calcium channel

NCLEX Pharmacology Medical Suffixes

  • -amil = calcium channel blockers
  • -caine = local anesthetics
  • -dine = anti-ulcer agents (H2 histamine blockers)
  • -done = opioid analgesics
  • -ide = oral hypoglycemics
  • -lam = anti-anxiety agents
  • -oxacin = broad spectrum antibiotics
  • -micin = antibiotics
  • -mide = diuretics
  • -mycin = antibiotics
  • -nuim = neuromuscular blockers
  • -olol = beta blockers
  • -pam = anti-anxiety agents
  • -pine = calcium channel blockers
  • -pril = ace inhibitors
  • -sone = steroids
  • -statin =antihyperlipidemics
  • -vir = anti-virais
  • -zide = diuretics
D&D Homebrew Poisons

So, im working on a mini series for badassdanddpics and was wondering if you guys had any ideas. im calling the mini series “Bewildering Botany and Perilous Poisons” that will basically showcase magical plant homebrew that will aid adventures and villains alike. for the poison section of it, i put together some basic information from D&D about the rules as well as how they are applied and used against others as well as common symptoms from plants in the real world.

different poisons are applied to victims by

  • contact
  • ingested
  • inhaled
  • injury
  • smoke from being burned

common rules (for 5th edition D&D regarding poison)

  • A weapon coated with poison will dry out in one minute.
  • When you are poisoned, you will usually suffer from the poisoned condition.
  • Poison can be bought or crafted using the downtime rules and a poisoner’s kit.
  • Cures for poison include low level spells or anti-toxin.
  • Truth Serum is listed under poisons, and is something I think could be useful in your campaign in many different ways.
  • Poisoned: A poisoned creature has disadvantage on attack rolls and ability checks.
  • each round until you make a saving throw.

Common symptoms of poisoning include nausea, vomiting, convulsions, liver failure, disables nerves, lowers blood pressure, and can stop the heart, muscle twitches, and sometimes paralysis, irritation of skin throat and mouth, swelling, burning pain, breathing difficulties and stomach upset. dilated pupils, sensitivity to light, blurred vision, tachycardia, loss of balance, staggering, headache, rash, flushing, dry mouth and throat, slurred speech, urinary retention, constipation, confusion, hallucinations, delirium, convulsions and photo-toxicity

underneath the “keep reading” i have included some actual plants that could help with creating realistic homebrew.

Keep reading

Quick fact. Ready?
Magnesium is one of the most abundant minerals in our body, 35% of it being stored in our bones.

A deficiency in Magnesium can lead to an increase in blood pressure, impaired glucose intolerance, or an excitation of neurons.

Often times, Magnesium makes one feel tired or relaxed due to the affect that it has on calcium channels in the brain.

The best sources of Magnesium are green leafy vegetables like spinach or kale, not only because of their high content, but because of their higher absorption rates.

anonymous asked:

hi aunty!! what would dying of takotsubo cardiomyopathy look like/feel like? i have a character whose son dies and then he's supposed to die shortly after of a "broken heart" but nothing will tell me what that's supposed to look like ;;. thanks in advance and thank you for running this blog!!

Hey there nonny! 

Dying of heart failure – really, any kind of heart failure – sucks pretty heart. 

Takotsubo cardiomyopathy – TCM for the remainder of this post – basically looks like a heart attack. The character will present with pain in their chest, possibly radiating down the left arm or into the jaw. They might also present with fainting or shortness of breath. 

On an EKG, they would have a finding called ST-segment elevation (ST elevation for short), which is indicative of a heart attack. 

On bloodwork, they would be positive for a kind of cardiac enzyme called troponins, which are released during a heart attack (and the only way to be sure, by the way, that a character is having a heart attack). Doctors might call this “positive troponins” or “elevated troponins”. 

But here’s where the diagnosis of TCM (or SCM, stress cardiomyopathy) starts to veer apart from the diagnosis of myocardial infarction (heart attack). The definitive treatment for an MI is usually to get the character into the cardiac cath lab, which will allow doctors to thread a wire into the coronary vasculature and find the blocked artery, so that the blockage can be cleared and blood flow restored. 

