HLA associations mnemonic

Hi everyone!
Here’s a complete guide on how to remember the HLA associations. Let’s catch em all!

Doctors (DR) will turn into MD’s someday.. The thought makes you go, “Aah”
Starting with 2 and ending with 5, your mnemonic for DR associations is "MD.. AAH!"
HLA DR2 - Multiple sclerosis
HLA DR3  - Diabetes mellitus type 1
HLA DR4  - Arthritis (Rheumatoid, also the one associated with Lyme’s disease)
HLA DR5  - Anemia (Pernicious, causing B12 deficiency)
HLA DR5  - Hashimoto’s thyroiditis

If it’s not too much, you can remember “Hey! This Doctor is going to be good MS someday” to remember Hay fever, Goodpasture’s syndrome and Multiple Sclerosis for HLA DR 2.

Hi5 is another way you can remember about Hashimoto’s relation to DR5.
HiPA5 will help you remember Pernicious Anemia with it too (If the A’s of Arthritis and Anemia confuse you!)

I use rhymes for all the other associations, make sure you sing em with a funny tone!

"Two, three S-L-EE.
Three, four, not so sour.”

HLA DR2 and HLA DR3 is associated with SLE
HLA DR3 and HLA DR4 is associated with Diabetes mellitus type 1
(not sour - sweet - sugar - diabetes lol)

You can also remember with the pokemon, "Two, three, butterfree" for the butterfly rash in SLE.. Whatever suits you.

A threeFrEaking three.
HLA A3 is associated with Hemochromatosis.
(fe3+ - iron - hemochromatosis)

Be there at eight, don’t be late.
HLA B8 is associated with Grave’s disease.
(late - dead - grave)

Seven, heavenly pee.
 HLA DR7 is associated with steroid-responsive nephrotic syndrome.
(pee - kidney - nephrotic syndrome)
Seven rhymes with heaven, lee rhymes with pee, I don’t know what I was even thinking when I made this!

For HLA B27, the PAIR mnemonic is famous.
Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome.

The above mnemonics will suffice for the exam.

The below facts are not very high yield, but for the sake of completion here you go -
SCAM 3 - Sjogrens syndrome, Chronic active hepatitis, diabetes mellitus type 1 for HLA DR3.

If you extend the line in 4, it looks like an A.
A for Arthritis. Flip the A and it looks like V.
V for vulgaris, pemphigus vulgaris.
So HLA DR 4 is associated with Arthritis as well as Pemphigus vulgaris,

That’s all!
Hope it helps you all < 3

Credits here.

This post is awesome!

How to differentiate between Lateral Pontine Syndrome vs Lateral Medullary Syndrome.

What is lateral medullary syndrome?

Neurological symptoms due to injury to lateral part of the medulla. Also called Wallenberg’s syndrome.

 When does it happen?

When the posterior inferior cerebellar artery (PICA) is occluded.

What is lateral pontine syndrome?

Neurological symptoms due to injury to lateral part of the pons.

When does it happen?

When the anterior inferior cerebellar (AICA)  artery is occluded.

What do both the lesions have in common?

  •  Ipsilateral horner’s syndrome.

Why? Descending hypothalamic tracts affected.

  • Contralateral loss of pain and temperature.

Why? Lateral spinothalamic tract affected.

  • Ipsilateral cerebellar ataxia.

Why? Cerebellar peduncles affected. (Inferior cerebellar peduncle in medullary and middle cerebellar peduncle in pons.

  • Nausea, nystagmus, vertigo, vomiting.

Why? Vestibular nuclei involved.

  • Ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia).

Why? Spinal trigeminal nucleus and tract involved.

  • Ipsilateral hearing loss.

Why? Cochlear nuclei and intraxial nerve fibers involved.

So how do I tell the difference between the two?

 Lateral medullary syndrome:

 Dysphagia, dysarthria, dysphonia

Why? Nucleus ambiguous involved.

Lateral pontine syndrome:

  •  Ipsilateral paralysis of the upper and lower face (lower motor neuron lesion).
  • Ipsilateral loss of lacrimation and reduced salivation.
  • Ipsilateral loss of taste from the anterior two-thirds of the tongue.
  • Hyperacusis.

Why? Facial nucleus and facial nerve involved.

 All the credits go to the brilliant medicowesome !!

