AOS Fic - Finally

Originally posted by cindyctw75

My contribution to the Jim Kirk Birthday Bash.

Posting now because tomorrow is gonna be killer for me. 

No real warnings, just a blatant disregard for canon and shameless pseudoscience. I am a creature of consistency. 

McKirk, ‘cause it’s always McKirk.

March 22, 2256

Len doesn’t think anything of it when Jim doesn’t stumble into his room at 3 am on March 22.

It crosses his mind that maybe things are going better with Ruth. He really isn’t bothered.

It’s a little weird when Jim isn’t sprawled on his couch when he finally finishes his day at the clinic. 

“Jim?” Len calls, dropping his pack on the floor.

Blessed silence greets him.

Len sighs and settles heavily into the cushions, toeing off his boots.

Finally, some peace and quiet.

Keep reading

anonymous asked:

Can you do something like a chapstick challenge for the boyfriends? The challenge is basically that one would cover his eyes while the other put on a flavored chapstick and the former will have to guess what that flavor is while smooching the latter.

“I call bullshit,” Cloud said, crossing his arms.

Zack’s grin was practically audible, even though Cloud couldn’t see it due to the blindfold that was currently blocking his sight. “Aw, Cloud. It’s just a quick test to see if your senses have been enhanced since your last mako shot, the labs do it all the time.”

“Somehow I severely doubt that whatever you’re planning is the same as what they do in the labs.”

“Well, we thought we’d make it a little bit more fun.”

Cloud sighed and sank back into the sofa cushions. He turned his head towards where he had last seen Sephiroth and Angeal standing. “You’re really going along with this?” Cloud asked, deadpan.

“You do not yet know what is to come,” Sephiroth pointed out.

“Zack’s grinning like an idiot, so it’s probably something stupid. I can figure that much out already.”

Sephiroth coughed, hiding a quiet laugh. “Perhaps it is unorthodox. But please be assured that you will not find the process unenjoyable.”

Cloud was quiet for a moment, turning the statement over in his head. It didn’t help. He still had no idea what they were up to, or how in Hel Zack managed to get all their boyfriends in on the game. At least, he assumed it was all their boyfriends. Genesis was absent, and that didn’t bode particularly well either.

“Fine,” Cloud sighed. “What do you need me to do?”

Keep reading

Quick fact. Ready?
Enzymes are proteins that participate in almost every single bodily function. These enzymes, however, cannot function without their cofactors or coenzymes. These helpers are usually the essential vitamins and minerals that we must obtain on a daily basis; such a the B vitamins, vitamin C, and those of A, D, E, and K!

anonymous asked:

Could you tell me all about magnesium for horses? It sounds really interesting and may be worth knowing!

Magnesium is part of the micromineral group, which also contains sodium, chloride, potassium, calcium, phosphorus and sulfur. It is cofactor in over 300 enzyme systems, which are responsible for biochemical reactions including protein synthesis, muscle and nerve function, blood glucose control and blood pressure regulation (to name a few). It is essential in energy product (particularly ATP), is required for the synthesis of DNA and RNA. It plays a role in the active transport of calcium and potassium ions across cell membranes and in the immune system [1, 2

Magnesium is important for so many more functions but I don’t want to turn this into a megapost so I’ll stop here.

Horses are commonly deficient in magnesium for various reasons. Soil quality for starters. Deficiencies mainly occur on sandy acid soils (or) in high rainfall areas. This soil type is particularly common in Australia. [3] As a result, most grass or crop that is grown on this type of soil will also display a lack of magnesium.

Calcium is also a major concern for magnesium intake. Because calcium is so heavily supplemented (in almost everything) it is really important to also supplement magnesium.  “Calcium supplementation often reduce magnesium absorption and retention. Magnesium supplementation actually improves the body’s use of calcium.” [4]

Per new research, the calcium to magnesium ratio should be a minimum of 1:1 (preferably a 1:2), compared to the 2:1 recommended previously. [5] This leads me to the nutrient profile of hay!