A patient with TCM will get a coronary cath, which will find…. nothing. Absolutely nothing. No blockage of any kind. (This is actually part of the diagnostic criteria for Takotsubo’s.) 

Also, the heart typically has abnormal wall motion, evident on ultrasound or CT. (CT is performed during the cardiac cath, because these procedures require fluoroscopy; that is, being able to see an X-ray or CT in real-time.) 

Now. You asked specifically about dying of TCM. This is going to look like most other kinds of heart failure following MI. 

The character may get chest pain and have their heart simply fail on them. This can happen quickly or fairly slowly. 

Chest pain and worsening shortness of breath are both very likely, as is difficulty walking, fatigue, and other nonspecific cardiac symptoms. The character may wind up with fluid in his lungs (since, if the left ventricle fails, blood basically backs up into the pulmonary system), he may be pale and sweaty, he may feel as though he’s about to die – this is an actual symptom of heart failure (and most kinds of shock). 

If the pulmonary edema (fluid backup in the lungs) gets bad enough, he may have some pink, frothy spittle, and he might feel like he’s drowning, because he is – in his own blood. 

However, there’s something important to know about TCM. Takotsubo cardiomyopathy is usually not a lethal condition. Mortality is only 1-3%, and most patients make a full recovery in 4-8 weeks. 

Treatment, by the way, is usually supportive: beta blockers or calcium channel blockers are used to reduce stress levels (since the physiological manifestation of stress is high adrenaline levels), and worse comes to worst the character might get put on a balloon pump (which basically inflates a balloon in the aorta to support the heart and reduce workload). 

So I hope that gives you what you need to know about Takotsubo cardiomyopathy!! 

Thanks for your ask and write a kick-ass story! 

xoxo, Aunt Scripty

[disclaimer]

Patreon: a magical land where the ask box never closes. Care to visit?  

Ebook for Free! 10 BS “Medical” Tropes that Need to Die TODAY!

To remember about SVT, all you need to remember is the cause and you know the symptoms and treatment!

SVT occurs due to accessory conduction pathway through the AV node.

A - ABCD

Adenosine

Beta blockers

Calcium channel blockers

Digoxin

V - Vagal maneuvers

Valsalva

Ice immersion

Carotid massage

SVT: Start Vagal Treatment - - > If fails, use pharmacotherapy (ABCD drugs)

The P in Pvst reminds us that it presents with Palpitations in a hemodynamically stable patient (HR: 160-180/min)

*PVST: Paroxysmal supraventricular tachycardia

Interesting fact: In an asthmatic patient with SVT, you can’t give adenosine or beta blockers. The drug of choice in an asthmatic patient is therefore, diltiazem (A calcium channel blocker)

That’s all!

-IkaN

GPCRs/7-transmembrane receptors (7TM receptors)

G-protein-coupled receptors (GPCRs) are the largest and most diverse group of membrane receptors in eukaryotes. 

Structure

  • single polypeptide chain comprising of seven transmembrane α-helices
  • extracellular N-terminal domain of varying length, 
  • intracellular C-terminal domain.
  • length of the extracellular N terminus and the location of the agonist binding domain determines family.
  • The long, third cytoplasmic loop couples to the G-protein 
  • Usually particular receptor subtypes couple selectively with particular G-proteins
  • For small molecules, such as noradrenaline, the ligand-binding domain of class A receptors is buried in the cleft between the α-helical segments within the membrane. Peptide ligands bind more superficially to the extracellular loops

G protein system

GPCRs interact with G proteins in the plasma membrane when an external signaling molecule binds to a GPCR, causes a conformational change in the GPCR.  G-proteins comprise a family of membrane-resident proteins
whose function is to recognise activated GPCRs and
pass on the message to the effector systems that generate
a cellular response. 

  • G proteins are specialized proteins with the ability to bind the nucleotides guanosine triphosphate (GTP) and guanosine diphosphate (GDP). 
  • The G proteins that associate with GPCRs are heterotrimeric, (alpha beta and gamma subunits)
  •  alpha and gamma are attached to the plasma membrane by lipid anchors 
  • Trimer in resting state 
  • activated alpha monomer and beta/gamma dimer

Guanine nucleotides bind to the α subunit, which has enzymic activity, catalysing the conversion of GTP to GDP. The β and γ subunits remain together as a βγ complex. All three subunits are anchored to the membrane through a fatty acid chain, coupled to the G-protein through a reaction known as prenylation.

