Fact(s) of the day!

[jfgavina]

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So this thread works for the people that are taking the examination in the next few weeks to write facts so others can learn! we can put a fact here each day or more if you want! and try to write it w/o consulting the book 🙂 others can correct if its wrong

 

[jfgavina]

my fact of the day!!

:

SNc stimulates motion by 2 mechanisms:

1. Stimulating the excitatory pathway
2. Inhibiting the inhibitory pathway


1.1. Dopamine is released from pars compacta activating D1 receptors in striatum (which is composed by caudate (for cognition) and putamen (for motion))
1.2. Striatum releases GABA and substance P which is going to inhibit GPi and SNr
1.3. SNr and GPi stop doing their usual job of inhibiting VA and VL nucleus of thalamus
1.4. thalamus is free to stimulate motor cortex allowing movement!

2.1. Dopamine is released from SNc to bind D2 receptors which inhibit GABA and enkephalin release
2.2. striatum stops releasing GABA which would eventually inhibit GPe
2.3. GPe is free to inhibit subthalamic nucleus
2.4. subthalamic nucleus stops stimulating GPi
2.5. GPi stops inhibiting VA and VL of thalamus because its not being stimulated by subthalamic nucleus
2.6 thalamus is free to stimulate cortex


clinical pearl:

-lesion is substantia nigra pars compacta is going to stop stimulation of stimulatory and inhibition of inhibitory therefore you get bradykinesia .

-lesion in subthalamic nucleus is indirectly going to prevent inhibition of thalamus via stopage of GPi stimulation resulting in less modulation of movement in thalamus resulting in contralateral hemibalismus!

-atrophy of striate nuclei lead to less inhibition of movement and dementia (huntington's)


hope my fact was useful for you and I'm waiting for yours!

 

[1badvette]

Factor V " NAD+ that is needed for H-influenzae can be supplemented by growing H.influ around a colony of S.aureus ..

Burkitts Lymphoma can also have a T(8-22) and T(2:8) not just T(8:14) ..

Plasmacytoma --> soft tissue myeloma found commonly in lungs , nasopharynx and nasal sinuses , plasma cell proliferation , IgG M spike with no lytic bone lesions .

 

[jfgavina]

medial medullary syndrome - occlusion of the anterior spinal artery:

- contralateral hemiparesis
- contralateral loss of proprioception and touch
- ipsilateral hypoglossal damage (tongue deviates to side of lesion)

lateral medullary syndrome - occlusion of PICA:

- loss of temperature and pain sensation over the contralateral body due to damage of spinothalamic
- loss of ipsilateral temperature and pain sensation of face due to damage of trigeminal
- ipsilateral dysphagia, hoarseness and loss of gag reflex due to damage of nucleus ambiguous (contains vagus and glossopharyngeal)
- ipsilateral nystagmus, vertigo, nausea/vomiting due to vestibular damage
- ispilateral ataxia due to damage of inferior cerebellar peduncle
- ipsilateral horner's syndrome due to damage of descending sympathetic trunk


lateral inferior pontine syndrome - occlusion of AICA

-ipsilateral facial nerve lesion and loss of taste from anterior 2/3 of tongue due to damage of facial nucleus and solitary tract
-ipsilateral deafness, tinnitus, vertigo and nystagmus due to damage of vestibulo cochlear
- ipsilateral loss of temperature and pain sensation of face due to damage of trigeminal nerve
- contralateral temperature and pain sensation of body due to damage of spinothalamic
-ipsilateral ataxia due to damage of middle and inferior cerebellar peduncle
-ipsilateral horner's syndrome due to damage of sympathetic descending trunk


and enough of memorizing medullary syndromes, if other appears will use exclusion technique because only God knows how much it cost me to memorize these ones. I have HY neuro back in my home so if someone knows a good website where I can see the actual medulla gross cuts w/ corresponding syndromes I would be thankful

 

[rahul0515]

that last post was i think word for word on the DIT handout

 

[jfgavina]

you're right! I think FA is too incomplete on these

 

[jfgavina]

Angiotensin II causes contraction alkalosis by enhacing Na/H transporter on PCT putting more H+ outside which in turn causes HCO3- reabsorption. also, by stimulating release of aldosterone will cause indirectly more excretion of H+ from alpha-intercalated cells in collecting duct, and further generation of HCO3- to be reabsorbed in exchange for Cl-

 

[pbnj003]

The normal function of CFTR is to not ONLY secrete Cl- ions into lumen but also inhibit Na reab back into the cell.

Therefore in a case with CFTR mutation one test is the obvious Sweat Test. However, in cases where theres a mild mutation, sometimes the sweat test comes back normal. In such cases Nasal transepithelial potential difference is the diagnostic test.

Since the CFTR channel is mutated it is not able to inhibit the Na reab from the lumen, widening the potential difference between the surface of the respiratory epithelium and interstitium.

This was a question in UWorld that totally bugged me! If it werent for this question I probably wouldv only stuck with "CFTR secrets Cl" and forgotten about its other functions!

 

[jfgavina]

-in PDA, late reversal of left-to-right to right-to-left will manifest as differential cyanosis, cyanosis of lower extremities only

 

[jfgavina]

- atrial contraction is required for s4 sound production (a/w stiff hypertrophiated left ventricle)

- PCWP will not reflect left ventricular end diastolic pressure in cases of mitral stenosis

- -xabans are a newer class of anticoagulants that inhibit factor X

- Congenital long QT syndromes are a/w dysfunction in K+ channels, preventing rapid efflux of + during repolarization phase


- http://www.youtube.com/watch?NR=1&v=0QPWHBmqOAA nice song for some pre-exam relaxation

 

[jfgavina]

- comedocarcinoma: a pattern of DCIS of the major duct of the breast marked by areas of central necrosis


did RR goljan bioch margin notes today and RR goljan path images. tomorrow will review some neuro images and CTs and start my last FA read (I've been reading it so many times that I'm actually feeling depressed knowing it is my last time. try to read a bood more than 5 times to see if it doesn't happen lol)

 

[1badvette]

Pneumocystis Jiroveci --> can lead to over production of type 2 pneumocytes and surfactant rich exudate filling the alveolar sac and causing death by asphyxiation " choking"