Lucerne (or Alfalfa to you weird fairy bread hating Americans) is possibly the most widely fed type of hay. As is evident by the diagram below the calcium to magnesium ratio is around 6:1. (!!! OMG !!!).  So it is really important to provide “stand alone” magnesium in your horses diet.

(source: FeedXL)

What to look for: common signs of magnesium deficiency include (in horses);

  • Nervous, anxious temperament
  • Sudden shying at familiar 
  • Violent pulling-back when tied
  • Dislike of grooming
  • Aggression towards owners or herd-mates
  • Separation anxiety, herd-bound
  • Restless under saddle, unable to focus on rider
  • Bucking
  • Poor hoof quality, footsore without shoes or boots on hard or rough ground
  • Short stride with inappropriate toe-first hoof landing
  • Laminitis
  • Grass belly
  • Insulin resistant with heavy crest
  • Stiff, braced posture with deep ‘V’ behind withers
  • Front feet placed far back under body when resting
  • Tight, sloping croup
  • Stifle catch
  • Tying-up
  • Excessive sweating in hot weather, shivering in warm, wet weather
  • Dry, flaky skin
  • Sweet-Itch
  • Watery eyes

Fudge (my pony) for example has/had about 11 of these symptoms.

“Ok, Emmy, but where do I get magnesium from?”

Well, there are heaps of magnesium supplements available. The two most common forms of magnesium for oral supplementation are magnesium oxide, and magnesium chloride.

Magnesium oxide is a common compound in the earths crust, however it has one of the lowest degrees of bioavailability, as low as 4% according to one study.

Magnesium chloride has the highest bioavailability of all types of magnesium, due to its superior solubility in water. It is extracted from brine or sea water (I recommend this one!).

Bioavailability: the extent to which nutrients can be absorbed and utilised by the body.

Magnesium chloride comes in a flake form, and can be found in bulk online or in store. It’s important when buying online that you purchase a “certified food grade” product. However it is more expensive than regular grade magnesium chloride because of the costly process they go through to get it certified. I buy my magnesium chloride flakes from a bulk food supplier (The Source Bulk Foods) and although it isn’t “certified food grade” it is just as good (according to the manufacturer and a chemical comparison I forced my chemistry teacher to do). 

Feeding MgCl [6]

  1. Dissolve 15g (1 tbsp) flakes in 150ml water and add 10ml of the resulting solution to each feed, preferably twice daily.   Increase by another 10ml every 2 or 3 days until 50ml is being added to each feed.  Starting with this very weak solution allows the horse’s body time to adjust to a new source of magnesium. Increasing quantity or strength too quickly may cause scouring.
  2. Slowly increase the strength of the solution by increasing the quantity of flakes being dissolved, again increasing the amount given to the horse by 10ml every 2 or 3 days.
  3. Continue slowly increasing the strength of the solution over a period of some six weeks or so until signs of deficiency have disappeared, or until a slight softening of the manure is noticed.  If this happens, reduce the amount of magnesium chloride fed each day to the previous level, then maintain at this level provided manure consistency is normal.

For interests sake, Fudge is currently getting two-three tablespoons of magnesium a day with awesome results. He no longer has a “watery” eye issue and his stifle lock is practically non existent - among other things.

It’s also good to know that excess magnesium is excreted and not stored through urine and faeces (which is why you should stop increasing the dosage when you see soft manure) so the risks of over feeding are low. [7]

The only exception is with animals (and humans) with pre-existing severe renal (kidney) problems so if you’re uncertain about the presence of kidney problems it is best to check with your vet.

Anyway, that’s about all you really need to know, but if you have any questions feel free to shoot me a message or do your own research using some of the sources provided. Hope you got something out of this post and if you start feeding magnesium as an extra supplement I would love to hear how it goes! 😊


I always mix up the stupid B vitamins and their actual names vs their number, and I told my internal med attending this and now I have to do a mini presentation tomorrow about B vitamins. So here is the handout I came up with, all basically from Step 1 First Aid.


