mental defense mechanisms - psych stuff

first off, sorry for the lack of updates. am up to my ears with catching up on studies. however, my notebook is already half filled with REALLY GOOD stuff i'll upload over my summer break.

for now, here's an easy way to remember all the different type of defense mech, using the husband and wife examples.

the dude that came up with this is a genius!

1. Husband attracted to another woman goes back and make love to his wife.
2. Husband attracted to another woman goes back and offer flowers to his wife.
3. Husband attracted to his student then he becomes her mentor.
4. Husband having affair with another woman justifies to himself by saying this will make me appreciate my wife more.
5. Husband attracted to another woman then he thinks that his wife is cheating on him.
6. Husband attracted to another woman and explains to his friend that how sexual desires are instinctual and cannot be controlled.
7. Husband attracted to another woman then goes and write about how bad cheating husbands are in the newspaper.
8. Husband fought with his wife then went fighting at a football game.
9. Husband told of grave diagnosis and tells his wife "Honey, I need your help without you I cannot fight".

Answer key

1. Displacement
2. Undoing
3. Sublimation
4. Rationalization
5. Projection
6. Intellectualization
7. Reaction formation
8. Displacement
9. Regression

reaction formation = doing the extreme opposite of what you long/ desire for.
undoing = not extreme opposite, somewhat same direction as desire (eg: giving flowers = sign of love and affection).

let's play some more

1. you get a 30 y.o. male who has been experiencing severe pruritus (itching) for the past 2 weeks. he has a history of ulcerative colitis (UC) for the past seven years, and is on sulfasalazine and cortisone enemas. he has diffuse excoriations on his extremities and trunk. his labs reveal a mild iron deficiency anemia and normal electrolytes. LFTs are normal, except for an increase in alkaline phosphatase: 322 U/L (normal <110 U/L). What is the most likely explanation for his symptoms?
   
   Primary Sclerosing Cholangitis (PSC)
   the patient has had longstanding UC and has now developed pruritus in the setting of an elevated alkaline phosphatase. this sclerosing process involves both the intra- and extrahepatic ducts and is diagnosed by ERCP.
   
   PSC occurs most often in young men and is commonly associated with IBDs, especially UC. PSC has a triad of progressive fatigue, pruritus and jaundice. there may also be upper quadrant pain, fever, hepatosplenomegaly or cirrhosis.
   
   complications of PSC include progression to decompensated cirrhosis, PHT, ascites, and liver failure. treatment is generally supportive and include antibacterial treatment for superimposed bacterial cholangitis.
   
   Primary biliary cirrhosis also presents with pruritus and an elevated alkaline phosphatase, but it is typically seen in middle-aged women and has no association with ulcerative colitis, thus ruling it out from the differential.
   
   
2.  this case is a gem: a 64-year-old man who is currently undergoing chemotherapy, experiences the occasional nausea and vomiting, for which he is given IV prochlorperazine to help ease the symptoms. after several days of therapy, he complains that he feels restless, agitated and he cannot stop moving his legs. what medication should you have given to him at the beginning of his therapy to prevent this reaction? choose between Haloperidol and Lorazepam.
   
   LORAZEPAM.
   
   why? because this patient has akathisia, a syndrome characterized by unpleasant sensations of "inner" restlessness that manifests itself with an inability to sit still or remain motionless (definition from wiki). this the feeling of restlessness sometimes occurs as a side effect of neuroleptic drugs, such as prochlorperazine and haloperidol. akathisia can be prevented by administering IV benzodiazepines, such as lorazepam, concomitantly with the neuroleptic drug. this is especially vital in a patient whose immune system and metabolic activity is compromised.
   
   
3. here's an obstretic pearl. let's say a pregnant woman comes for her antenatal check up. everything is a ok, except her urine dipstick shows bacteriuria (asymptomatic because she doesn't have dysuria, increased frequency, a temperature or increased urgency). whaddya do?
   
   asymptomatic bacteriuria is present in about 5% of pregnant women. because it may cause preterm delivery/low birth weight, it is vital that all pregnant women be screened for asymptomatic bacteriuria early in the pregnancy and be treated if affected by it.
   
   e. coli is the main organism most of the time. other gram-negative organisms (e.g: klebsiella, enterobacter, and proteus species) and gram-positive cocci (e.g: enterococci and group B strep) may be responsible as well.
   
   treatment choices include: trimethoprim-sulfamethoxazole, nitrofurantoin, and cephalexin. ampicillin and amoxicillin may be administered as well (bear in mind though that e.coli may be resistant to these drugs).
   
