacolon


Three mechanisms of protein-losing enteropathy

#1.   Malabsorption
#2.   Right-sided cardiac failure

#3.   Lymphedema and poor lymphatic return



Carcinoid
Diarrhea secondary to carcinoid does not happen until metastasis to the liver.
We will therefore go looking in the liver with an ultrasound prior to the fancy expensive serotonin/histamine metabolite urinalysis.


When calculating stool osmolality gap he did not actually need the stool unless you or ruling out factitious diarrhea, in the words of Arora "the sole function of the GI tract is to maintain stool osmolality that of plasma"


"The likelihood of ERCP complication is inverseley proportional to the to the indication of needing it"

Strong indications for ERCP: Common bile duct stone or ascending  cholangitis  or bilirubin greater than four
Melanosis coli finding on colonoscopy indicative of laxative abuse however can also be seen with chronic senna use
Alanine aminotransferase  is not elevated and alcoholic liver disease because  this enzyme is  dependent upon  vitamin B6  which is usually deficient in alcoholics.



Extrahepatic manifestations of hepatitis
1. are normally immune complex regulated and result in deposition to the glomerular basement membrane
2. As well, these circulating immune complexes  are termed mixed cryoglobulinemia and deposit in the vessels and joints.



Councilman bodies- acidophilic degeneration at the bedside secondary viral disease an immune response



Worldwide hepatitis B surface antigen carriers number greater than 350 million
In the words are, "Hep B surface antigen positivity is either acute or chronic"

Incubation period for hepatitis
  hepatitis A-15-45 days
  Hepatitis B and D-3 -180 days
  Hepatitis C  15-160 days mean seven weeks

 



Trivia: What is the eponym for Hepatitis B presentation in children?
  Giannotti-Crosti syndrome -  lymphadenopathy & papular acrodermatitis







What is the differential diagnosis of terminal ileitis?
Inflammatory bowel disorder
   Infection 
       tuberculosis Yersinia actinomyces histoplasmosis CMV
    malignancy lymphoma T-cell, carcinoid
Infiltrative diseases such as amyloid and sarcoid
Vasculitides such as ? and Behçet's disease
Vasoconstrictive medications such as amphetamine cocaine



Clinical triad chronic mesentery ischemia
#1 postprandial pain
#2 sitophobia - abnormal aversion to food
#3 weight loss


**acute mesenteric ischemia CT abdomen is completely normal early on
You need to get selective mesenteric angiography with papaverine

Clinical clue: constipation and renal failure watch for hyperkalemia

Mechanisms of action of lactulose
#1 ammonia ion trapping
#2 catharsis
#3  changing the colonic microFlora to increase nitrogen fixation


infiltrative disorders of the liver commonly present with isolated elevated alkaline phosphatase



Eosinophilic esophagitis
Six food elimination diet -Eggs dairy soy seafood tree nuts wheat
*Dairy and wheat comprised 60% of the clinical response and six food elimination diet
Treatment of eosinophilic esophagitis -proton pump inhibitor - a second line is intranasal budesonide


Gastrografin can cause pneumonitis but less likely mediastinitis  so if suspecting esophageal perforation use this contrast however unfortunately it has low sensitivity
Barium in the mediastinum is bad news so do not use it if you are suspecting esophageal perforation
CT of the chest as the highest specificity and sensitivity for assessing for esophageal perforation



Clinical clue: Drug-induced cholestasis most likely offenders of antibiotics are clavulanic acid and trimethoprim sulfamethoxazole


Clinical clue: differentiating hyperkeratinemia from jaundice - not likely to find scleral icterus in patients that have hypervitaminosis A.


Landmark study - new England  journal of medicine medicine 1999-
Spontaneous bacterial peritonitis trial arms were antibiotics versus antibiotics plus albumin mortality 30% decreased to 15% in the antibiotics/albumin arm
pathophysiological mechanism: albumin decreased acute kidney injuries #1 driver and mortality benefit
The one year relapse rate of spontaneous bacterial peritonitis roughly 70%.
-> with antibacterial prophylaxis this is less than 10% annually
*drawbacks include increased microbial resistance

Why are we using ceftriaxone as a treatment for spontaneous bacterial peritonitis?
because cultures are showing increased enterococcus so you want gram positive coverage.

Recurrent ascites?
#1 salt restriction- this works less than 10% secondary to nonadherence
#2 furosemide : spironolactone ratio 1:2.5 spironolactone has the mortality benefit furosemide is incorporated to maintain potassium homeostasis
#3 large-volume paracentesis versus TIPS
#4 transplant
TIPS are good for variceals bad for ascites meld score greater than 18
bad prognosis for TIPS




Clinical clue: Wilson’s - picking up the diagnosis
Young female acute liver failure hemolyzing
Decreased alkaline phosphatase? secondary to zinc depletion because of copper overload
increases in AST? - RBC membrane rich in AST
The treatment is liver transplant can be lifesaving.





Little known treatment for obscure GI bleed:
Thalidomide 100 mg daily for four months side effects: edema fatigue constipation


Ascorbic acid in high doses can cause a calcium oxalate crystals because vitamin C tablets often contain oxalic acid



Causes of hepatic encephalopathy...
Hypovolemia
Gastrointestinal bleeding
Hypokalemia secondary to ammonia production
Portal vein thrombosis shunting
Hypoxia
Infection SBP
Hepatocellular carcinoma although rare
Sedatives

Clinical clue: reversal sleep wake pattern is seen in hepatic encephalopathy







Ammonia (serum)
Venous or arterial? arterial is better but must be kept on ice the longer and since the higher will go up
only 20-30% of people with hepatic encephalopathy will have abnormal ammonia level making its negative predictive value weak



CELIAC DISEASE
Fun fact: Celiac disease is named such because pathologic bowel is found to be perfused by this arterial branch
lymphoma associated with celiac disorder is enteropathy associated T-cell lymphoma



Diagnostic criteria for celiac disease he need all three if you do not have all three reconsider your diagnosis
#1 positive serology
#2 small bowel biopsy
#3 positive response to gluten-free diet



What is the differential diagnosis of intrahepatic cholestasis?
Hepatitis
drug-induced
PBC
postop
pregnancy
graft-versus-host
sepsis


Differential diagnosis of benign extrahepatic cholestasis?
Postop cholestasis
PSC
IgG4
AIDS
cholangiopathy
Mirizzi syndrome



Malignant etiologies of extrahepatic cholestasis?
cholangiocarcinoma
adenopathy secondary to a systemic disorder (lymphoma)
pancreatic cancer



Contraindications for corticosteroids with people who have high discriminate function?
Renal failure
infection
GI bleed

Silver stool? Thoman’s sign- happens with the combination of acholic stools and gastrointestinal bleeding, will turn silver-colored.

celiac and familial adenomatous polyposis have a 5% overlap

Daptomycin:  Monitor creatinine kinase weekly or you will be sued, another complication his pulmonary infiltrates with eosinophilia AKA PIE, and finally its deactivated by surfactant so don’t use it for pneumonia

Risk for hepatocellular carcinoma with hepatitis B can happen prior to developing cirrhosis
The risk for hepatocellular carcinoma with hepatitis C happens after progression to cirrhosis


In familial adenomatous polyposis after resection of the colon the next most common presentation is ampullary tumor in the duodenum

Bililrubins greater than 20 are always intrahepatic cholestatic.