Vitamin B1 (th1am1ne)

  • What does it do: cofactor for all the things in glucose breakdown
  • Deficiency: impaired glucose breakdown = ATP depletion. Wernicke-Korsakoff. Beriberi (wet/dry). Seen in folks whose primary diet is husked white rice. Dx = increase RBC transketolase following thiamine administration

Vitamin B2 (riboflavin/r2b2)

  • What does it do: component of FAD and FMN (source of e-), cofactors, kind of a big deal
  • Deficiency: cheilosis, corneal vascularization, magenta-colored tongue

Vitamin B3 (niacin/sunglasses cat face–> B3 )

  • What does it do: NAD+ and NADP+, redox rxns, Derived from tryptophan. Synth from B2 and B6. Used to tx dyslipidemia (lowers VLDL/raises HDL)
  • Deficiency: glossitis. Pellagra (anything that decreases tryptophan absorption or inc metabolism) = diarrhea, dementia, dermatitis
  • Excess: facial flushing, hyperglycemia, hyperuricemia


Vitamin B5 (pantothenate/5 pants)

  • What does it do: essential component of CoA and other things
  • Deficiency: dermatitis, enteritis, alopecia, adrenal insufficiency

Vitamin B6 (pyridoxine/siX)

  • What does it do: synthesis of lots of things (neurotransmitters, heme, molecules) and cofactor of transamination
  • Deficiency: convulsions, hyperirritability, peripheral neuropathy, microcytic sideroblastic anemia, cheilosis/stomatitis. MCC etoh and isoniazid.

Vitamin B7 (biotin/ALMOST has 7 letters)

  • What does it do: Cofactor for adding 1-carbon group
  • Deficiency: dermatitis alopecia, enteritis, fasting hypoglycemia. Can be caused by eating too many raw egg whites (avidin binds biotin).


Vitamin B9 (folic acid/9 months of pregnancy)

  • What does it do: converted to THF; synthesis of nitrogenous bases for DNA/RNA.
  • Deficiency: macrocytic megaloblastic anemia, hypersegmented PMNs, glossitis, NO NEUROLOGIC SX. Increased homocysteine, normal methylmalonic acid. MCC deficiency in US, dt etoh or pregnancy.

 10 and 11 ARE SILLY NUMBERS!!!

Vitamin B12 (cobalamin but who calls it that let’s be real)

  • What does it do: cofactor for important things
  • Deficiency: macrocytic megaloblastic anemia, hypersegmented PMNs, parathesias, subacute combined degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts. Increased homocysteine AND methylmalonic acid.
Pentose Phosphate Pathway

Pentose phosphates (including ribose-5-phosphate) are required for synthesis of

  • nucleic acids
  • ATP
  • cofactors
  • precursors to amino acids

glucose-6-phosphate is catabolised to form a pentose phosphate and CO2. NADP+ is reduced to NADPH in the oxidative stages

Stage One: Oxidative stage

3 enzyme catalysed steps

The dehydrogenases reduce NADP+ to NADPH

In the last step, 6-phospho-gluconate is decarboxylised. 

Stage Two: Non oxidative steps

Ribulose-5-phosphate is a pentose phosphate, but it’s not very useful. It can react in 2 initial reactions to produce more useful phosphates.

  • both are isomerations catalysed by phosphopentose isomerase
  • both are readily reversible
  • relative concentrations determine which way

Ribose-5-phosphate is a component of nucleotides, cofactors etc

Xylulose 5-phosphate gives excess ribulose-5-phosphate something to react with in the second stage of the PPP

-This makes molecules that can enter glycolysis from excess pentose phosphates formed in the first stage.

Only the first stage is controlled - NADP+ and NADPH compete for binding to glocose-6-phosphate dehydrogenase - therefore if there is lots of NADPH production of it, and pentose phosphates, will decrease

However not all cells require pentose phosphates and NADPH in equal amounts.

the PPP can operate in 3 modes

to supply necessary NADPH and pentose phosphates and make use of any excess materials

Equal requirement 

As above. 1 olecule of lucose-6-phosphate produces 1 molecule of ribose 5-phosphate and 2 NADPH

More ribose-5-phosphate required

eg in rapidly dividing cells - required for nucleotide synthesis

  • 1st oxidative step missed out
  • 2nd runs in opposite direction

More NADPH required

in cells conducting lots of biosynthesis eg fat cells carrying out fatty acid synthesis

  • 1st oxidative stage working full capacity
  • ribulose-5-phosphate is converted into glycolytic intermediates in the 2nd stage 
  • these then catabolised to produce ATP or used in glucogenesis to form glucose

anonymous asked:

I've been watching that kiss on repeat for like two straight weeks now and read all kinds of angst and I'm moving on to the next stage of fitzsimmons... I'm in desperate need of some science nerd /SMUT/. Can you hook a poor fangirl up with some pwp hotness?