  • G-proteins are freely diffusible so a single pool of G-protein in a cell can interact with several different receptors and effectors 
  • When GPCR is activated by an agonist, a conformational change causes it to acquire high affinity for αβγ (G protein)
  • bound GDP dissociates and is replaced with GTP, which in turn causes dissociation of the G-protein trimer, releasing α-GTP and βγ subunits - the ‘active’ forms of the G-protein
  • which diffuse in the membrane and can associate with various enzymes and ion channels
  • Signalling is terminated on hydrolysis of GTP to GDP through the GTPase activity of the α subunit.
  • resulting α–GDP dissociates from the effector, and reunites with βγ
  • Attachment of the α subunit to an effector molecule increases its GTPase activity
  • GTP hydrolysis is termination –> activation of the effector tends to be self-limiting

Second messenger targets for G proteins

Main targets:

  • Adenylyl cyclase (responsible for cAMP formation)
  • Phospholipase C (inositol phosphate and diacylglycerol (DAG) formation)
  • Ion channels, particularly calcium and potassium channels
  • Rho A/Rho kinase (system controlling the activity of many signalling pathways for cell growth and proliferation, smooth muscle contraction, etc.)
  • Mitogen-activated protein kinase (MAP kinase) system controlling cell functions eg division.

(notes on these coming soon)

Key Drug Suffixes!

-amil = calcium channel blockers

-caine = local anaesthetic

-itidine = H2 (histamine) receptor antagonists/blockers

-done = opioid analgesics

-lam/pam = anxiolytics

-micin/mycin = antibiotics

-mide/zide = diuretics

-olol = beta blockers

-sone = steroids

-statins = cholesterol drugs

-vir = anti-virais

Happy Studying!

Internship diaries: Calcium channel blockers and peripheral edema mnemonic

As you all know, I am doing internship or housejob and it’s really tiring but a good learning experience. Lemme share what I learnt / revised today!

In my medicine OPD, we start most newly diagnosed hypertensive patients on amlodipine, a calcium channel blocker. Many of the patients, after a few weeks of therapy, come back complaining of lower extremity edema. You check their electrolytes, LFT’s and RFT’s and they are all normal.

Then it dawns on you - Edema is a side effect of calcium channel antagonists like amlodipine!

You explain to them that it is a side effect of the medication, change the medication if it is really severe, otherwise you keep them on the same regimen.

It’s nice to learn a fact from the book and then see it in practice :)

Oh and I made a small mnemonic for this - Dipines make your legs dip in watery edema! :D

That’s all!

-IkaN

My Uworld notes- 6
  • serum sickness is a type 3 HSR characterized by deposition of circulation complement fixing immune complexes and resulting vasculitis. Associated findings include fever, urticaria, arthralgias, glomerulonephritis, lymphadenopathy and a low serum c3 level 5-10 days after intravascular exposure to antigen. type 3 HSR typically activate complement at local site where immune complexes containing IgG and or IgM complement fixing antibodies have been deposited. This often results in hypocomplementemia including decreased C3 level

  • liver dz-a/w AFP

  • carcinoembryonic antigen (CEA) a/w colorectal cancer

  • CA125 -ovarian cancer. Both CEA and ca125 are fr monitoring purposes

  • PSA prostate specific antigen is most useful in establishing extent of prostate cancer and evaluating response to prostate cancer tx.