   10 days after completing the course of antibiotics, the patient should have a follow-up urine culture to make sure the causative agent of bacteriuria has been eradicated.
   
   
4. ok, bonus question. you have to be able to answer this (or it's time to hit those patho books again): pitituary adenomas, what hormone level will be elevated?
   
   PROLACTIN!
   
   
5. all right, i know most of us didn't like public health/ public service medicine too much as a subject, but statistics play a big role in diagnosing a patient right too.
   
   let's go back to 2 basic points before i give you the question:
   
   
   
   • sensitivity = (positive)/ (positive + false negative) x100.
     a sensitive screening test detects DISEASED individuals.
     usually used to screen for disease with low prevalance.
     remember: sensitivity rules out. (SnOUT).
   • specificity = (negative)/ (negative +  false positive) x 100.
     a specific screening test detects HEALTHY individuals.
     usually used as a confirmatory test after a positive sensitive test.
     remember: specificity spins in (SpIN).
   
   now...you get a 70 y.o male come to you to complain about his very red and swollen right toe, that hurts severely. he is not on any medications and denies abusing alcohol. you know it's gout, but which method will you use to make that diagnosis? pick from colchicine response or checking his uric acid levels.
   
   colchine response. u.a levels may be elevated in gout, but it is also increased at tumor lysis syndrome and other diseases. so the results won't be specific enough.
   
   so give oral colchicine hourly until the patient develops improvement in joint pain and inflammation.
   
   
   
   
   
   of course the most specific method of diagnosis, would be joint aspiration and seeing negatively birefringent needle shaped crystals under the microscope. but think CHEAP, get the right diagnosis and your chief of medicine will love you for saving his the bucks.
   
   
   
   until the next round folks =)

let's play the diagnosis game

1.            you have a 50-year-old man with ringing in his ears and he feels the room spinning around him. he also tells you his hearing in his left ear has slowly gotten worse. he says that this all began a while ago, along with a slight feeling of unsteadiness. he has no chronic medical conditions and does not take any medications. examination shows nystagmus. what is the most likely diagnosis?

Dx: meniere's disease, which is characterized by tinnitus, vertigo, and progressive hearing loss (his hearing got worse slowly). it is thought to be related to a degeneration of the vestibular and cochlear hair cells. treatment includes bed rest, a low-salt diet, dimenhydrinate, cyclizine or meclizine. 

perhaps you considered it being benign positional vertigo, but recall that, BPV is characterized by paroxysmal vertigo and nystagmus. it is brought on by certain changes in position and hearing loss is not present. therefor, you can rule it out of the differential.

2.            an 18-year-old male student is admitted for psychosis. he is put in seclusion because he is highly aggressive and a threat to others. he was given haloperidol intramuscularly twice so far. suddenly, he has acute torticollis and twitching of the mouth and face on that side. what reaction did this patient most likely have?

acute dystonia, an involuntary spasm of a particular group of muscles that can involve the neck, jaw, tongue, eyes, or the entire body. it can be an early adverse effect of antipsychotics, and it is more common in younger men. it is more common with typical antipsychotics. the treatment of choice is parenteral administration of anticholinergics.

 3.            a 15-year-old, obese boy complains of persistent knee pain for several weeks and came into your office, limping. he sits in the examining table with the sole of the foot on the affected side pointing to the other leg. however, physical examination is normal for the knee, but shows limited hip motion. when the hip is flexed, the leg goes into external rotation and cannot be rotated internally. which of the following is the most likely diagnosis: avascular necrosis of the femoral head OR slipped capital femoral epiphysis?

slipped capital femoral epiphysis, an orthopedic emergency. it has a classic clinical picture: a chubby male, early teens, who is limping and cannot rotate his leg internally. also, this hip pathology will produce knee pain, but the knee is normal on physical examination.

avascular necrosis is seen in younger children, around 6 years of age.

dermatomes!