We’re right in that kiss-watching boat with you, Anon!  Thankfully, this fandom has some excellent smut writers (and check out our smut tag as well as our season 1 smut recs). 

We can certainly recommend some in-world smutty fic (assuming that’s what you mean by science nerd pwp hotness) but you should definitely check out these authors’ AO3 pages so that you can appreciate their many sexy fics! 

@lavendergaia, Touch of Blue (Touch of You)

@mech-bull, The Morning After

@0hcicero, Sex Ed With Skye

@memorizingthedigitsofpi, Saucy

@madalayna, Afraid of the Light

@agentverbivore, Wide Awake

@lono285, Cofactors to the Catalyst

@pleaseletmeshowyou, The Value of Communication

@quibbler, A Series of Firsts

@jessssicajones, it’s a sharp shock to your soft side

@natasharommanoff​, From your skin to mine

@mrsleopoldfitz, Dublin

@engineerleopoldfitz, Paint Me By Numbers

heartlines, Operation Sandwich Fail

@snarkysweetness, Don’t Leave Me

@blogginghaley, Getting There

@unbreakablejemmasimmons, More Adventurous

@elizabaethhenstridge, the lights glimmer around us like a thousand golden stars (blinding, dizzying, don’t let it stop)

@stillnotapepper, The Whole Dom Time

@eclecticmuses, A Gross Lack of Communication (not in-world, but we don’t mind)

@daftmunky, Now I See (The Colours of You and Me) (not in-world, but we don’t mind)

@plinys, it’s just the woman in you (that brings out the man in me) (not actually that smutty, but we don’t mind)

@monolithjemma, Nine Little Words  (not actually that smutty, but we don’t mind)

@everyl1ttleth1ng, Conviction (not actually that smutty, but we don’t mind)

@amanda-rex, Misunderstandings (slightly less porn than plot, but we don’t mind)

And you might keep an eye on @happilyshanghaied‘s Turnabout!  It doesn’t include any Fitzsimmons smut yet, but it might soon!

Hope that helps!  Happy reading!


Our new video about enzymes is out! We explain enzymes and how they remind us of Pacman!

Vocabulary covered includes active site, induced fit, coenzyme, and cofactor. Also the importance of ideal pH and temperatures for enzymes are discussed.

5) Healthy foods for runners/anyone!

These are foods that are good for anyone, but I’ll explain why they can be specifically applicable for runners! I believe that food can play a major role in performance so I thought I’d share some of my knowledge with you because running fast is so much fun!!

First, I’ll lay down some ground rules for general healthy eating for performance!

1. Stay with the good carbs.

The carbs that you should aim for should have a low glycemic index (GI). GI is basically a measurement on how fast the carbs are released in your blood, so the slower, the better because it would give you a more steady supply of energy. Low GI foods mostly contain lots of fiber because fiber takes longer to digest. Some examples include fruits, vegetables, beans, and yogurt!

2. Protein!!

Protein digests slower than carbs, so it will also provide you with a steady supply of energy! It will also help you build all those lovely muscles!! It’s recommended that you aim for one gram of protein per pound of bodyweight. Runners generally need more protein because we’re constantly breaking our muscles down everyday by running. I’m a huge fan of egg whites, fish (especially tuna and salmon!!), and yogurt! Whey protein powder mixed with almond milk tastes great as well!

3. Frequent meals

If you eat more frequently, lets say every 3 hours, then you will be providing your body with a constant supply of energy throughout the day. For me, I usually only do this when I have a race because sometimes I find it inconvenient.

