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el Sáb Mayo 09, 2009 7:25 pm
Recuerdo del primer mensaje :

Lo siguiente es para ayudarme a repasar y recordar temas de medicina. Anotare por areas o temas. En ciertas areas estaran en español y/o ingles. Quizas a unos les sirva o les valga pero aqui sere egoista y honestamente la pongo para mi beneficio. Cada que pueda agreagre mas informacion. Si alguien desea agregar adelante.Si escribo algo de manera incorrecta por favor corrijanme. Gracias y buen dia!

Trantornos en la cavidad oral:

El transtorno congenital mas comun es el labio leporino y mas comun en hombres. Herencia multifactorial y esta asociada con el paladar hendido en un 50% de los casos. Esto resulta por falta de la union de los tejidos antes de nacer. Normalmente esto se corrige con varias cirugias, la primera siendo el primer año de vida. Este transtorno puede producir problemas con la alimentacion, el habla e infecciones de oido.

Aqui se encuentran las glandulas salivales las cuales producen la alfa-amilasa la cual se encarga de las uniones alfa-1,4 que se encuentran entre la glucosa y residuos alimentarios de almidon.

Los procesos inflamatorios que aqui se pueden encontrar son la aftas la cuales pueden ser de origen autoinmune y estas se pueden encontrar en cualquier parte de la cavidad oral. La glositis es causada por deficiencia cronica de hierro, Vit. B12 o deficiencia de folato, escorbuto o fiebre escarlatina.


Universidad : Universidad Autonoma de Guadalajara
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el Lun Mar 21, 2011 11:21 pm
Glomerular Crescent formation:
-Due to proliferation of epithelial cell and infiltration by monocyte and macrophages. Crescents suggest rapidly progressive glomerulonephritis.

Berge Disease
-IgA deposition in glomerular mesangium, which may contain C3, properdin, I gG and IgM.
-It is thought to be casued by trapping of large Iga-antigen complexes in the glomeurli, leading to activation of al alternative complement pathways.

-ADH:Stored in post. pituitary and produced in Hypothalamus.
-Inserts additional water channels into the apical membrane cells of the (distal) renal collecting ducts. Therefore it can retain water and concentrate urine without affecting sodium and potassium excretion.
It does not affect the proximal tubule where most water and ELECTROLYTES are reabsorbed.

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el Miér Mar 23, 2011 7:01 pm
Chromosomal Translocations;

t(9:22) Philadelphia Chromosome = C.M.L.(bcr-abl hybrid)
t(8;14) Burtkitt's Lymphoma (c-myc activation)
t(15:17) M3 type of A.M.L.(Responsive to all-trans retinoic acid)
t(11;22) Ewing's Sarcoma
t(11;14) Mantle Cell Lymphoma

Auer bodies (rods) are peroxidase positive cytoplasmic inclusions in granulocytes and myeloblasts. Commoly seen in Acute Promyelocytic Leukemia(M3).
Treatment of A.M.L. M3 can release Auer Rods and cause a disseminated intravascular coagulation.

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el Mar Jun 07, 2011 6:21 am
Daunorubibin y Doxorubicin se intercalan entre las bases del ADN por lo tanto inhiben la funcion de la Topoisomerasa II. Estos medicamentos son utilizados como parte del tratamiento de las leucemias.

El cisplatin se une al ADN causando alteracion en la estructura y funcion de este.
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el Mar Jun 07, 2011 6:46 am
Durante el crecimiento o recuperacion post-parto, cirugia, etc. que amino acido es de gran importancia en esta etapa?


Cual otro amino acido de importancia durante el crecimiento?


Otra funcion importante de la arginina es la eliminacion de la amonia!!
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el Mar Jun 14, 2011 2:00 pm
1-Prader Willi Syndrome:

Patient, young, with obesity, hypotonia, mental retardation, short stature, hypogonadotropic hypogonadism, strabismus, and small hands and feet.

Treatment is with Growth Hormone

2-Pt w/ symptoms include tall stature, ectopia lentis, mitral valve prolapse, aortic root dilatation, and aortic dissection? What gene is missing and what is treatment of choice?

Marfan's Syndrome . Defect in fibrillin gene. Treat the aortic dissection with B-Blockers. Warn about pneumothorax and strenous exercise. Tell patients that they are AD inheritance. Warn them about things like an elevator that travels up too fast.

3-IF you are given a diagram with an LDL receptor molecule, and ...
then if you are asked what ion binds to it, what would you guess?
Choices: Na, Ca, Fe?


4-Uric acid stones (which are transLUCENT on x ray unlike Ca stones), are common in what three diseases? Bonus: what do uric acid stones cause symptom wise?

HGPRT deficiency
PRPP synthetase overactivity
Glucose-6-phosphatase deficiency
The stones will present most commonly with hematuria, then fever/nausea/vomiting, then UTI!!

5-What is the primary treatment for the uric acid stones? 2nd treatment if refractory?
1st thing is to alkalinize the urine and hydrate! Wait for the stone to pass.
If that doesn't work, give ALLOPURINOL! BUT, if the stone is more than .5cm, then use lithotripsy because the stone will not pass by itself!

