Friday, April 21, 2017
Wednesday, April 12, 2017
Palpating Carotids Bilaterally
Why should you not palpate your patient's carotids arteries bilaterally?
I remember being told it could cause less blood flow to the brain. However would that caused by the pressure you place on the vessels? Do you cut off the blood supply?
It is actually because of the carotid body located near the bifurcation of the carotid artery. The carotid body is a bundle of mechanoreceptors that reacts to changes in pressure. If you were to increase the pressure on the carotid body, it would set of the baroreceptor reflex. It signals to the brain that there is an increase in systemic pressure, and then the brain signals the body to lower blood pressure. As a result, there is less blood flow to the brain.
Thanks to Dr. Koehler and Danny!
I remember being told it could cause less blood flow to the brain. However would that caused by the pressure you place on the vessels? Do you cut off the blood supply?
It is actually because of the carotid body located near the bifurcation of the carotid artery. The carotid body is a bundle of mechanoreceptors that reacts to changes in pressure. If you were to increase the pressure on the carotid body, it would set of the baroreceptor reflex. It signals to the brain that there is an increase in systemic pressure, and then the brain signals the body to lower blood pressure. As a result, there is less blood flow to the brain.
Thanks to Dr. Koehler and Danny!
Monday, April 10, 2017
RA Treatment
NSAIDs and glucocorticoids are used to treat the symptoms of rheumatoid arthritis, while traditional and biologic DMARDs are used to treat active RA.
NSAIDs inhibit either COX-1 or COX-2, or even both. In the treatment of rheumatoid arthritis, these drugs inhibit the production of prostaglandins from arachidonic acid leading to a decrease in inflammation. One adverse effect is decrease in cytoprotection in GI via inhibition of COX-1.
Aspirin-irreversibly blocks COX-1 and COX-2, hypersensitivity (bronchospasms), Reye's syndrome, acute and chronic salicylate poisoning (ion trapping)
Acetaminophen-metabolism via sulfation/glucuronidation + CYP2E1+ glutathione detoxification, NAC for toxicity
Traditional NSAIDs
Propionic Acid Derivatives
Ibuprofen-close ductus arteriosus, inhibit aspirin
Naproxen-can be used to treat pain and fever in children>12yo
Acetic Acid Derivatives
Indomethacin-close ductus arteriosus, gout, tocolytic
Ketoroloac-non-selective, seasonal allergies, does not penetrate CSF
Diclofenac-mostly COX-2, hypersensitivity
Enolic Acid Derivative
Meloxicam-OA and RA
Coxib
Celecoxib-COX-2 selective, no GI effects or bronchospasm but higher risk of CVD
Glucocorticoids interfere with the HPA by acting like cortisol, which then represses transcription. In turn humoral and cellular immunity are suppressed. Glucocorticoids are started and taper down in dose. The adverse effects of glucocorticoids can be summed up as Cushing Syndrome.
Methotrexate (first line traditional DMARD) inhibits DHFH, TYMS, and AICAR formyl transferase. The inhibition of DHFH and TYMS leads to decrease in DNA and RNA synthesis, and so less cell proliferation. The inhibition of AICAR formyl transferase leads to an accumulation in adenosine, which is responsible for MTX's anti-inflammatory effects. MTX can cause GI problems because it is a folate analog, so to treat these adverse effects the patient can take folate (Leucovorin). MTX can also interact with various drugs like penicillin, NSAIDs, aspirin, sulfonamides, probenecid (gout treatment) via competition with OAT. MTX can be displaced by salicylates, doxycycline, phenytoin (prevent seizures).
Other traditional DMARDs include Sulfasalazine (unknown mechanism but is capable of displacing MTX + hypersensitivity), Choloroquine (stabilizes lysosomal membranes and inhibits enzymes responsible for cartilage breakdown), and Leflunomide (inhibits DHODH-->inhibits de novo pyrimidine synthesis). Leflunomide is a teratogen (cause malformation of embryo).
The biologics can be divided into TNF-alpha antagonists and lymphocyte modulating biologics.