4. Great foods!!!!! Keep in mind that everything in this list is of equal awesomeness.

-Bananas! good for before and after your workout. It’s full of carbs and vitamin b6. Vitamin b6 acts as a cofactor for proteases which helps you digest protein after a workout, so you should eat bananas with protein after a workout!

-Fish! My favorites are tuna and salmon. Fish contain omega 3 fats which help keep the not-so-good fat in your blood (triglycerides) in balance!

-Oatmeal! Oatmeal is a low GI carb so it’s a great pre-race food because it will provide you with a steady supply of energy!

-Yogurt! contains protein, calcium, potassium. Calcium is important for building your bones and potassium is important for initiating muscle contractions! Hence those sodium potassium pumps on your neurons!! It’s also full of good bacteria to live in your large intestine~ i like to eat it in the morning. i tend to stick with nonfat because whole milk makes my stomach extremely upset.

-Energy bars! I don’t consume them often because I’d rather get my energy from real food. But when i do, it’s before a race because it’s quick and densely packed with calories so it doesn’t take much space in my stomach. My favorites include cliff and kind bars.

-Milk! It contains both protein and carbs and it’s a great post workout because you need to refuel your energy stores and you also need that energy for your body to build muscles!

-Almonds! They are full of vitamin E which function as antioxidants which helps protect your cells! They also contain omega 3 fats. I like to sprinkle them on my yogurt in the morning and have them as a snack throughout the day. I also like to munch on almonds in the bus before a race!

-Eggs! Because eggs are animal protein, they contain all the essential amino acids! chose omega 3 enhanced eggs so you get more healthy fat. They also contain vitamin K, which are good for bones, and chloine, which are good for brains eyes. Hard boiled eggs are a great snack for anytime!!

-Sweet potatoes! My favorite pre-race meal!! I always “carb load” on sweet potatoes instead of pasta before races. Containing vitamin C and A, potassium, iron, manganese, and copper, they are packed with way more nutrients than pasta!! I like to microwave/steam slices and eat them plain because they are already full of wonderful flavors so appetizing to my taste buds!

-Beans! Full of lots of wonderful protein and fiber! Also, folate is good for your heart and circulation! Beans and legumes are low GI foods so they are slowly released in the body so you receive a steady supply of energy by having a controlled blood sugar level. I love black beans!

-Fruits and vegetables! This one is a given. Eat the rainbow. All fruits and vegetables are my favorite!!

-Skinned chicken! Great source of protein.

-Green Tea! Basically contains lots of antioxidants which protect your cells from damage! I wake up to a cup of lovely green tea every morning!

There are obviously a lot more, but those are just some of my favorites.

5. Pre-race foods

-Night before: Sweet potatoes, lot of healthy green vegetables, and fish/chicken

-Breakfast (if it’s in the afternoon): Yogurt topped with almonds, berries, and chia seeds plus a banana. (I have this every morning)

-Pre-race meal: Several bananas, almonds, dried fruit (sometimes), pita bread (I specifically looked for the one with the lowest fiber at trader joes so it wouldn’t give me stomach problems)

-Before warming up: A few bites of a cliff bar

-Between races: Any fruit, cliff bar, almonds

swimming-to-djibouti  asked:

Actually, science supports veganism in many ways, and the reason it's not found in any traditional cultures is because people never had the option to survive this way.

In reply to your other “ The only benefit of eating meat (that I’ve found) is b12.” ask, 

It’s more than just B12 (I don’t understand how this is the only one you’ve ‘found’, seeing as this is the first thing listed when you Google is being vegan/veggie is good for you.)

  • Animal protein contains all the essential amino acids in the right ratios. It is important for muscle mass and bone health, to name a few. Vegans don’t get any animal protein, which can have negative effects on body composition (2, 3, 4, 5).
  • Creatine helps form an energy reservoir in cells. Studies show that vegetarians are deficient in creatine, which has harmful effects on muscleand brain function (6, 7, 8).
  • Carnosine is protective against various degenerative processes in the body and may protect against aging. It is found only in animal foods (9, 10, 11).
  • Docosahexaenoic Acid (DHA) is the most active form of Omega-3 fatty acids in the body and primarily found in animal foods. The plant form of Omega-3s, ALA, is inefficiently converted to DHA in the body (12, 13, 14).
  • Not surprisingly, vegans and vegetarians have much lower testosterone levels than meat eaters.   - Popular Science

K2. You can eat as much calcium as you want but it won’t strengthen your bones unless it is accompanied by vitamin K2.

