CASE 1
What is the underlying cause of the "little red spots" the patient presents with?
What is the underlying cause the skins "yellow tinge" the patient presents with?
Thrombocytopenia
Elevated Bilirubin, secondary to hemolysis
What types of cells are seen on the blood smear? (Be specific)
Helmet Cells --> "Schistocytes"
What is the function of 2,3-BPG?
It decreases hemoglobin's affinity of oxygen, in order to release more oxygen to the peripheral tissues.
What is deficient in Bernard-Soulier Syndrome and what does that alter? What is the characteristic presentation on blood smear?
Glycoprotein IB receptor of platelets, altering the binding of platelets to vWF (adhesion).
Enlarged Platelets would be seen on smear.
APGAR stands for what?
Appearance/Color
Pulse
Grimace/Reflex
Activity/Muscle Tone
Respiration
Describe common complications of TTP
Anemia (due to hemolysis), thrombocytopenia, headaches, confusion, mental changes, speech abnormalities, partial paralysis and seizures.
What do increased serum haptoglobin and serum lactate dehydrogenase indicate?
Destruction of RBCs (hemolysis)
What is the MOA of Warfarin? Also name the "most important" AE seen during initial use of the medication, what causes it and how it can be prevented?
Inhibition of Vitamin K Epoxide Reductase
Warfarin Induced Skin Necrosis, due to the inhibition of protein C and S during initial use. It can be prevented by conjunctional use of Heparin.
Opponens digiti minimi and Flexor Digiti Minimi would be affected, therefore the actions lost would be opposition of the 5th digit as well as flexion of the carpometacarpal and metacarpophalangeal joints of the 5th digit.
In evaluation of occipitoatlantal joint a patient has a deeper right sulcus compared to the left. The sulcus become symmetric in flexion.
What is the diagnosis.
Help with remembering....
DR.SS --> Deep Rotated, Shallow Sidebending
OA --> Opposite Always (or Always Opposite)
What was the utility of asking if the patient had any N/V/D and recent illness or contacts?
(One thing in specific I am looking for)
Most likely to r/o Typical HUS, which is caused by the toxin of E.Coli as the present very similar as well as to r/o other infectious microorganisms.
The point of running the CMP was to r/o which particular disease process?
(although, there may be a couple, which is the one that we should be really be focused on)
HUS as it classical presents with renal impairment
Invasion of apoptosis
Self-Sufficiency | Self-renewal
Immortality
Invasion/Metastasis
Angiogenesis
Dysregulation of Metabolism
Genome Instability
What nerve on the palmar aspect of the hand is not affected by carpal tunnel syndrome? and why is that the case? Is it sensory or motor?
Palmar Branch of the Median N
Because it branches off the median nerve prior to entering the carpal tunnel and then runs over the carpal tunnel to supply cutaneous innervation
List the NEW components of the SOAP note that are now required in unit 3.
*Bonus Points. What is one component is now included in the grading, but not part of the SOAP note.
Past Medical History
Health Maintenance: Cancer screenings
Family History
Surgical History
Impression
*Compassion*
TTP: Plasmapheresis as the ADAMTS13 levels can be replenished and/or levels of vWF can be taken back to normal range with new plasma.
HUS: Treat the symptoms as the it most common caused by a microorganism (infection) and this will usually resolve symptoms.
The coagulation studies were used to differentiate TTP from which disease process?
DIC. (not going to say why because pathogenesis of DIC is discussed later)
What are laboratory results that would appear in iron deficiency anemia v anemia of chronic inflammation?
(Serum Iron, TIBC, % Saturation, Ferritin and Hepcidin)
Iron Deficiency: Decreased serum iron, Increased TIBC, Decreased % Saturation, Decreased Ferritin and Decreased Hepcidin
Anemia of Chronic Disease: Decreased serum iron, Decreased TIBC, Decreased % Saturation, Increased Ferritin and Increased Hepcidin
*Daily Double (Must be fully correct in order to take points away from another team)
Outline the lymph drainage of the breast.
Lateral:
Subareolar lymphatic plexus --> Humeral, Pectoral and Subscapular Nodes --> Central Node --> Apical Node --> Supra/Infraclavicular nodes --> Thoracic duct or Right Lymphatic Trunk
Medial:
Subareolar lymphatic plexus --> Parasternal Nodes --> Bronchomediastinal trunk --> Thoracic duct or Right Lymphatic Trunk
They are 7 counterstrain points for the UE, what are they?
*Points for at least 4
Infraspinatus, Supraspinatus, Levator Scapulae, Subscapularis, Pectoralis Minor, Supinator and Pronator Teres
What is the pathogenesis of TTP?
What is the role of the deficient enzyme?
ADAMTS13 is deficient, either due to a genetic mutation or autoimmune destruction of it.
The role of ADAMTS13 is to degrade vWF when it is no longer needed.
Compare the pathogenesis of HUS to that of DIC
DIC: Abnormal amounts of Thrombin and Fibrin in the circulating blood, thus creating a hypercoagulable state and can use up all the coagulation factors, leading to bleeding in other places. Usually occurs as a secondary complication to other syndromes/disease, such as AML.
HUS
What is the MOA of Eptifibatide? (100)
What is the MOA Clopidogrel? (150)
What is the MOA of Paclitaxel? (250)
Eptifibatide is a competitive inhibitor of the glycoprotein IIb/IIIa receptor, which stops the binding of fibrinogen.
Clopidogrel is a competitive inhibitor of the P2Y12 receptor on platelets, which stops the binding of ADP from binding to platelets (therefore stopping platelet activation and expression of GPIIb,IIIa)
Paclitaxel binds to beta-tubulin enhancing ploymerization, therefore blocking microtubule separation during anaphase.
If a patient severes the MEDIAL CORD of the brachial plexus, which muscles would lose motor function.
Hint* 5 individual muscles and 2 compartments.
*Points for 3 individual and 1 compartment*
Medial cord gives rise to:
Upper Subscapular --> Subscapularis
Middle Subscapular (Thoracodorsal) --> Latissimus Dorsi
Lower Subscapular --> Subscapularis and Teres Major
Axillary --> Deltoid and Teres Minor
Radial --> Posterior Compartment of arm and forearm
A patient has restriction in pronation of the forearm, what is the radial head somatic dysfunction diagnosis?
Bonus points*
What would be the position and motion of treatment for HVLA of the dysfunctional radial head?
Anterior Radial Head
*Patients arm would be put into pronation (directly into the barrier), you (the physician) will have your thumb on the anterior surface of the radial head. Then the arm would be flexed and during that motion you would push the radial head posterior with a gentle thrust.