For more posts like these follow medicowesome on tumblr or http://medicowesome.blogspot.in/p/blog-page_1239.html

Awesome blog: MEDICOWESOME

Hey guys! there’s this blog that i’ve recently started following and reblogging a lot! 

If you haven’t started follow her/him, start now!!! She/he explains everything perfectly and in a very easy to learn way :) 

This is the blog: medicowesome

Enjoy ;)

R.

Watch on nakimedicalblog.tumblr.com

How to draw the tympanic membrane

7
How to remember lipoprotein disorders

Hello everyone!

Click here to read about Lipoproteins and apoproteins if you need a quick revision before we get started :)

In this blog post, I’ll be talking about lipoprotein disorders, how to remember them and some facts that you need to know about the disorders.

Type I hyperlipoproteinemia
Chylomicrons increased in childhood.
VLDL increased later in life.

Lab findings: Increase in serum triglycerides.

Why?
CPL (Capillary lipprotein lipase) hydrolyzes triglycerides in lipoproteins.
It requires apo-CII as a co-factor.

Clinical findings: Acute pancreatitis (Pancreatic vessels filled with chylomicrons rupture), eruptive xanthomas.

Type II hyperlipoproteinemia
Serum LDL is increased.

Lab findings:
In IIa, only cholesterol is increased.

Why?
Liver cholesterol synthesis is deprived of negative feedback.

In IIb, cholesterol and triglycerides are increased.

Why?
Liver overproduces VLDL in IIb

Acquired causes: Primary hypothyroidism, nephrotic syndrome, extrahepatic cholestasis.

Clinical findings: Tendon xanthomas, Xanthelasma, premature coronary artery disease and stroke.

Type III hyperlipoproteinemia
This dysbetalipoproteinemia is also known as “remnant disease”.

Lab findings: Elevation in cholesterol and triglyceride levels.

Why?
Apo E is required to remove chylomicron remnants and IDL (remnant of VLDL).

Clinical findings: Palmar xanthomas, increased risk for coronary artery and peripheral vascular disease.

Type IV hyperlipoproteinemia
Increase in VLDL.

Lab findings: TG accumulates
in preference to cholesterol, like IIb.

Acquired causes: Excess alcohol, OCPs, Diabetes mellitus, chronic renal failure, thiazides, beta blockers.

Clinical findings: Eruptive xanthomas, increased risk for coronary artery and peripheral vascular disease.

Type V hyperlipoproteinemia

Increase in chVlomicrons and VLDL.

It is a mixture of types I and IV familial dyslipidemias.

Lab findings: TG levels are high, whereas cholesterol concentration increases only moderately.

Clinical findings: Like type I, but unlike type IV, there is no major risk of atherosclerosis, so that pancreatitis and eruptive xanthomas remain the main complications.

For the sake of completion, I’d like to add another disease -
Tangier disease is due to lack of ABC1 cholesterol transporter gene.
Cholesterol accumulates inside cells. Blood HDL and cholesterol are low.
The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.

*phew* That’s all!

Like I always say, if you stare at a word long enough, you find the mnemonic in the word itself :P
I made these myself, hope you find them helpful ^__^

Happy Indian Independence Day :)

-IkaN

2

Hey everyone!

We recently got 500 followers on tumblr & I couldn’t think of a more fun way to celebrate it!! =D

I missed the 500th follower though ^__^”

I’d love to thank all of my followers for reblogging & liking my posts :)

Especially, My Notes for USMLEDr. Cranquis’ Mumbled Gripes

Thank you so much everyone for your love and support <3

As for the emoticon game, I won’t be posting the answers online but you can email me on medicowesome@gmail.com for the answers and I’ll get back to you as soon as I can!

That’s all!

-IkaN

Southern, Northern, and Western blot mnemonic

Hello everyone!

The mnemonic to remember blotting techniques is “SNoW DRoP

S -    Southern - DNA     - D
N -   Northern - RNA     - R
O -   Oooooo - Ooooo    - O
W -  Western - Protein   - P

That’s all!

Hope you won’t go, “Which direction was that again?” in the exam =P

-IkaN

Competitive and non competitive inhibitors simplified

image

Let me present to you the most understandable, simplified, awesome analogy for explaining competitive and non competitive inhibitors =D

image

When you are hungry, you have affinity for food.
Hunger has affinity for food like enzymes have affinity for substrates.

image

Rice is the substrate for your hunger.
You happily eat it at some random rate.

image

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.

image

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.

image

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.

image

Say, you were hungry.. Until you saw something gross and it ruined your appetite.
The “gross thing” is a non competitive inhibitor.

image

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.

image

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.

image

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

-IkaN

10

I feel reviewing from Blogger is easier in such long posts.. Click here to view the post on the website.

