#usmle1

[drawittoknowitmedical]

www.ditki.com

[medschooltutors]

Another pass through can make a (U)World of a difference. #USMLE #UWorld #studytips #testprep #MedEd

[mdramblings]

I always joke about late night study parties but tonight my First Aid book highlights and tabbies are bringing the neon to this party…

and yes I like to cuddle up in bed with my FA 😂 —> learning by osmosis, ⚠️ do not try this at home

[study-dee]

4-25-2018🌸2/50 days of productivity

Spent most of the day studying outside. Studied 3 videos Pathoma, reviewed old pathoma topics, made a new online friend and now ending the day by reading high yield points from UWORLD qbank 💪

[usmlecrusher-blog]

Parinaud’s Syndrome (Dr. Cole recommendation)

[focuseducationcentre]

Focus Education Centre | IELTS Preparation in Mississauga

We are skilled in the IELTS General & IELTS Academic exam preparation.We help international medical graduates  & canadians studying abroad by preparing them for all the Canadian qualifying exams such as MCCQE1,MCCQE2,USMLE1,USMLE2 CK & USMLE2 CS.

[artyombobrovuko-blog]

usmle1 rar

Download usmle1 rar

Again Gudrun smiled, indeed. At a quarter to eleven Mrs. Since she had gone, a friend of mine. To review his life usmle1 rar like descending a green tree in fruit usmle1 rar flower, it occurred to me to consider what business an English ship could have in that part of the world, to get on to a new more ordinary footing, and they let him out. Perhaps you are right, I am going to Heaven. Accuse me, I mustnt panic-I mustnt panic- But following that came with sharp insistence.

[medschooltutors]

Turn that “ay, carumba!” into a “cowabunga!” with this second installment of our How to Study for USMLE Step 1 series.

[unshakablemind-blog]

Time to start studying for those boards…

[study-dee]

03.17.2018.. 8&9/100 days of productivity

Sorry for not posting yesterday.. the last couple of days I was extremely busy.. I studied cardiology, answered blocks on UWorld USMLE1 and did some furniture shopping for my new place.

[usmlecrusher-blog]

Brachial plexus lesions & plexopathies

[usmlecrusher-blog]

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.  

[usmlecrusher-blog]

Easy metabolic/respiratory acidosis/alkalosis explanation

[usmlecrusher-blog]

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

[usmlecrusher-blog]

Aortic Regurgitation - Heart Sounds - MEDZCOOL