One more 10 hour shift to go, and then VACATION!
Always think Beta = Booster; which means stimulation of:
- Beta 1 receptors -> increase renin secretion
- Beta 2 receptors -> increase insulin secretion
And for Alpha receptors it’s the reverse, which means stimulation of:
- Alpha 1 receptors -> decrease renin secretion
- Alpha 2 receptors -> decrease insulin secretion
Beta & Alpha 1 for renin
Beta & Alpha 2 for insulin
Vd: volume of distribution
Co: plasma [ ] at zero time
Cp: plasma [ ]
t1/2: half life
Cl: clearance = free fraction x GFR
Ko: infusion rate
Css: steady state [ ]
LD: loading dose
MD: maintaining dose
Are all about one of my top 5 favorite things - cheeseburgers (with fries).
Class IA = A Double Quarter Pounder (disopyridine, quinidine, procainimide
Class IB = 1 Burger with Lettuce, Tomato, Mayo, Pickles (lidocaine, tocainide, mexiletine, phentoyin)
Class IC = Can i have More Fries Please (moricizine, flecainide, propafenone)
Let me present to you the most understandable, simplified, awesome analogy for explaining competitive and non competitive inhibitors =D
When you are hungry, you have affinity for food.
Hunger has affinity for food like enzymes have affinity for substrates.
Rice is the substrate for your hunger.
You happily eat it at some random rate.
But *plot twist* if you’re given a hamburger at the same time..
OBVIOUSLY, your affinity for the burger is more so you eat the burger instead.
The burger acts as a competitive inhibitor.
Lesson learnt: Competitive inhibitors reduces enzyme-substrate affinity.
Say you’re still hungry and your burger is surrounded by rice.. *Another twisted plot*
The only way to reach the burger is to eat the rice..
So you eat the rice (since you are hungry anyway, duh!)
Lesson learnt: Competitive inhibitor concentration can be overcome by increasing the substrate concentration.
What ultimately made you eat the rice?
The increased concentration of the substrate!
Km, the substrate concentration to produce half of Vmax, had increased.
Lesson learnt: Km increases in presence of a competitive inhibitor.
Say, you were hungry.. Until you saw something gross and it ruined your appetite.
The “gross thing” is a non competitive inhibitor.
Even if there is food on the table, you won’t wanna eat it or uhh, say if you were gonna eat it really fast, now you roll your eyes and yeah, eat slowly.
Vmax, the maximum rate of a chemical reaction, decreases.
Lesson learnt: Vmax decreases in presence of a non competitive inhibitor.
And since you have a decreased appetite, no matter how much rice is given to ya, you’ll eat it at the same slow rate.
Lesson learnt: Increasing substrate concentration will not affect the action of a non-competitive inhibitor.
When it comes to drugs, there are terms such as efficacy, potency and complex things such as graphs you need to remember - Here are some mnemonics that may help you out.
That’s all! <3
ANTIBIOTICS CHEAT SHEET :)
* Sulfonamides compete for albumin with:
- Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies
- Warfarin: increases toxicity: bleeding
* Beta-lactamase (penicinillase) Suceptible:
- Natural Penicillins (G, V, F, K)
- Aminopenicillins (Amoxicillin, Ampicillin)
- Antipseudomonal Penicillins (Ticarcillin, Piperacillin)
* Beta-lactamase (penicinillase) Resistant:
- Oxacillin, Nafcillin, Dicloxacillin
- 3°G, 4°G Cephalosporins
- Beta-lactamase inhibitors
* Penicillins enhanced with:
- Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)
- Aminoglycosides (against enterococcus and psedomonas)
* Aminoglycosides enhanced with Aztreonam
* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)
* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)
* Both inhibited by Probenecid during tubular secretion.
* 2°G Cephalosporines: none cross BBB except Cefuroxime
* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.
* Cephalosporines are ”LAME" bc they do not cover this organisms
- L isteria monocytogenes
- A typicals (Mycoplasma, Chlamydia)
- M RSA (except Ceftaroline, 5°G)
- E nterococci
* Disulfiram-like effect: Cefotetan & Cefoperazone (mnemonic)
* Cefoperanzone: all the exceptions!!!
- All 3°G cephalosporins cross the BBB except Cefoperazone.
- All cephalosporins are renal cleared, except Cefoperazone.