• C6-C8: 
• C6 covers the thumb and index finger (medial half). to remember this, make the number 6 with your left hand by touching your index finger to your thumb.
• then, remember C8 the is the lateral digit (baby finger) and half of the 4th
• which leaves C7 getting whats inbetween C6 and C8
• L5 vs S1
• intervetebral discs herniation happens at this level
• L5 affects the big toe
• L5 = Largest of the 5
• L5 root is compressed by a herniated disc at the L4-L5 level
• S1 affects the smallest toe
• S1 = the smallest one
• S1 root is compressed at the L5-S1 level
• L1 = Skin overlying the inguinal ligament
• L for ligament, 1 for 1nguinal
• S5 = Anus
• S5 is the doodie hive (got this off the net: doodie being another word for poop and hive = house...so erm yeah)
• Others:
• T10 = Umbilicus
• Bellybut-TEN
• C3, 4, 5 keeps the diaphragm alive
• L4 = Knee
• L4 hits the floor (when kneeling)

M & M & M & M

what?    

• Mycoplasma pneumoniae (causes atypical pneumonia aka walking pneumonia: insidious onset, headache, non productive cough, diffuse infiltrate, respiratory symptoms don't dominate)

who? 

• Military and Minors and Misfits (prisoners)

how? 

• IgM (which causes cold agglutination and lysis of rbc which can lead to hemolytic anemia)
• bullous Myringitis (bullae on the tympanic membrane)

Tx = erythromycin or tetracycline. resistant to penicillin because? come on gander a guess (think MOA of penicillin and you'd understand immediately).

if you guessed coz it has no cell wall, good for you =) it's the only bacterial membrane with cholestrol. so it can't be seen on gram stain.

vitamin B

to a med student, knowing their B1, 2, 3, 6, 12 is as intrinsic as a preschooler knowing their A, B, Cs. sometimes the difference between an A grade and a B grade, is getting the right vitamin B type.

B1 thiamine	In thiamine pyrophosphate (TPP) a cofactor for: Pyruvate DH (glycolysis) Alpha ketoglutarate DH (TCA) Transketolase (HMP) Branched chained aa DH	At malnutrition or alcoholism (secondary malnutrition and malabsorption) Impaired glucose breakdown leading to ATP depletion, so first organs affected are the brain and heart (highly aerobic tissues). Wernicke-Korsakoff syndrome. Wernicke: confusion opthalmoplegia, ataxia Korsakoff: memory loss confabulation personality change Beriberi: §         wet beriberi (high output HF, dilated cardiomyopathy, edema) §         dry beriberi (polyneuritis, symmetrical muscle atrophy) mnemonic: ber1ber1
B2 riboflavin	Cofactor in oxidation and reduction (FADH2)	2 Cs: Cheilosis Corneal vascularization mnemonic: riboFlavin = FAD, FMN= 2 ATP
B3 niacin	Redox rxn (NAD+, NADP+) Derived from tryptophan Synthesis requires B6 *excess: facial flushing (seen at pharmacological doses of treating hyperlipidemia)	3 Ds of pellagra: Dermatitis Diarrhea Dementia Severe deficiency caused by: 1.      Hartnup’s disease (decreased tryptophan absorption) 2.      Malignant carcinoid syndrome (increased tryptophan metabolism) 3.      INH (decreased B6)
B5 pantothenate	Cofactor for acyl transfers and FA synthase	Dermatitis Enteritis Alopecia Adrenal insufficiency
B6 pyridoxine	·        Required for synthesis of B3 from tryptophan ·        Converted to pyridoxal phosphate, a cofactor for: «     transamination (eg: ALT, AST) «     DC reactions «     Glycogen phosphorylase «     Cystathione synthesis «     Heme synthesis	§         Convulsions §         Hyperirritability §         Peripheral neuropathy §         Sideroblastic anemias Deficiency can be caused by INH and OCPs.
B12 cobalamin	·        Cofactor for homocysteine methyltransferase and methylmalonyl COA mutase (transfers CH3 group as methylcobalamin)	§         Macrocytic, megaloblastic anemia §         Hypersegmented PMNs §         Neuro symptoms such as paresthesias, subacute combined degeneration (abnormal myelin) o Only vitamin stored (in liver). Other vitamin Bs are flushed out of the system o Deficiency due to: à      Pure vegan diet à      Sprue à      Enteritis à      Diphyllobothrium latum à      Lack of intrinsic factor (gastric bypass, pernicious anemia) à      Absence of terminal ileum (Chron’s)

renal pearls 3: getting neurotic with nephrotic syndrome

NEPHROTIC SYNDROME:

