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Arterial supply to the brain

Brown Sequard syndrome

A spinal cord hemi-section results in ipsilateral spastic weakness (Corticospinal tract), ipsilateral decreased vibration/proprioception (Fasciculus gracilus and cuneatus), and contralateral decreased pain and temperature.

Degeneration of dopamine producing neurons

Less dopamine will stimulate D1 receptor less, produce less GABA going to output nuclei (inhibit output nuclei less), so these put out more GABA to VA nucleus

More inhibition of VA = less glutamate to motor cortex

Indirectly, less inhibition of D2, will put out more GABA to external GP (inhibit it more), will put out less GABA to subthalamic nucleus, will release more Glutamate, which will stimulate internal GP to produce more GABA, inhibit VA more, less glutamate to the Cortex

The five areas of trauma that cause urine leakage: 1 = Rupture of the "Superior Wall of the Urinary Bladder" (Dome) results in extravasation of urine into the "Peritoneal Cavity" (PC). 2 = Rupture of the "Anterior Wall of the Urinary Bladder" results in extravasation of urine into the "Retropubic Space of Retzius (RPS). 3 = Rupture of the "Urethra Above the Urogenital Diaphragm"(UG) results in extravasation of urine into the "Retropubic space of Retzius". 4 = Rupture of the "Urethra Below the Urogenital Diaphragm" results in extravasation of urine into the "Superficial Perineal space". *Note that extravasated urine within the superficial perineal space can extend into the scrotal, penile, and anterior abdominal wall areas. 5 = Rupture of the "Penile Urethra" with INTACT Buck Fascia results in extravasation of urine "Beneath the Deep Fascia of Buck" and will remain "Confined to the Penis" *Note that If "Buck Fascia get SEVERED" in Penile Urethral Injury, urine will make it into the space Underneath Dartos Fascia" and from here it can spread to scrotum, superficial perineal space and anterior abdominal wall. PS = pubic symphysis; dots = urine.

#anatomy #penile fracture #pelvis #reproductive organs #TC5 #Gross Anatomy #USMLE1 #Step 1 #Medical school #Diagrams

Parinaud’s Syndrome (Dr. Cole recommendation)

#Parinaud's #USMLE1 #Neurology #Medical school #TC5 #videos

Addison’s vs Cushing’s disease

#Endocrinology #TC5 #Physiology #Renaldisorders #addison's disease #Cushing's disease #medical school #MS1 #google image results #personal table #original table #medical tables

Renal acid/base balance

Kidneys contribute to the maintenance of body pH (7.35-7.45) via 3 B's: Buffer, Breathing, and Blood [HCO3-]

Extracellular & intracellular Buffers:

Extracellular buffers include the HCO3- buffer system, plasma proteins, and Phosphate (in order of importance)

Bicarbonate Buffer: uses the enzyme Carbonic Anhydrase to convert CO2 + H2O <--> H+ HCO3-

Albumin in the blood has histidine binding sites that can bind and release H+ as necessary

Low concentration of phosphoric acid allows H2PO4 <--> H+ + HPO4

Intracellular and Bone buffers:

Hemoglobin acts similarly to albumin, uses histidine + dissociable proton

40% of buffering during an acute acid load is mediated by Bone (similar to extracellular bicarb). H+ taken up in exchange for Na, K+, and dissolution of bone material to produce buffers, i.e. NaHCO3, KHCO3, CaCO3, & CaHPO4. Chronic acidosis results in kidney stones (from excreted Ca2+) and weak bones.

Within the proximal tubule and thick ascending limb, HCO3- can only be reabsorbed after being broken down into either OH- + CO2 or H2O + CO2.

Proximal tubule: brush border Carbonic Anhydrase breaks HCO3- down into CO2 which diffuses into the cell and OH- which combines with H+ secreted into the lumen by Na/H exchanger (#2) and H+ ATPase (#3) to form H2O. Inside the cell, CO2 combines with H2O to form H+ and HCO3-. The H+ is recycled into the lumen to help reabsorption of more HCO3-, and the HCO3- is reabsorbed via Na/HCO3- symport (#4) and Cl/HCO3- antiporters (#5).