- Disulfiram-like effect
* Against Pseudomonas:
- 3°G Cef taz idime (taz taz taz taz)
- 4°G Cefepime, Cefpirome (not available in the USA)
- Antipseudomonal penicillins
- Aminoglycosides (synergy with beta-lactams)
- Aztreonam (pseudomonal sepsis)
* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.
* Covers VRSA: Linezolid, Dalfopristin/Quinupristin
* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.
* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)
* Phototoxicity: Q ue S T ion?
- Q uinolones
- T etracyclines
* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides
* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis
* Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.
* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.
* Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.
* QT prolongation: macrolides, sometimes fluoroquinolones
Good question Anon!
As you know electronic copies are much cheaper than buying the physical copy, but your access to them sometimes expire, or you lose the access code, etc., whereas a physical book is always readily available for reference. For me, it really depends on the book. For example, I was required to buy Potter & Perry’s Fundamentals of Nursing my first year. There was the option to buy an electronic version, but I opted to buy the physical copy because this text is required for multiple classes and is a great reference for the future.
Here are my thoughts for each option:
- available for reference in the future
- no expiry date
- ability to highlight (this is not always possible on all online versions)
- ability to read in areas with no internet access
- can resell in the future (provided there hasn’t been major changes in the next edition)
- takes up space on your bookshelf
- editions change almost every year, so you may not be able to resell, or your resell value will be very disappointing
- you can read it on the bus, but that also means you have to lug it around all day (nursing textbooks are HEAVY!)
- many textbooks are available for permanent download. This means that you can save it on your desktop or external hard drive and still use it as a reference without taking up space in your small, small apartment or dorm room.
- WAY cheaper, and no need to try and resell
- more environmentally friendly
- the ability to use a search function to find specific terms and passages
- if it is a permanent download you can read your text in internet-less areas without having to lug around a heavy book
- if it is a rental or time-limited edition then you will not have access to the text after a set period of time
- electronic files sometimes have a way of getting lost. If you lose your textbook due to a virus and it is a one-time download then you are in trouble.
- laptop batteries die, physical textbooks never do.
- can’t resell
SO, I think I’ve covered it all. Like I said it differs for each textbook. I tend to go for electronic if it is a course that is required but I don’t think I will use again because of the monetary savings.
Hope this helps!
Last week of full time work and summer vacation! Is it strange that I’m excited for school to start so I can get a little bit of a break?
Be prepared for sweet nursing notes to be posted in the upcoming weeks!
Good luck, everyone with the first few weeks of the semester!
Our cat just jumped off/fell off our fifth floor balcony and came out with only a small laceration on her tongue. WTF.
So happy she is okay, but also having a many small sequential panic attacks thinking about how much worse it could have been.
Thank you! That’s a great question. I also struggle with this, but I’ve found a great solution — be flexible.
It may seem counterintuitive to have flexible breaks when I am scheduling every minute of my week, but I have found that this works the best for me. I usually change the time of my break depending on what I have going on in the week. My ultimate goal is to finish all my school work, so first I estimate how long this is going to take. Say, it may take three hours to study two chapters, so I will work from 8:30 am until 11:30. For my break I like to have some human interaction (like grabbing coffee with a friend), or if this is not possible I will have a short nap or watch a 30 minute episode of something on Netflix. I give myself a time limit as to how long this will take (usually from 30-40 minutes), and then it is back to work!
A good tip that I was given is to schedule your study day like an 8-hour work day: start at 8:30, work until 10 and then take a 15 minute break, work until 12, take a 30 minute lunch break, work until 2 and take a 15 minute break, and finish at 4:30. I like this structure, as I tend to get side-tracked when I am studying alone.
Another important aspect for me is giving myself an evening to myself. I do not think it is wise or productive to work every night of the week, so I will sometimes work from 8:30-5:00 on a Saturday and do something fun in the evening, like see a movie. If I do something too fun that night and sleep in the next day, I will simply move my schedule up in the day, and finish later at night.
During midterms and finals my breaks are shorter as I have more material to study, and my breaks, also shorter, consist of me doing speed walking laps through the library stacks (I probably look crazy, but there’s nothing like blood flow to increase study success!).
So, in conclusion, create breaks that feel like breaks, schedule your day like a work day to maximize the studying/break ratio, do something fun with your down time, and study more/take less breaks during midterms (duh).
Thanks for following, Anna! I hope this helps!