• proteinurea >3.5g per 24 hrs
• hypoalbuminimea (due to loss of protein in urine)
• pitting edema (due to decreased oncotic pressure brought on by loss of protein)
• hyperlipidemia (the liver senses the loss of proteins and synthesizes more, including lipoproteins whose function is to circulate lipids)  and fatty casts in urine

renal pearls 2: getting neurotic with nephritic syndrome

first, a reminder of what a normal glomeruli looks like:

there are 2 types of GN: nephritic and nephrotic. it cannot be both at the same time, but nephritic can progress to nephrotic.

NEPHRITIC SYDROME

• hematuria (active damage to glomeruli)
• rbc casts 
• protein spill but less than 3.5g in 24hrs (mild to moderate proteinurea)
• oliguria (because you have an inflammation of the glomerulus = decrease GFR)
• HT (because of the decreased GFR, there is no filtering of Na and a build up of it)

there are FOUR diseases that can cause this syndrome:

1. proliferative GN:
   
   
   • diffused inflammation of all glomeruli plus active proliferation of cells
2. post strep GN:
   
   
   • had strep throat/ scarlet fever week(s) prior and then comes in with puffy face (edema) and cola coloured urine (hematuria).
   • IC deposits in subepithelial space
   • treat with corticosteroids
   
   
   
   
   hypercellularity of post-infectious glomerulonephritis is due to increased numbers of epithelial, endothelial, and mesangial cells as well as neutrophils in and around the glomerular capillary loops. this disease may follow several weeks after infection with certain strains of group A beta hemolytic streptococci. patients who have had a strep infection typically have an elevated anti-streptolysin O (ASO) titer.
   
   
3. lupus GN
   
   
   • almost always young woman (~30-35 y.o) with serum ANAs.
   • six types but most important = diffuse proliferative GN
     
     
     • lots of nuclei
     • wire loops
   • subendothelial deposits
     
     
     
     
     extensive immune complex deposition in the thickened glomerular capillary loops, giving a so-called wire loop appearance
     
     
4. crescentic GN
   
   
   • also known as Rapidly Progressing GN because of its fast progression to acute RF 
   • RPGN is a description not a specific disease. the diseases that can causeit: SLE, post strep GN, goodpasture's syndrome, vasculitis (polyarteritis nodosa, wegner's granulomatosa) or it could even be idiopathic
     
   • the glomerulus is surrounded by proliferating cells that are epithelial cell. the glomeruli damage is so severe, fibrinogen leaks into the bowman's space inducing epithelial proliferation.
   
   
   
   
    
   anti IgG ab deposits as seen in Goodpasture's: linear appearance on immunoflorescence
   
   
   
   
   crescents made up of proliferating epithelial cells
   
   
   

   to be continued...

renal pearls 1

i have my therapy (internal medicine) exam coming up, so the next few posts are going to be related to topics i need to cover for the exam.

let's start with my second least favourite system: the renal system.

the nomenclature of kidney diseases alone give you a good idea of what it represents:

diffuse: it just means EVERY glomerulus is involved.
focal: only some glomeruli (in one foci) is involved.
focal segmental: the diseased is localized to the kidney and only some of the glomeruli are affected. technically, it should be called focal focal, but you if try saying that out loud fast a couple of times, you'd realise why they chose to call it focal segmental instead.
proliferative: increased number of cells. it's a microscopic presentation of lots of nuclei.
membranous: thickened membranes.
membranoproliferative: both increased cell count and thickened membrane.

before i explain the twins of renal diseases (nephritic and nephrotic syndromes), let's do a quick overview of the physiology of the glomeruli:

podocytes line the bowman's capsule. they have slitpores between them. they synthesize the glomerular basement membrane (GBM).

what keeps albumin out of the urine normally? the strong negative charge of the BM.
what causes this strong negative charge? a GAG called heparan sulfate.

so if when there's damage to the visceral epithelium, there's automatically a damage to the BM and therefore a spill of protein into the urine.

say, i gave you the results of a renal biopsy of an abnormal kidney, and it shows a linear pattern on immunoflourescent IgG tag, what should you be thinking of?