Unlike vitamin K1, plants do not provide vitamin K2.(The one and only exception to this rule is natto, a fermented soybean product. One problem, however, is that natto is, for the majority of humans and animals, repulsive to eat). Like other fat-soluble vitamins, Vitamin K2 is found fatty sources – Mother Nature packages the vitamin with the cofactors required to absorb it. You’ll get vitamin K2 in pastured egg yolks, milk and cheese from grassfed animals, liver, beef, and chicken.” - Link

Vegetarians have a higher risk of developing nutritional deficiencies caused by lack of animal protein in their diet than meat-eaters. The more restrictive the diet, the higher potential for vitamin B-12, protein, calcium and iron deficiencies. Food from animals supplies all the essential amino acids, the building blocks for protein, while most plant proteins, with the exception of soy and the grain quinoa, do not contain all the essential amino acids. Vegetarians must consume foods that contain different amino acids over the course of the day to ensure that they get all the amino acids they need. While plants contain iron, your body absorbs the iron they supply, called nonheme iron, less efficiently than heme iron from meat. Consuming foods high in vitamin C along with plants high in iron increases iron absorption. Many vegetables contain substances that reduce calcium absorption, increasing the risk of calcium deficiency and bone loss in vegetarians who don’t consume dairy products. Beans, lentils and vegetables such as spinach contain iron.” - Healthy Eating 

Any negative effects of eating meant listed in those links can be countered by simply eating healthy, lean meats… no need for supplements and or having to cease consumption entirely. And therefor, flip side, any “benefits” of being vegan (low cholesterol. etc) can be achieved on an omnivorous diet as well. They aren’t exclusive. Unnatural additives or bad fats that harm you can be found in both diets and can be avoided or consumed with both. 

Oh by the way, you know how soy is listed as an alternative protein in most of those links? Long term, high soy consumption is terrible for you and terrible for the environment. Soy increases estrogen, which can lead to all sorts of issues. 

So you’re saying it’s not naturally sustainable? Sounds like a good argument against it on a logical level and on a health level. 

Most of the pros on this list are canceled out by the cons (#s 1-4,9-22,etc), or can be achieved just the same by eating a healthy omnivorousness diet (#7,9, etc)

I’m not seeing a good argument for it.  When I Google reasons to go vegan or for things telling you that soy isn’t bad, I’m getting sources like Peta and blogs like “celestial healing”…

My UWorld notes- 5

To those who were waiting yesterday for this post, I’m extremely sorry. For some reason I Thought yesterday was sunday -____- but here it is. 

  • reflex tachycardia caused by nitrate can be prevented by administering beta adrenergic blockers w

  • prazosin- selective alpha 1 adrenergic blocking medication used for HTN and BPH

  • hydrochlorothiazide is a weak diuretic

  • phenylephirine is an alpha agonist which is classified as a vasopressor agent. Its used in cases of shock and severe hypotension

  • hydralazine is a direct acting arteriolar dilator . It causes a reflex tachycardia which can also be prevented with administering beta blocker

  • ataxia telangiectasia an autosomal recessive d/o characterized by DNA hypersensitivity to ionizing radiation. Cerebellar atrophy leads to ataxia that occurs in first years of life. . Patients with ataxia telangiectasia also have sever immunodeficiency with repeated sinopulmonary infections. This risk of cancer in these patients in increased significantly b/c of inefficient DNA repair

  • XP is characterized by DNA hypersensitivity to UV radiation causing premature skin agin and increased risk of skin cancer (malignant melanoma and squamous cell carcinoma)

  • Fanconi anemia is caused by hypersensitivity of DN TO CROSS LINKING AGENTS

  • Bloom syndrome is characterized by generalized chromosome instability. Increased susceptibility to neoplasms is present