  • Iced water think cold – cold think cold agglutinins – cold agglutinin associated with infection with mycoplasma pneumonia

  • another cold agglutinin is EBV

  • free air in peritoneal cavity= bowel perforation

  • pancreatic calcification= chronic pancreatitis

  • heavily calcified vessels = atherosclerosis and vascular dz

  • distended bladder= urinary retention

  • air in billiary tract a/w gallstone ileus

  • fluoxetine a/w anorgasmia and decreased libido and increase latency to orgasm. They can however be used to tx premature ejaculation

  • phenelzine= MAO-I used in tx of depression monoamine oxidase is a mitochondrial enzyme that deaminates primary and secondary aromatic amines

  • tricyclic antidepressants can cause orthostatic hypotension example imipramine

  • trazadone- priapism

  • paroxysmal breathlessness and wheezing in young patient unrelated to ingestion of aspirin, pulmonary infection inhaled irritant stress and or exercise should raise a strong suspicion for extrinsic allergic asthma. The granule containing cells in sputum are most likely eosinophils and the crystalloid bodies are most likely Charcot Leyden crystals (contain eosinophil membrane protein)

  • chronic eosinophilic bronchitis in asthmatics involves bronchial wall infiltration by numerous activated eosinophils largely in response to IL5 released by TH2 cells

  • digestion and absorption of nutrients primarily occurs in small intestine. SI cells produce enzymes responsible for nutrient absorption. Proteins in ingested food exist primarily as polypeptides and require hydrolysis to dipeptides tripeptides and amino acid for absorption. Hydrolysis of these polypeptides is accomplished by proteolytic enzymes such as pepsin and trypsin

  • these enzymes are secreted inactive proenzymes trypsinogen and pepsinogen from stomach and pancreas

  • trypsin activates other proteolytics enzymes including chymotrypsin carboxypeptidase and elastase. Activation of trypsinogen to trypsin is achieved by enteropeptidase (or enterokinase)an enzyme produced in duodenum

  • enteropeptidase deficiency results in defective conversion of trypsinogen to active trypsin

  • lipase secreted from exocrine pancreas is the most important enzyme of digestion of triglycerides. Chronc pancreatitis is a painful condition that causes lipase deficiency. This leads to poor fat absorption and steatorrhea

  • secretin is a peptide hormone secreted by S cells of duodenum un response to low duodenal pH. Secretins timulates secretion of bicarbonate from the pancreas and gall bladder and reduces acid secretion in the stomach by reducing production of gastrin. Neutralizing the acidic pH of food entering the duodenum from the stomachis necessary for proper function of pancreatic enzymes (amylase, lipase)

  • trisomy 18 (47XX: Edwards syndrome

    • face: micrognathia, microstomia, eye defects (microphthalmis, cataracts) low set ears and malformed ears prominent occiput

    • CNS: microcephaly, neural tube defects (meningocele, anencephaly), holoprosencephaly, arnold chiri malformation, severe MR delayed psychomotor development

    • musculoskeletal: clenched hands with overlapping fingers (index finger overrides the middle fingerand fifth finger overrides the fourth finger) rocker bottom feet short sternum and hypertonia

    • cardiac: VSD, PDA

    • distinguishing features: clenched hands and or overlapping finger

    • GI: Meckel diverticulum, malrotation

    • ultrasound: intrauterine growth restriction and polyhydramnios especially ina fetus with abnormal hand arrangement

  • unlike patients with Edward’s syndrome neonates with Patau syndrome (trisomy 13) have cleft lip and palate, polydactyly and omphalocele. Patau syndrome is not a/w low set ears and overlapping fingers but do present with rocker bottom feet also

  • 47XXX karyotype is clinically silent however, some affected women have slightly decreased IQ scores. Female newborns with this karyotype are phenotypically normal with no obvious dysmorphism

  • 47XXY Kleinfelter’s syndrome: may be a/w mild mental retardation or normal intelligence. The typical patient is tall mall adult with gynecomastia small testes and infertility. Male newborns with this karyotype are phenotypically normal with no obvious dysmorphism. The clinical findings do not become apparent until adulthood.

  • Sudden onset of abdominal or flank pain hematuria and left sided varicocele together suggests renal vein thrombosis a well known complication of nephrotic syndrome. Nephrotic syndrome is a hypercoagulable state d/t increased loss of anticoagulant factors especially anti thrombinIII (responsible for the thrombotic and thromboembolic complications of nephrotic syndrome)

  • venous drainage from left testes travels throught the left testicular vein into the left renal vein and from there the IVC. In contrast to the right testicular vein which empties directly into the IVC. This difference in venous drinage gives diagnostic significance to left sided varicocele in that it often indicates an occlusion of the left renal vein by a malignant tumour or thrombus

  • malaise low grade fever followed by a facial rash. Feels better now but still has the rash- red flushed cheeks with – clinical presentation of erythema infectiosum aka fifth dz. As the facial rash fades an erythematous rash in reticular lace like pattern often appears on trunk and extremities. The rash of erythema infectiosum is thought to result at lest partly from local immune complex deposition once serum levels of virus specific IgM and IgG have attained high enough levels.

