Thursday, January 26, 2012

Cold Agglutinins

Cold agglutinins are clinically relevant antibodies that are implicated in intravascular hemolysis. At normal body temperature, these antibodies do not cause hemolysis. However, when RBCs get out into the periphery and temperatures drop, the antibodies can attach to red blood cells, causing hemolysis primarily through the complement system. They are called cold agglutinins because when they are placed in cold temperatures in a laboratory setting, the antibodies will attach to RBCs and cause agglutination.

Remember the 3 M's of cold Agglutinins:
IgM
Mycoplasma pneumoniae (can trigger cold agglutinins)
Mononucleosis (EBV, CMV infection)

Warm agglutinins are caused by IgG. To remember the difference, you can remember that
"Maine is colder than Georgia."


Wednesday, January 25, 2012

K+ sparing diuretics

How do you get your potassium? Potassium Sparing Diuretics

"Some EAT bananas" (as in some people eat bananas to get potassium? Maybe? No?)

Spironolactone, Eplerenone, Amiloride, Triamterene

Background: act in the distal collecting tubules
S and E: block the cytoplasmic steroid receptor for aldosterone.
A and T: block the sodium channel (ENaC) that is upregulated by aldosterone

By the way, the aldosterone receptor is a zinc finger. It'll go into the nucleus and bind DNA to induce transcription. Did you know that? Probably not that high yield, but it's important to remember to tie concepts like that together!

Sunday, January 22, 2012

Heart Auscultation

"All Patients Trust Me" - Aortic, Pulmonic, Tricuspid, Mitral

When listening for abnormalities, auscultate in these areas:

Aortic: right sternal, 2nd intercostal space
Pulmonic: left sternal, 2nd intercostal space
Tricuspid: left sternal, 4th intercostal space
Mitral: left midclavicular (near PMI), 5th intercostal space

2 things you should figure out:

1) Is it a R or L heart problem? R-sided heart sounds increase intensity with inspiration (you suck more blood into the right heart from the system, exacerbating heart sounds). L-heart sounds increase intensity with expiration.

2) Is it systolic or diastolic? Systolic is (as you well know) increased pressure in the ventricle due to ventricular contraction. Valvular defects that manifests: AV valves forced to close (Mitral/Tricuspid regurgitation audible), and blood must be pumped through aortic or pulmonic valves (Aortic/Pulmonic stenosis audible). Diastolic heart sounds are the opposite.

Also, did you know that the S1 and S2 heart sounds are not actually the sound of the valves closing, but the sound of turbulent blood flow hitting the valves AFTER they closes? I thought that was interesting.

Wednesday, January 18, 2012

Adrenal Cortex Layers


Think of an adrenal gland chilling on a kidney in a swim suit, drinking a margarita...

When drinking a margarita, you get "salt, sugar, then sex... the deeper you go, the sweeter it gets!"

Also, it's on the kidney, so it can observe the "GFR" - corresponds to the layers of the cortex.

Adrenal cortex layers from most superficial to deep:
Zona Glomerulosa: produces aldosterone
Zona Fasciculata: produces mostly cortisol
Zona Reticularis: produces mostly androgens

Monday, January 16, 2012

DiGeorge Syndrome

DiGeorge Syndrome. Main problem is related to the immune system, due to aplasia of the thymus (T cells are unable to mature). The parathyroid glands are also generally absent, leading to problems with calcium absorption and maintenance (no PTH). The syndrome is commonly due to a deletion on chromosome 22 (22q11.2). Though the syndrome can have a spectrum of symptoms, you can memorize the general symptoms with this mnemonic:

CATCH-22

Cardiac Abnormalities (especially Tetralogy of Fallot)
Abnormal Facies
Thyroid aplasia
Cleft Palate
Hypocalcemia
-
22: found on chromosome 22

Saturday, January 14, 2012

Learning: Acid-Base Disorders

I always had trouble with Acid-Base Disorders, so I thought I'd share this. People always say that they're not too difficult if you know what you're doing. Sure you can look at the pH, but how do you tell if the offense is a metabolic acidosis vs. a respiratory acidosis?

First of all, you're dealing with pH, PCO2, and bicarbonate.

1. Look at the pH. Is it low or high? High pH= alkalosis. Low pH = acidosis.

2. Now all you have to do is figure out which organ (lungs or kidney) is messing up and causing the pH dysfunction. For example, let's say we have a low pH. What can cause that? Either low bicarbonate or high PCO2. Note: you will never have both. So if you have a low bicarbonate, you will have a low PCO2, and visa versa. You can take my word for it, or you can see the explanation below(*). Now all you have to do is look at which one corresponds to the pH level. If you have a low pH and you have a low bicarbonate, you KNOW it's the kidney that isn't making enough bicarbonate to balance all that acid. Thus, metabolic acidosis. If you have low pH and high PCO2, you know that your lungs are messing up, making it a respiratory acidosis. Essentially the name of the disorder (i.e. respiratory acidosis) refers to the organ that isn't functioning properly (lungs in this case) and the pH value (acidosis in this case).

Just two steps. Not too shabby.

*here's an example to understand. If you have a low pH (acidosis), you're really just asking what causes it. The other organ, either the lung or the kidney, is going to try to compensate for that lack. So again, low bicarbonate is causing the acidosis, your lungs are going to try to compensate by expelling out CO2 (decreasing PCO2). Reason your way through this with any scenario. Another example if you're still confused: if you have a respiratory alkalosis, that means your lungs are messing up (low PCO2 gives you a high pH) and thus your kidneys will try to compensate by decreasing the bicarbonate.