GOODPASTURE'S SYNDROME, a HSII where there are IgG directed against the BM of glomeruli (and alveoli in lungs). so, you get a linear pattern because IgG will attach to all BM.
 
but say i gave you instead a biopsy showing a granular bumpy pattern? what's big and gets in the way of things?

IMMUNE COMPLEXES, which are ab-ag complexes (ie at lupus: anti-DNA + DNA). these IC float around and then deposit at certain places (HSIII). because they consist of both ag and ab, naturally they are larger than just plain abs and can be of different sizes, depending on what forms the complex, so they don't fit nice and neat in the glomeruli. 

you'd get subendothelial deposits in lupus because the IC is too big to go past the BM. in post step GN, you'd get subepithelial deposits because the ICs are small and soluble enough to pass the BM.

you can't see the ICs on immunofluorescence (won't be stained), but you can on EM (they're electron dense).

to be continued...

(almost) everything meninges

the meninges are the covering for the brain, so think of them padding the brain=

P-pia mater
A-arachnoid
D-dura mater

the pia mater is very popular, and others like sticking to it. the dura attaches to it via denticulate ligaments and the arachnoid attaches to the pia via trabeculations.

(however i can't forsee anyone ever being asked this during an exam or clinically, but still betcha didn't know that fact! everyone just thinks the three layers are atop of each other)

the pia forms the filum terminale at the end of the cord, and this joins the dura at S2.

infection of the meninges = meningitis.

Most Common Causative Agents:

newborn: group B strep
children: strep pneumoniae
adults: n. meningitidis
elderly: strep pneumoniae
HIV patients: cryptococcus neoformans (remember that post on capsulated organisms? it's a form of yeast with a capsule; stain with india ink)

(children and old people afflicted by same organism)

so clinical picture for meningitis: fever, headache, photophobia, neck stiffness.
physical examination: positive Kernig's and Brudzinki's signs.
Dx: LP to analyse CSF.

1. CSF in bacterial meningitis: high protein, high pressure, high WBC, low glucose (bacteria use up glucose)
2. CSF in viral meningitis: high protein, high lymphocyte, normal glucose (viruses have no use for glucose) 
3. TB meningitis: CSF same as viral meningitis EXCEPT glucose level would be very low.

complications of meningitis:

• encephalitis: sharp triphasic complexes on EEG
  *herpes encephalitis causes olfactory hallucinations and has mononuclear pleocytosis, along with RBCs in CSF
• adrenal haemorrhage (Waterhouse-Friderichsen syndrome): shell like calcifications on XR.

treatment:

1. DOC: 3rd generation cephalosporins + vancomycin
2. for cryptococcus neoformans: amphotericin B + flucytosine
3. prophylaxis for close contacts: rifampicin

and one last pearl before i end this post:

if patient has meningitis along with extremely high amylase levels, with no clear abdominal source (liver disease etc), think of acute viral parotitis.

Symbol of Medicine

Most of us are too caught up with the science of medicine and often ignored the meaning of the symbol of medicine.

The Rod of Asclepius/Asklepios, an ancient symbol associated with medicine and healing, consist of a rod entwined by a serpent. (Asclepius is the son of Apollo, a medicinal practitioner in ancient Greek mythology)

Another symbol is a staff entwined by 2 serpents and surmounted by wings, is known as Caduceus. It is often confused with Rod of Asclepius, which has only one snake and no wings. It is the magic staff of Hermes, the god of commerce, eloquence, invention, travel and theft, and hence is the symbol of heralds and commerce, not medicine.

The association of snake and medicine can be interpreted in a few ways:

- shedding of skin and renewal symbolized rejuvenation
- snake venom can be fatal or have medicinal properties (developed into antivenom), reflecting ambiguity of the use of drugs, which can help or harm.

The rod also represents resurrection and healing, or that of an itinerant physician.

History of Presenting Complaint

the SOCRATES questions should be asked:

Site
Onset
Characteristics
Radiation
Associations
Timing/duration
Exacerbating or alleviating factors
Severity