Darrow-Yannet Diagrams simplified

What are Darrow Yannet diagrams?

They are graphs that tell you the osmolarity and volume changes of body fluids.

X axis represents volume.
Y axis represents solute concentration.

Total body water = 2/3 ICF (Intracellular fluid) + 1/3 ECF  (Extracellular fluid)

Remember:
All volume disturbances originate in the ECF compartment.
Changs in ICF are in response to changes in ECF.

How to make the graph in your head -
Step 1. Figure out what happens to the osmolarity and volume in theECF compartment (ECF is the smaller compartment)
Step 2. Think how is ICF affected?

Let’s review some examples to make sure we understand the concept!

Loss of whole blood, adult diarrhea.

What will happen to volume in ECF compartment?
Will decrease.

What will happen to osmolarity in ECF compartment?
Will not change. (Why? Isotonic fluid is lost.)

What will happen to ICF volume and osmolarity?
No osmotic gradient, therefore, will not change :)

That was easy!
Let’s look at a similar example.

Infusion of excessive isotonic saline.

What will happen to volume in ECF compartment?
Will increase.

What will happen to osmolarity in ECF compartment?
Will not change. (Why? Isotonic fluid is lost.)

What will happen to ICF volume and osmolarity?
No osmotic gradient, therefore, will not change.

See? It’s very simple!

Loop diuretics, Addison’s disease.

(Loops make you lose sodium and water, but more of sodium than water.
Addison’s disease is adrenal insufficiency. Aldosterone makes you retain sodium so in the absence of aldosterone, you will lose sodium.)

What will happen to osmolarity in ECF compartment?
Will decrease. (Why? You are losing sodium.)

What will happen to volume in ECF compartment?
Will decrease. (Why? Fluid moves from ECF to ICF)

What will happen to ICF volume?
Will increase. (Decrease in osmolarity shifts the fluid into ICF)

SIADH, compulsive water drinker.

(SIADH: You are conserving too much water due to ADH.
Water drinker: You are having too much water =P )

What will happen to osmolarity in ECF compartment?
Will decrease. (Why? You are diluting by adding water.)

What will happen to volume in ECF compartment?
Will  increase. (Why? You are adding fluid.)

What will happen to ICF volume?
Will increase. (Decrease in osmolarity shifts the fluid into ICF)

Right heart failure, Cirrhosis, Nephrotic syndrome.

What will happen to osmolarity in ECF compartment?
Will decrease.

What will happen to volume in ECF compartment?
Will  increase.

What will happen to ICF volume?
Will increase.

Can’t figure why? Well.. Here’s why!

In all three conditions, there is a decreased effective circulatory volume (Effective arterial blood volume)
[See diagram]

This leads to decreased renal blood flow and pressure and increased ADH secretion and activates the renin angiotensin aldosterone system, increasing sodium and water reabsorption.

Note: Total body sodium is increased, however, serum sodium is decreased.
Why?
The alteration in Starling forces redirects the sodium containing fluid in the interstitial space (leading to edema)

*phew* That was work! Let’s see what happens during sweating ;)

Sweating.


What will happen to volume in ECF compartment?
Will decrease.

What will happen to osmolarity in ECF compartment?
Will increase. (Why? Hypotonic fluid is lost.)

What will happen to ICF volume?
Will decrease.

Your sweat doesn’t taste salty.. That’s how I remember it’s hypotonic, not hypertonic like tears T_T

Insensible water loss in fever, diabetes insipidus, alcohol.

What will happen to volume in ECF compartment?
Will decrease. (Water is lost. Why? ADH action is lost in Diabetes insipidus, alcohol inhibits pitutary secretion of ADH, water evaporates from the warm skin surface in fever)

What will happen to osmolarity in ECF compartment?
Will increase.

What will happen to ICF volume?
Will decrease.

Note: The ECF contraction is mild because there has been no loss of sodium.

Next one is easy too.. Keep going! <3


Infusion of sodium bicarbonate, sodium containing antibiotics.

What will happen to osmolarity in ECF compartment?
Will increase.