  • Erythema infectiosum= non enveloped DNA virus called parvo B19. The blood group P antigen globoside is a parvovirus B19 is highly tropic for erythrocyte precursors particularly erythrocytes and erythroid progenitor cells

  • Parvo B19 replicates predominantly in the bone marrow

  • anthracyclines daunorubicin doxorubicin epirubicin and idarubicin are chemotherapeutic agents a/w severe cardiotoxicity because of their unique ability to generate free radicals.. Dilated cardiomyopathy is dose dependent and may present months after discontinuation of the drug . Swelling of sarcoplasmic reticulum is the morphologic sign of early stage doxorubicin associated cardiomyopathy. Followed by loss of cardiomyocytes and its symptoms are those of biventricular CHF including dyspnea on exertion orthopnea and peripheral edema

  • dexrazoxane prevents Doxorubicin associated cardiomyopathy because dex is a iron chelating agent that decreases formation of free radicals by anthracyclines.

  • Restrictive cardiomyopathy a/w hemochromatosis amyloidosis sarcoidosis and radiation theraapy : remember -osis

  • hypertrophic cardiomyopathy caused by mutation of beta myosin heavy chain

  • focal cardiomyopathyscarring commonly results in MI

  • pericardial fibrosis usually follows cardiac surgery radiation therapy or viral infections of the pericardium

  • PCP aka angel dust aka phencyclidine commonly associated with violent behaviour

  • LSD can also cause aggressive behaviour but it is more typically characterized by affective liability thought disruption )delusion) and visual hallucination whereas PCP produces more psychomotor agitation including clonic jerking of extremities

  • angel dust can be put on marijuana and smoked LD is ingested orally

  • secobarbital is a street barbiturate a CNS depressant which leads to drowsy drunken state of consciousness without the violent behaviour

  • heroin (opioid) produces CNS psychomotor depression and respiratory depression miosis and bradycardia are common

  • dry tap with no splenomegaly or lymphadenopathy – think aplastic anemia which causes pancytopenia

  • aplastic anemia= hypo cellular bone marrow with fat cells and fibrotic stroma

  • hyper cellular marrow with increased blasts found in myeloproliferative d/o and certain leukemias

  • most common side effect of streptokinase= hemorrhage . Streptokinase is a thrombolytic agent that acts by converting plasminogen to plasmin which subsequently degrades fibrin. It is a foreign protein derived from streptococci and induce HSR.

  • Dissection of ascending aorta manifests as tearing chest pain that radiates to the inter-scapular area commonly occurs in hypertension marfans and ehlers danlos

  • hyperactive jaw jerk reflex when lightly tapped= chvostek’s sign- Hypocalcemic – facial m contraction elicited by tapping facial nerve just anterior to ear. The most common cause of outpatient hypocalcemia is primary hypoparathyroidism which is often d/t prior loss of parathyroid tissue during thyroidectomy

  • scotoma is visual defect that occurs d/t pathologic processes that involve parts of retina or optic nerve resulting in discrete area of altered vision surrounded by zones of normal vision. Lesions of macula cause central scotomas.. examples would include MS, diabetic retinopathy and retinitis pigmentosa

  • verapamil is a calcium channel blocker that slows SA and AV node phase 0 depolarization (in nodal cells, the phase of depolarization is mediated by calcium influx)

  • phase 0 depolarization of cardiac conduction system occurs during diastole thus verapamil slows diastolic depolarization

  • action potential: *activates voltage-gated ion channels*
  • voltage-gated calcium channels: *open*
  • calcium ions: *enter the cell*
  • synaptic vessicles: *fuse with the cell membrane and release neurotransmitter molecules into the synaptic cleft*
  • neurotransmitter molecules: *bind to postsynaptic receptors and create an excitatory or inhibitory postsynaptic potential*
Diseases and their twins.