  • HNPCC d/t to defect in DNA mismatch repair enzymes leading to increased susceptibility to colon cancer

  • caudate nucleus atrophy- huntington dz

  • Lewy bodies- Parkinsonism

  • loss of neurons in substantia nigra- Parkinson’s dz

  • neurofibrillary tangles in neocortex – Alzheimer’s dz

  • double vision while walking down the stairs or while reading the newspaper- palsy of cranial nerve 4 (trochlear nerve)

  • optic nerve (CN2) transmits visual info to brain damage causes loss of vision

  • CN3 occulomotor nerve innervates superior rectus medial rectus inferior rectus and inferior oblique. Which all collectively perform most ye movement. Palsies of this nerve can cause vertical and horizontal diplopia and an enlarged nonreactive pupil

  • abducens nerve CN6 innervates lateral rectus which is responsible for abdcution of eye. Palsy of this nerve can cause horizontal diplopia and inward deviation ( inward deviation)

  • MLF lesion a/w internuclear ophthalmoplegia, which presents with impaired horizontal eye movement and weak adduction of affected eye with simultaneous abduction nystagmus of contralateral eye

  • at low doses atenolol is a selective beta 1 adrenergic antagonist . Beta 1 receptors are found in cardiac tissue and on renal juxtaglomerular cells but not on vascular smooth muscle. The beta 1 receptor is G protein coupled receptor a/w Gs G protein which increases cAMP levels. Blockage of beta receptor therefore means decreased cAMP levels in cardia and renal tissue without affecting cAMP levels in vascular smooth muscle

  • pure red cell aplasia is a rare form of marrow failure characterized by sever hypoplasia of marrow erythroid elements in setting of normal granulopoiesis and thrombopoiesis. Pure red cell aplasia is a/w thymoma lymphocytic leukemias and parvovirus B19 infections

  • deficiency of 21 hydroxylase is MC type of CAH. . These patients present with cortisol and aldosterone deficiency combined with androgen excess.. genitalia of females infants may be masculinized to some degree; male infants however are normal in appx

  • When asked a question regarding DKA know that ph is decreased H2PO4 is increased (it is titratable acid) and also bicarbonate excretion is decreased. This response is overtime meaning these changes are made because of the acidosis that the patient has . Therefore in order to fix metabolic acidosis d/t DKA bicarbonate excretion is decreased and urinary ph is decreased and titratable acid excretion is increased.

  • Musculocutaneous nerve innervates flexor muscles of upper arm and provides sensory innervation to lateral forearm. Musculocutaneous nerve is derived from upper trunk of brachial plexus and can be injured by forceful injuries that cause separation of neck and shoulder. It is derived from C5-C7 ventral rami

  • posterior arm and forearm are both innervated by the branch of the radial nerve which is posterior cutaneous nerve of the arm and posterior cutaneous nevre of the forearm

  • thenar eminence is innervated by recurrent branch of median nerve

  • g6pd deficiency – cant convert glucose 6 phosphate to 6 phosphogluconate . G6Pd requires NadPH as a cofactor to work

  • urine sample turned black= alkaptonuria which is an autosomal recessive d/o in which lack of homogentisic oxidase blocks the metabolism of phenylalanine and tyrosine at the level of homogentisic acid leading to accumulation of homogentisic acid. Turns black because homogentisic acid excreted in urine undergoes oxidation when exposed to oxygen in air

  • alkaptonuria cause ochronosis a blue black pigment evident in ears nose and cheeks

  • conversion of phenylalanine to tyrosine is defective in PKU and usually occurs d/t defect in phenylalanine hydroxylase

  • small percentage of PKU cases are also d/t dihydrobiopterin reductase deficiency

  • branched chain a.a. Are valine isoleucine and leucine

  • blastomyces dermatidis is a dimorphic fungus that is seen in tissue as round yeasts with doubly refractive walls and broad based budding. Endemic to great lakes and ohio and Mississippi river regions, present in soil and rotten organic matter

  • blastomyces mold form (branching hyphae) predominates in environment with average temperature 25-30 degrees Celsius. In the human body it assumes yeast form (single cells)