TNF-alpha Antagonists (need to screen for exposure to Hep B/C and tuberculosis)
Infliximab-binds to both soluble and membrane cytokine
Etanercept-binds to both soluble cytokine
Adalimumab-human mAb
Golimumab-human mAb
Certolizumab-lacks Fc fragment on antibody-->does not induce complement activation
Lymphocyte Modulating Biologics
Abatacept-inhibit T cell activation
Rituximab-inhibit B cell activation
Tocilizumab-IL-6 antagonist
Anakira-inhibits IL-1 receptor
Tofacitinib-inhibit JAK3 enzyme (cannot phosphorylate STAT-->affects transcription)
NSAIDs inhibit either COX-1 or COX-2, or even both. In the treatment of rheumatoid arthritis, these drugs inhibit the production of prostaglandins from arachidonic acid leading to a decrease in inflammation. One adverse effect is decrease in cytoprotection in GI via inhibition of COX-1.
Aspirin-irreversibly blocks COX-1 and COX-2, hypersensitivity (bronchospasms), Reye's syndrome, acute and chronic salicylate poisoning (ion trapping)
Acetaminophen-metabolism via sulfation/glucuronidation + CYP2E1+ glutathione detoxification, NAC for toxicity
Traditional NSAIDs
Propionic Acid Derivatives
Ibuprofen-close ductus arteriosus, inhibit aspirin
Naproxen-can be used to treat pain and fever in children>12yo
Acetic Acid Derivatives
Indomethacin-close ductus arteriosus, gout, tocolytic
Ketoroloac-non-selective, seasonal allergies, does not penetrate CSF
Diclofenac-mostly COX-2, hypersensitivity
Enolic Acid Derivative
Meloxicam-OA and RA
Coxib
Celecoxib-COX-2 selective, no GI effects or bronchospasm but higher risk of CVD
Glucocorticoids interfere with the HPA by acting like cortisol, which then represses transcription. In turn humoral and cellular immunity are suppressed. Glucocorticoids are started and taper down in dose. The adverse effects of glucocorticoids can be summed up as Cushing Syndrome.
Methotrexate (first line traditional DMARD) inhibits DHFH, TYMS, and AICAR formyl transferase. The inhibition of DHFH and TYMS leads to decrease in DNA and RNA synthesis, and so less cell proliferation. The inhibition of AICAR formyl transferase leads to an accumulation in adenosine, which is responsible for MTX's anti-inflammatory effects. MTX can cause GI problems because it is a folate analog, so to treat these adverse effects the patient can take folate (Leucovorin). MTX can also interact with various drugs like penicillin, NSAIDs, aspirin, sulfonamides, probenecid (gout treatment) via competition with OAT. MTX can be displaced by salicylates, doxycycline, phenytoin (prevent seizures).
Other traditional DMARDs include Sulfasalazine (unknown mechanism but is capable of displacing MTX + hypersensitivity), Choloroquine (stabilizes lysosomal membranes and inhibits enzymes responsible for cartilage breakdown), and Leflunomide (inhibits DHODH-->inhibits de novo pyrimidine synthesis). Leflunomide is a teratogen (cause malformation of embryo).
The biologics can be divided into TNF-alpha antagonists and lymphocyte modulating biologics.
TNF-alpha Antagonists (need to screen for exposure to Hep B/C and tuberculosis)
Infliximab-binds to both soluble and membrane cytokine
Etanercept-binds to both soluble cytokine
Adalimumab-human mAb
Golimumab-human mAb
Certolizumab-lacks Fc fragment on antibody-->does not induce complement activation
Lymphocyte Modulating Biologics
Abatacept-inhibit T cell activation
Rituximab-inhibit B cell activation
Tocilizumab-IL-6 antagonist
Anakira-inhibits IL-1 receptor
Tofacitinib-inhibit JAK3 enzyme (cannot phosphorylate STAT-->affects transcription)
Sunday, April 9, 2017
Wednesday, March 15, 2017
Thursday, March 2, 2017
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