What will happen to volume in ECF compartment?
Will increase. (Why? Fluid moves from the ICF to ECF)

What will happen to ICF volume?
Will decrease.

..And the last one!!! :D

Hyperosmolar nonketotic coma, diabetic ketoacidosis.


What will happen to osmolarity in ECF compartment?
Will increase. (Why? Glucose is an osmotically active particle)

What will happen to ICF volume?
Will decrease. (Why? Fluid moves from the ICF to ECF)

This gets a little tricky.. ^__^”

What will happen to volume in ECF compartment?
Will decrease.
Why?
Glucose in urine acts as an osmotic diuretic and the water from ECF is lost.


That’s all!

This blog post took me forever to write.. I feel the color coding makes it easier to see the changes in the diagrams :)
Hope you had fun learning and revising with me and see you in the next post <3

-IkaN

Case scenarios: When you don't give patients 100% O2 and why

Clinical scenario #1: Chronic lung disease patient.

The ventilatory drive of patients with chronic lung disease is primary due to their hypoxemia, rather than CO2 levels. This is because pCO2 receptors are adaptive. Chronically elevated pCO2 makes central receptors unresponsive in COPD patients. Administration of a high O2 mixture to relieve the hypoxemia is contraindicated because this removes the hypoxic drive, leading to severe hypoventilation.

Clinical scenario #2: Drug overdose where central receptors are blocked.

In morphine or heroine overdosed patients, central receptors are knocked out and the hypoxic drive is what keeps them breathing. Administration of a 100%  O2 mixture to relieve the hypoxemia is contraindicated too because this removes the hypoxic drive which kept them breathing.

Clinical scenario #3: Tracheostomy following prolonged respiratory obstruction.

Apnea in patients is due to washing out of CO2 which was acting as a respiratory stimulus. Treatment is to administer 5% CO2 in oxygen or assisted ventilation.

I know there are many such scenarios but I can’t think of any more at the moment. The basic concept in such cases is the same - understanding which receptor acts as a drive for respiration and not messing with it! Lemme know if you recall any more and we’ll add more scenarios here =)

I was super super excited to share this mnemonic with you ^__^

What is lateral medullary syndrome?
Neurological symptoms due to injury to lateral part of the medulla
(also called Wallenberg syndrome)

When does it happen?
When the posterior inferior cerebellar artery is occluded

What is lateral pontine syndrome?
Neurological symptoms due to injury to lateral part of the pons

When does it happen?
When the anterior inferior cerebellar artery is occluded


What do both the lesions have in common?
 

Ipsilateral horner’s syndrome
Why? Descending hypothalamic tracts affected

Contralateral loss of pain and temperature
Why? Lateral spinothalamic tract affected

Ipsilateral cerebellar ataxia
Why? Cerebellar peduncles affected
(Inferior - medulla, middle - pons)

Nausea, nystagmus, vertigo, vomiting
Why? Vestibular nuclei involvement

Ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia)
Why? Spinal trigeminal nucleus and tract involved

Ipsilateral hearing loss
Why? Cochlear nuclei and intraxial nerve fibers involved


So how do I tell the difference between the two? @__@


Lateral medullary syndrome:
Dysphagia, dysarthria, dysphonia
Why? Nucleus ambiguus involved

Lateral pontine syndrome:
Ipsilateral paralysis of the upper and lower face (lower motor neuron lesion)
Ipsilateral loss of lacrimation and reduced salivation
Ipsilateral loss of taste from the anterior two-thirds of the tongue

Hyperacusis
 Why? Facial nucleus & facial nerve involved


Cool fact:

There is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face

This finding is diagnostic

That’s all!

I created the mnemonic all by myself =D
Hope that was fun and helpful :)

-IkaN

Kawaii means cute in Japanese.
Helps you remember Kawasaki’s disease, also known as mucocutaneous lymph node syndrome, with strawberry tonguecoronary artery aneurysms and Asian predisposition.

That’s all!

PS: I love Japanese culture & kawaii things :3
I wanna visit Japan someday, wear a kimono, eat Sushi & Onigiri, color my hair pink, cosplay anime and watch cars drift ^__^
I love how this post allowed me to express my love for Japan & calligraphy =D

-IkaN

Normal arterial blood gas values and serum electrolytes mnemonic

Know the normal pH of blood 7.35 - 7.45.. That’s all you need to remember I promise!

