Here's a playlist I made from a few Youtube videos. Heart Murmurs Many thanks to Thinklabs for having so many examples.
Of course we also need to know how they change with maneuvers.
Wednesday, March 28, 2018
Monday, March 26, 2018
Microbiology Review
I've attached some charts for microbiology. The yellow boxes are for characteristics that are used to differentiate species. It's also a good idea to add notes on each bug. ^.^
Tuesday, March 6, 2018
Review Questions
A 55 yo patient presents to the ER with subacute endocarditis. Patient’s history was significant for a recent dental procedure. What allows for the organism to bind to damaged heart valves?
A. Pili
B. Dextrans
C. Biofilm
D. TSST-1
E. Protein A
A 6 month old child presents to the clinic with hypotonia. History was significant for ingestion of honey containing spores of a gram (+) rod. What is the mechanism of the toxin produce by this organism?
A) cleavage of SNARE protein inhibiting GABA release
B) damage of cell membranes
C) inhibition of Ach release
D) depolymerization of actin
E) ADP-ribosylation of EF-2
A 10 yo patient presents to the clinic with hematuria. 2 weeks ago, patient had a honey crusted lesion on his face but did not see a physician. Another infection by this organism is pharyngitis. A complication of pharyngitis is a result of antibodies to which portion of the organism?
A. Capsule
B. Protein A
C. Cell wall
D. M protein
E. Erythrogenic toxin
22yo female presents with fatigue for the past few days. Patient became a vegetarian 3 months ago. Blood tests show a decreased MCV but normal ferritin. Patients experienced no other symptoms. What is the cause of RBC damage in this condition?
A) lack of membrane protein that anchors DAF
B) glutamate to valine mutation
C) iron deficiency
D) tetramers of excess globin chains
E) Vitamin B12 deficiency
B
C
D
D
A. Pili
B. Dextrans
C. Biofilm
D. TSST-1
E. Protein A
A 6 month old child presents to the clinic with hypotonia. History was significant for ingestion of honey containing spores of a gram (+) rod. What is the mechanism of the toxin produce by this organism?
A) cleavage of SNARE protein inhibiting GABA release
B) damage of cell membranes
C) inhibition of Ach release
D) depolymerization of actin
E) ADP-ribosylation of EF-2
A 10 yo patient presents to the clinic with hematuria. 2 weeks ago, patient had a honey crusted lesion on his face but did not see a physician. Another infection by this organism is pharyngitis. A complication of pharyngitis is a result of antibodies to which portion of the organism?
A. Capsule
B. Protein A
C. Cell wall
D. M protein
E. Erythrogenic toxin
22yo female presents with fatigue for the past few days. Patient became a vegetarian 3 months ago. Blood tests show a decreased MCV but normal ferritin. Patients experienced no other symptoms. What is the cause of RBC damage in this condition?
A) lack of membrane protein that anchors DAF
B) glutamate to valine mutation
C) iron deficiency
D) tetramers of excess globin chains
E) Vitamin B12 deficiency
B
C
D
D
Saturday, March 3, 2018
Heparin + Warfarin
Why do we give heparin before starting long-term warfarin? Warfarin knocks out Vitamin K epoxide reductase in the liver. This decreases factors 2, 7, 9 and 10. It also decreases protein C and S, which inactivate the coagulation cascade. Although synthesis is stopped, there are still pre-existing factors within the blood. The first ones to decrease are protein C and S. Uh oh...that means you still have coagulation factors floating around and nothing to stop them. This hypercoagulable state could result in skin necrosis! Not to worry. This is why we give heparin to transition the patient onto warfarin therapy. What does heparin do? It binds to antithrombin 3 which inhibits factors 2 and 10.
Vit B12 Deficiency
Vitamin B12 is carries a methyl group from tetrahydrofolate to homocysteine. Homocysteine is then converted in methionine. Without B12, the methyl group cannot be added, increasing levels of homocysteine which makes the blood hypercoagulable.
Thursday, March 1, 2018
Neuro Pathology
Parkinson Disease
Loss of dopaminergic cells in substantia nigra pars compacta (in the basal ganglia) disrupts movement. Classic presentation is tremor, cogwheel rigidity, akinesia, postural instability, and shuffling gait. The condition is associated with Lewy bodies, which are aggregates of α-synuclein.
Huntington Disease
Treatment:
levodopa
carbidopa
entacapone/tolcapone
selegiline
benztropine
bromocriptine, pramipezole, ropinirole
amantadine
Huntington Disease
Huntington disease is an autosomal dominant CAG repeat disorder on chromosome 4. This trinucleotide expansion can result in a gain-of-function that disrupts the normal transcriptional repression by huntingtin. This increases histone deacetylation (so increased transcriptional repression), silencing the genes necessary for neuronal survival. Condition is characterized by chorea, aggression, depression, and dementia.
Alzheimer Disease
APP is usually degraded into A-α but in Alzheimer's, it is degraded into A-β amyloid forms seniles plaques. Neurofibrillary tangles formed from hyperphosphorlyated tau proteins, which are normally in the cytoskeleton.
Treatment:
tetrabenazine, reserpine
haloperidol
Alzheimer Disease
APP is usually degraded into A-α but in Alzheimer's, it is degraded into A-β amyloid forms seniles plaques. Neurofibrillary tangles formed from hyperphosphorlyated tau proteins, which are normally in the cytoskeleton.
Plaques will lead to widespread cortical atrophy, which can present as hydrocephalus ex vacuo. ApoE2 is associated with decreased risk, while ApoE4 is associated with increased risk. Alzheimer is also associated with APP, presenilin-1, and presenilin-2.
Treatment:
memantine
donepezil, galantamine, rivastigmine
Frontotemporal Dementia
Inclusions of hyperphosphorlyated tau proteins form Pick bodies. Frontal lobe involvement results in behavioral changes. Temporal lobe involvement results in aphasia.
Lewy Body Dementia
Lewy bodies are aggregates of α-synuclein. Condition presents as dementia first, then parkinsonian symptoms.
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