There a few diseases which quite resemble an other disease in presentation and sometimes pathology.Here’s a list I made-

1. Wolf-Parkinson-White and
   Lown-Ganong-Levine syndrome-

   -What’s similar?
    The tachycardia, short PR    
     interval, pre- excitation

  -What’s different?
    While in WPW syndrome,the
    culprit is a naughty extra pathway,
    the bundle of Kent, in LGL the AV
    node itself is naughty.(The
    hypothesized bundle of James  
    hasn’t been discovered yet)
    Conduction through the AV node
    occurs rapidly.
   
    ECG findings- WPW syndrome has
    a short PR interval and a Delta
    wave on the QRS complex. No
    Delta waves occur in the LGL
    syndrome.
   
    Also, the risk of sudden death
    remains lower in LGL syndrome.


2. Myasthenia Gravis and Lambert
   Eaton syndrome.

   -What’s similar?
    The muscle weakness.

  -What’s different?
   Oh almost everything. In MG,
   autoantibodies are formed against
   the nicotinic receptors whilst in
   LEMS(Lambert Eaton myasthenic  
   syndrome), the antibodies are  
   against ‘pre synaptic voltage  
   gated Calcium channels’.
   
    LEMS is mostly associated with
    underlying malignancies,
    making it a paraneoplastic
    syndrome.

     In contrast to MG, where
     distal musculature is affected
     the most, proximal musculature
     gets involved in LEMS. Arm
     muscles are frequently involved
     while MG prefers muscles of the
     leg.
     
     The autonomic nervous system
     also may be affected in LEMS.

    The most significant difference
    is that the strength actually
    improves on exertion in LEMS,
    known as ’Lambert’s sign’,  
    whereas in MG, weakness  
    prevails on repeated activity.


3. Multiple sclerosis and Devic’s
  disease
   
    -What’s similar?
    The demyelination and
    associated CNS symptoms.

    -What’s different?
     Many things. The optic nerve
     and spinal cord are affected more
     commonly in Devic’s. MS affects
     the CNS as a whole.

     Devic’s runs a more serious
     course than MS, the morbidity
     after an attack is more severe
     compared to it.

    MS is a T cell mediated
    autoimmune disease while IgG
    antibodies mediate Devic’s, more
    specifically the
    NMO(neuromyelitis optica)IgG.
    Oligoclonal bands are rare in
    Devic’s, and disappear after
    an attack.

    Uhthoff’s phenomenon, where
    symptoms worsen after exposure
    to higher temperatures,and the
    Lhermitte’s sign, where sudden,
    shock like sensation travelling
    through the spinal cord is felt,
    occur more commonly in MS.

4.Plague and Tularemia.
   
    -What’s similar?
      Those large, pus filled lymph
       nodes.
   
    -What’s different?
      Everything.Francisella
      tularensis is the causative agent,
      ticks and arthropods are the
      vectors, rabbits are the source,
      so on and so forth!

anonymous asked:

Have you ever made a med error and if so how did you handle it?

Yes. I promise, if you have been a nurse for longer than a week, you have made a med error.

If someone tells you they haven’t made a med error they are either 1. Lying or 2. Too dumb to realize it, which is really scary.

Here’s what I do: Don’t freak out, tell the doc, and go from there. I have been lucky, not to make a significant error that caused the patient harm.

Other med errors are scarier, just know that the sooner you come clean, the safer it is for the patient. One time, a new nurse was on orientation on my unit. There’s calcium channel blocker med we give to SAH patient to prevent vasospasm. The patient was intubated, so this med need to down the patient’s dobb hoff tube. The pill was a liquid capsule. So, what we would do was, insert a needle  with a 10 cc syringe into the capsule, draw out the liquid in a syringe and then give the med via the dobb hoff tube. This new nurse does that, then sees this 10cc syringe of liquid in her hand and it feels natural to give that IV, right? So she did. It was 60 mg of a calcium channel blocker given IV. So, what do you think happened? The patient’s ECG began to have dysrhythmias, he went into v-tach. The doc was called and ACLS was started. Around this time the new nurse realized her error. She told her preceptor off to the side and the preceptor told the doc. They began pushing calcium chloride and the patient improved, NSR was restored after a lot of calcium. The new nurse was written up. But the process was also changed. Pharmacy began supplying us with that medication already in the liquid form, so no more drawing up liquid out of a capsule pill. That was unsafe practice, so the system improved.