    • blastomyces in lungs assumes yeast form and induces granulomatous response

    • aspergillus fumigatus causes lung dz in immunocompromised and only has a mold form . It is seen as septate hyphae that branch at 45 degrees (angle)

    • oppotunistic mold with irregular non septate hyphae that branch at wide angles (>90)= mucor and rhizopus

    • starts with just a sinus infection and then you end up getting a rapid infection to the brain because this organism can penetrate the cribriform plate causing frontal lobe abscess – Mucor and rhizopus

    • cryptococcus neoformans can also cause lung dz but in addition causes meningitis in immunocompromised and in contrast to blastomycosis it forms narrow based buds and has thick polysaccharide capsule which stains with india ink

    • histoplasma capsulatum causes lung dz and is also a dimorphic fungus like blastomyces but the yeast form of histoplasma is found intracellularly within macrophages

    • coccidioides immitis is also a dimorphic fungus but is seen as spherules (round encapsulated structures containing many endospores) in tissue sample, barrel shaped arthroconidia a/w dust storms which causes San Joaquin Valley fever (inhalation of dust particles) 

X-linked Recessive Diseases List
  • Alport’s Sd: "hereditary nephritis", type IV collagen deficiency, alternating thickening & thinning of GBM, COL4A5 mutation, hearing loss, ocular abnormalities (lens & cornea), hematuria (gross or micro) since childhood.
  • Bruton’s Agammaglobulinemia: btk gene defect, no mature B cells or plasma cells, low lymphoid tissue, hepatitis, enterovirus infxs, first 6 months protected by maternal ab (no symptoms)
  • Becker’s Muscular Dystrophy: altered dystrophin gene, later onset than Duchene's, slow progression, relatively normal life span, less severe, rare cardiac involvement.
  • Chronic Granulomatose Disease (CGD): NAPDH oxidase deficiency, recurrent catalase (+) infxs, nitroblue tetrazolium test negative (yellow)
  • Congenital Aqueductus Stenosis: MCC of congenital obstructive hydrocephalus.
  • Color blindness (red-green): can't distinguish shades of red and green (usually blue-green)
  • Duchene’s muscular Dystrophy: dystrophin gene mutation (Xp21), absent dystrophyn protein, MC & severe of muscular dystrophies, normal until 5yo, short life span (<30yo), progressive muscle weakness, calf pseudohypertrophy, <3 failure, arrythmias, respiratory insufficiency and infxs (decreased mucociliary clearence). Pneumonias CC of death.
  • Fabry’s Disease: alpha Galactosidase A, Ceramide trihexose accumulation, angiokeratomas, renal failure, peripheral neuropathy.
  • Glucose 6-P Dehydrogenase (G6PD) Deficiency: chronic hemolytic anemia, MCC of enzymatic deficiency HA, Heinz bodies, bite cells. Triggers are infections, drugs (antimalarial), fava beans
  • Hemophilia A & B: factor VIII & IX deficiency respectively. PTT prolongation.
  • Hunter Disease: iduronate sulfatase deficiency, heparan sulfate accumulation, no corneal clouding, aggressive behaviour.
  • Inherited Nephrogenic Diabetes Insipidus: V2 receptors in collecting duct don't respond to ADH.
  • Lesch-Nyhan Sd: HGPRT1 deficiency, spastic cerebral palsy, self-mutilation, hyperuricemia, oral crystals in diapers, early death.
  • Menkes Disease: ATP7A gene mutation (copper efflux protein), Cu+ is lysil oxidase cofactor, Cu+ accumulates in intestine & kidneys; deficient in other tissues = deficient collagen cross linking; steely 'kinky' hair, MR, arterial tortuosity, hypotonia.
  • Ornithine Transcarbamoylase Deficiency: urea cycle, orotic aciduria + hyperammonemia (no megaloblastic anemia), orotic acid accumulation, increased glutamine . Cerebral edema, lethargy, vomiting, hyperventilation, convulsions, coma, death.
  • SCID: IL-receptor, Gamma chain deficiency
  • Wiskott Aldrich Sd: combined partial B & T immunodeficiency, IgM deficiency, thrombocytopenia, eczema.