Take the numbers after the decimal, 35 - 45; and that’s your pCO2.

Divide 45 by 2, approx 22; and that’s your bicarbonate levels.

Multiply 45 by 2, that is, 90; and that’s your pO2.

So in summary -
pH: 7.35 - 7.45
PCO2: 33 - 45 mm Hg
PO2: 75 - 105 mm Hg
Serum bicarbonate: 22 - 28 mEq/L

That’s all!

Eid mubarak to everyone :)

5
Aortic arch derivatives mnemonic images  -HD images here

I made these diagrams guessing these will be helpful ^__^

The greater part of the first and second artery disappear. In adult life first arch artery is represented by the maxillary artery and the second arch persists for some part of fetal life as the stapedial artery.
The mnemonic people use for that is, “First is max" & "Second is Stapedial" =)

Mnemonic for third arch artery:
C for Carotid, C the third letter of the alphabet.”

The third arch artery gives off a bud that grows cranially to form the external carotid artery.

The internal carotid artery is derived from the distal part of the third arch artery and cranial most part of the dorsal aorta.

The brachiocephalic trunk is formed by the right horn of the aortic sac.

Mnemonic for fourth arch artery:
"fOUR rhymes with AOR for Aorta.
fouRS for Right Subclavian.”

The ascending aorta is formed from the truncus arteriosus.

The arch of aorta is derived from the vental part of the aortic sac, it’s left horn and the left fourth arch artery.

Mnemonic for sixth arch artery:
Well, this is lame but the letter 6 looks like lungs to me =D

Pulmonary trunk is derived from truncus arteriosus.

Mnemonic for subclavian artery:
"7 is S."
Seventh InterSegmental Subclavian!

The right subclavian artery is derived from the right fourth arch artery and right seventh cervical intersegmental artery.

On the left side, the subclavian is derived entirely from the seventh cervical intersegmental artery.

That’s all!

Hope you had fun learning ^__^

-IkaN

Which cell secretes what? Gastrointestinal mnemonics

"pH" for Parietal cells secrete H+ ions.

"PC" for Pepsin is secreted by Chief cells.
(Alternate mnemonic: I think of master chef making food rich in proteins, peptides being degraded by pepsin and that’s how I remember the association that Chief cells secrete Pepsin).

G for G cells & G for Gastrin. (Hah! That was easy!)

S for S cells & S for Secretin! (Medicine is easy!)

You’ve probably heard of the iPhone.. Heard of iCDs? Coz they’re gonna help you remember the rest of the cells secretions- I cells secrete CCK. Delta cells secrete somatostatin. Go ICDS!

That’s all! <3
Wait.. Which cell secretes intrinsic factor? Do you know the IP address of that cell? IP.. Yes, yes. Parietal cells! Intrinsic factor - Parietal cells!

Obstructive and restrictive lung diseases

Happy friday everyone!
We’ll learn about obstructive and restrictive lung diseases today.
This is just a short summary for a quick review :)

Obstructive lung diseases - Characterized by airway obstruction
Increased compliance - Due to the loss of alveolar and elastic tissue
You have a problem getting air out of your lungs
Mnemonic: Obstructive Out

They breathe like “poof poooooof”
In and oooooout
They take infinity to get it all out =P
So, FEV1 / FVC is decreased

TLC and RV increased - Flow volume loop shifts towards left

Examples: Any pathology that decreases the ability to develop a positive intrapleural pressure
Chronic bronchitis
Asthma
Bronchiectasis
Emphysema
COPD

Restrictive lung diseases - restriction of lung expansion
Reduced compliance - lungs become fibrotic, lose their distensibility and become stiffer
You have a problem getting air into your lungs
Mnemonic: Restrictive Reduced compliance

They breathe like “poof pof”
In and out
They get everything out in one second =P
So, FEV1 / FVC is increased

TLC and RV decreased - Flow volume loop shifts towards the right

Examples: Any pathology that decreases the ability to develop a negative intrapleural pressure
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Pneumoconioses
Kyphoscoliosis
ARDS
Polio
Obesity

That’s all!

I know you must’ve found the “poof” sounds pretty weird because that isn’t the way you breathe
But they are a funny and they help me remember so I put it up anyway ^___^”
Just like “lup dubb” are official sounds for heart beats.. Which sounds would you assign to inspiration and expiration?

-IkaN

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