It’s not fun owning to a mistake, but it’s necessary.

*Phone rings*

Tech: Pharmacy, how can I help you? Oh, you want to speak to the pharmacist, sure thing.

Me: Hi, how can I help you Doctor?

Stupid, MD: I was wondering if you could answer a very important question, its in regards to a patient.

Me: Sure, go ahead, I’ll put on hold the other prescriptions i have to verify for the waiters and the PA that I was just about to call for.

Stupid, MD: What is almodipine used for?

Me:

It…is used for blood pressure, it is a calcium channel blocker…are you my cardio professor calling to check in on me to see if I still remember my pharmacology?

Stupid, MD: Oh! okay. What is the brand name?

Me: Norvasc

Stupid, MD: Ahh alright thanks.

Me:

Mint

How to Grow: Because mint tends to spread and grow so fast, resembling a weed in the way it spreads, you want to isolate it in some way. You can either put it in a pot by itself, or in it’s own bed. You need to keep the soil moist, so it’s a good idea to add water-retaining polymer, peat moss, or something similar to the soil. It does tend to prefer partial to full sun. If you’re harvesting often, it’s a good idea to add fertilizer regularly, as in every few weeks. Flowers bloom from June to September, and you can trim the buds off before they open to keep you plant under control. Mint is fairly frost tolerant, and will survive all the way up to USDA zone 5, some varieties will even keep to zone 3. Pro-tip: replant you mint every three years to keep the scent and taste strong.

Medicinal Properties: Mint has a long history as a medicinal plant. While each specific type of mint has different qualities, almost all mint is an analgesic, antimicrobial, antseptic, antispasmodic, diaphoretic, helpful in the aid of proper digestion, and a stimulant. They are commonly applied for use in treating headaches, fevers, sore throats, and upset stomachs. Applied topically, mint can repel biting insects, ease the heat and itchiness of bug bites and rashes, and treat fungal infections such as athlete’s foot. Drinking a cup of mint tea before or after each meal can help regulate irritable bowel syndrome. Be warned, a few people have the opposite reaction to mint, and find tit o actually cause heartburn and indigestion.

Be careful when giving mint, especially peppermint as the strongest of the family, to children. Do not use mint oil if you’re pregnant or attempting to become pregnant. See a doctor before starting a mint regimen if you’re using calcium channel blockers.

Magical Attributes: Money, Lust, Healing, Travel, Exorcism, Protection. Associated with air.

DISCLAIMER! I am not a trained herbologist, or a doctor. Plants, herbs, and natural remedies do not negate the need to see a doctor for chronic, ongoing conditions, sudden illnesses, or modern medication. This is just stuff I’ve read, or picked up over the years. Be sure to let your doctor know if you plan on starting any kind of herbal treatment, as it may interfere with your regular medications. If you explain to your doctor that you really want to try naturals, they’ll usually work with you to see what they can do.

This blog is normally about technology, medicine, and new innovations, but I’m taking an aside today. Perhaps it’s the fact that I am currently meeting new MS1s at OHSU that I feel like imparting this right now - take the time to enjoy life

One of my really good friends - that’s me carrying him above - stayed with me in Portland for the past few days. Despite being mired in cardiology for the past two weeks, I took time off from school to show him around. We had a blast, discovered a lot, and made some really good memories. I even convinced him, a diehard California stalwart, that living in Portland would be amazing. I didn’t get a lick of studying done.

Here’s the thing; medicine will always be there, opportunities to make memories with friends won’t.

If you’re stuck between memorizing verapamil’s calcium channel blocking mechanism and entertaining a friend on a road trip across America, choose the latter.

If you’re deciding between staying in the same place for break or flying 1,000 miles to discover someplace new with someone familiar, go the distance.

Say yes to making memories. Say yes to making connections. Don’t let medical school run your life, because medicine isn’t going anywhere. The ones who care about you, and the ones you care about, are.

Join them. There’s always UpToDate for later; speaking of which, I need to get back to studying.