Lead Poisoning

Lead Poisoning Clinical Presentations:


Just remember ABCDEFGH (I remember it as "A-GGHH! Lead poisoning!")

1. Anemia. Pb denatures enzymes (ferrochelatase, ALA dehydrase) leading to ringed sideroblasts (faulty heme synthesis, iron accumulates in mitochondria of RBC progenitors)
2. Basophilic stippling. Pb also degrades ribonuclease, which degrades ribosomes. Mature RBCs normally have no ribosomes.
3. Colic w/ Diarrhea. (lead deposits in GI tract. Can visualize with radiographic image)
4. Encephalopathy in children. δ-ALA accumulates, increasing vessel permeability (edema) and causing demyelination. Often presents as headaches and memory loss in adults
5. Foot drop. More specifically, peripheral neuropathy. Consequences: foot drop (perineal nerve palsy), wrist drop (radial nerve palsy), claw hand (ulnar nerve palsy)
6. Growth retardation and Gum deposition. Pb accumulates in epiphyses, causing growth retardation and increased densities on bone radiograph. Pb also lines your gums.
7. Pb causes Nephropathy. This can lead to impaired uric acid secretion (Gout/Hyperuricemia) and Hypertension

Friday, January 13, 2012

Fact of the Day: CO2 transport to the lungs

Fact:

When the tissues give of CO2 after undergoing metabolic oxidation, the CO2 enters into RBCs. This CO2 + H2O (with the help of carbonic anhydrase**) is converted into HCO3- and H+. The HCO3- is exchanged for Cl- (chloride shift), and drifts out into the plasma. This explains why the major form of CO2 is HCO3-! (80-90%)

So now the RBC is stuck with H+ in its cytoplasm. It turns out hemoglobin is a good buffer, but only in the deoxyhemoglobin form. Luckily, most of the O2 attached to hemoglobin has been released into the peripheral tissues, leaving a majority in the deoxyhemoglobin form, which readily attaches to H+.

When the RBC makes it to the lungs, the opposite happens. HCO3- is exchanged back into the RBC for Cl-, combines with H+ (again, with the help of carbonic anhydrase**), and reforms CO2 + H2O. The CO2 happily diffuses out into the alveolus, and the O2 enters back into the RBC to oxygenate hemoglobin.

So note, Cl- plays a crucial role in CO2 transport to the lungs.

**Technically, carbonic anhydrase is used for H2O + CO2 <--> H2CO3, and H2CO3 readily dissociates into HCO3- and H+

Tuesday, January 10, 2012

G-protein coupled receptors

G-protein coupled receptors (GPCRs) are essential for many processes. What receptors are GPCRs?

Before I get into this further, I must say that sometimes it's the dirty mnemonics that you remember best. That being said, I've created a mnemonic to memorize which receptors are GPCRs.

"Αlpha and βeta Males Don't Hate Vagina."

Receptors: Alpha, Beta, Muscarinic, Dopamine, Histamine, Vasopressin.

More facts you will need to memorize are to what class the G proteins belong. That is to say, if the G proteins that are coupled to the receptors are Gs (stimulatory), Gi (inhibitory), or Gq. Gs and Gi use Adenylate Cyclase as their effector and Calcium as their second messenger, while Gq receptors use Phospholipase C as their effector and IP3 and DAG as their second messengers.

Here is an easy mnemonic. Important: line up the receptors according to the above mnemonic (Alpha and Beta Males Don't Hate Vagina)

"qiss and qiq til you're siq of sqs" (kiss and kick til you're sick of sex)

α1   -   q
α2   -   i
β1   -   s
β2   -   s

M1  -   q
M2  -   i
M3  -   q

D1  -   s
D2  -   i
H1  -   q

H2  -   s
V1  -   q
V2  -   s

2 mnemonics for the price of one. Awesome.

Friday, January 6, 2012

Fact of the Day: Kids Hb Count

Fact:

Children have a lower hemoglobin count than adults (<11.5 g/dL is anemic).

Why is this? They have a higher serum phosphate, assumably from the increase in bone growth* and an increased metabolism in general. This higher phosphate leads to increased levels of 2,3 BPG, which we know causes a right shift in the O2 saturation curve. This means more oxygen is dumped into the tissues per hemoglobin molecule. Thus, less hemoglobin is required to transfer oxygen to the tissues.

*the main inorganic material of bone, hydroxyapatite, utilizes 10 Ca for every 6 Phosphorous (Ca10(PO4)6(OH)2). This leaves an excess of Phosphorous (since Calcium and Phosphorous usually come together in the form of CaPO4)

Mnemonic: Encapsulated Organisms

"YES, Some Killers Have Pretty Nice Capsules"

Yersinia Pestis (F1 capsule)
E. coli (some species)
Strept Agalactiae

Strept Pneumoniae
Klebsiella
Haemophilus Influenzae
Pseudomonas Aeruginosa
Neisseria Meningitidis
Cryptococcus Neoformans

Note there are other encapsulated species, but not as important. However, one to remember is Bacillus Anthracis, because unlike other bacteria, it has an amino acid (D-glutamate) capsule!

Important Notes:
Children are more susceptible to bacteria with polysaccharide capsules, because they do not have the proper antibodies against these organisms.
Asplenic patients are more susceptible to encapsulated pathogens. Watch out for functional asplenic patients with Sickle Cell Anemia! (Don't forget those Howell-Jolly bodies in asplenic patients!)