Thick Ascending Limb: Lacks carbonic anhydrase on the apical brush border, so HCO3- must first combine with secreted H+ before being able to dissociate into H2O + CO2. Inside the cell carbonic anhydrase can reproduce HCO3- and it can be reabsorbed via Cl/HCO3- antiporters. (Basically same reactions as proximal tubule except for location of CA)

The collecting duct has alpha-intercalated cells which reabsorb the remaining HCO3- via an HCO3-/Cl- antiporter and secretes the last bit of H+. During chronic alkalosis though, Beta-intercalated cells will become active to perform the opposite function.

The excess H+ secreted into the lumen that is not used for recapturing HCO3- must be neutralized, this is done via urinary buffers phosphate and ammonium.

#physiology #physio #notes #TC5 #USMLE1 #medicalschool #renalphysiology #incomplete

Easy metabolic/respiratory acidosis/alkalosis explanation

#videos #Physiology #Acid base physiology #acidosis alkalosis #USMLE1 #TC5

Movement of sperm through the male system

S - Seminferous Tubules E - Epididimys V - Vas Deferens E - Ejaculatory Duct N - Nothing U - Urethra P - Penis

#mnemonic #male reproductive system #Anatomy #Reproductive anatomy #TC5 #Anatomy mnemonic #MS1 #Medical school #biology

Created by Vishal Punwani. Watch the next lesson: https://www.khanacademy.org/test-prep/nclex-rn/rn-reproductive-system-physiology/rn-reproductive-system/v/m...

Khan academy remains clutch even in medschool.

#CSF #MS1 #Cell Structure and Function #Reproductive cycle #ovarian cycle #usmle1 #videos

Potassium Homeostasis

Remember HIKIN': HIgh K+ INtracellularly

K+ controls the membrane potentials of nerve and muscle cells, so hyper/hypopolarization and excitability is inversely related to the values of plasma [K+] (i.e. too much plasma [K+] will cause increased activation (depolarization) of your heart muscles--> lots of contractions aka arrhythmia and death)

98% of the K is within the cells and only 2% is extracellular, so shifts of K in/out of the cell will cause changes within the body and is highly regulated by 3 hormones: Insulin, Epinephrine, & Aldosterone

K+ regulation is via regulation of Na/K ATPase.

Uptake:

Epinephrine will stimulate B2-adrinergic receptors to increase K+ uptake via stimulating Na/K ATPase activity + insulin secretions (epinephrine aka adrenaline= sympathetic activation= stress, i.e. released by heart during MI to lower plasma [K+] )

Beta-blockers will cause hyperkalemia, B2-agonists will induce hypokalemia

Insulin is the most important [K+] regulating hormone!! Increases Na/K ATPase activity after meals

Lack of insulin with Diabetes mellitus causes rise in plasma K+ after K+ rich meal

High plasma [K+] ==> adrenal cortex glomerulosa cells depolarization==> Ca2+ influx==> aldosterone synthesis & secretion

Aldosterone activates Na/K ATPase (duh) but also increases activity of kidney principal cell ENaC==> increased K+ efflux/secretion (loss!) into nephron lumen in exchange for Na+ reabsorption. Which means too much aldosterone= hypokalemia!

Secretion:

Too much K+ = get rid of it (hyperkalemia= secret) Hyperkalemia ==> aldosterone (see above) Distal tubular flow rate is equivalent to the rate of K+ secretion because it increases the [Na+] and the rate of Na reabsorption

Na/K are always inversely related

Increased flow rate via diuretics or ECF volume expansion = increased K+ secretion

Decreased flow rate via NSAIDs or volume loss= decreased K+ secretion

Kassi might have a long-distant relationship, but she is still directly affected by Tub's flow.

Reabsorption:

Too little K+ = keep it (hypokalemia= reabsorb) Rate is ALWAYS 67% at Proximal Tubule and 20% at the Thick Ascending Limb Rate via H/K ATPase can increase at the Distal Convoluted Tubules/Collecting ducts if plasma [K+] decreases due to decreased K+ intake

#renal #MS1 #USMLE1 #Physiology #Physio #RenalPhysiology #TC5 #medical school notes

Brachial plexus lesions & plexopathies