6-A patient who had her gall bladder removed for stones STILL feels colicky pain, what could be the reason?

loss of inhibitory enteric innervation (motor).

7-injury to the SURGICAL neck of the humerus/or the dislocation of ANTERIOR shoulder will have which nerve injury?

AXILLARY nerve, not the radial nerve.

8-A woman who diets and cuts out all fats but still eats carbohydrates. Will she lower her LDL? HDL?

Chylomicrons are blood lipoproteins produced from dietary fat.
It is the VLDLs that are produced mainly from dietary carbohydrate. IDL and LDL are produced from VLDL. Thus, HER LDL level will still BE HIGH.

9-Diffuse demineralization of the bone associated with hypercalcemia, anemia, hypergammaglobulinemia, proteinuria, and normal serum alkaline phosphatase is most suggestive of?
Name of proteins: Bence-Jones proteins -Serum beta 2 microglobulin level
Dexamethasone, melphalan, thalidomide, lenalidomide, and bortezomib.

Drugs called bisphosphonates are used to reduce bone pain and prevent fractures.

Multiple Myeloma!!!!!!

10-A woman with sarcoidosis or with hypercalcemia (there are a thousand ways to ask this concept) enters your clinic, which is the diuretic of choice?

Furosemide, NOT thiazides or mannitol, or acetazolamide!

Gracias a TOMMY por compartir esta informacion!

11-Hardy Weinberg- If the number of homozygotes is 1/4900, can you tell me the number of heterozygotes?

Use q2 and then use equation 2pq.

12-Transgenic mouse with defect in B2 microglobulin gene. What is the immuno defect?

The B2 microglobin is part of the MHC Class I molecule. So, a defect here will cause a problem with CD8 + cells so cell mediated immunity is crushed!
The MHC includes a polymorphic set of genes encoding cell surface glycoproteins, designated class I and class II molecules, whose function is to present antigenic peptides to CD8+ and CD4+ T cells, respectively. Peptides generated in the cytosol from denaturated proteins fragmented by proteasomes, some components of which are MHC-encoded are transported into the endoplasmic reticulum (ER) by peptide pumps or transporters associated with antigen processing (TAP) whose encoding genes are again located in the MHC. Peptide binding to the class I heavy chain facilitates association with b2-microglobulin (b2-M) and stabilizes the complex allowing it to migrate to the cell surface.
B2 microglobin, a component of MHC I molecules, functions to transport MHC I to cell surface,ditto.
Lack B2 microglobin, no MHC on cell surface. CD8+ cytotoxic T cell needs to bind to MHC I molecules.
result: defect on CD8+ cytotoxic T cells mediated immunity!!!

13-A Bicornuate uterus, which prevents a woman from fertility, is caused by what?

Incomplete fusion of the PARAMESONEPHRIC ducts!!

14-Inhibited by acyl CoA and enhanced by citrate?

During fatty acid synthesis in the CYTOSOL, Citrate will activate acetyl CoA into malonyl CoA, Acyl CoA will block this.

15-Aside from drug abuse and high exercise, which is a given, what is the next most common cause of lactic acidosis?

Shock, like septic shock or hypoperfusion.

16-A child comes in with meconium ileus, other than Hirshsprung's, what is the other MAIN common disease you see?

Cystic Fibrosis.
It is too easy to merely ask about salty sweat and fatty stools.

17-Meconium ileus is a block of the terminal ileum and is the most common cause of obstruction and congenital GI anomaly. What is the other name of this that starts with the letter M?

Meckel's diverticulum, persistence of the vitelline duct!!!

18-A pt. comes in with overdose of scopolamine because she went on a roller coaster in Disneyland. The doctor in line slips her physostigmine instead of neostigmine, etc. why?

Physostigmine crosses the blood brain barrier to CNS.

Neostigmine is better for urinary retention after plastic surgery (or any surgery).

19-A med student grabs gentamicin for you to treat Bacteroides.Why? Mechanism of action?

Bacteroides is an ANAEROBE. Aminoglycosides do not work on anaerobes b/c they need O2 for uptake, thus blocking formation of 30S initiation complex!

20-Tetracycline has the famous concept of discoloring teeth and blocking bone growth in children, along with photosensitivity. Therefore do not give in children or teens!!

21-A football player comes in with an injury in the shaft of his humerus. What nerve is crushed (choices: radial, median, ulnar, axillary) and what prob. does he have?

Radial nerve is damaged. He is lose his triceps, brachioradialis, and have wrist drop.

22-The aforementioned athlete breaks his supracondyle of humerus. What nerve is crushed?

(Radial, median, ulnar, or axillary)

MEDIAN nerve is blown. He loses his finger flexing ability and some thumb movements and some loss of sensation over lateral palm and thumb and radial 2.5 digits.

23-A supermodel in a car crash looks at you with a "claw hand". What two cord segments contribute to the nerve which is damaged?

Cord segments are C8 and T1!

24-Adenosine deaminase def can cause what problem immunologically?

Adenosine deaminase def can cause SCID (Severe combined immunodeficiency).

25-There will be a person with a history of travel who goes to Mexico or thereabouts. Then he or she will return with bloody bloating crampy diarrhea. They will ask you either what is the bug and the disease, and the treatment. So what are the answers?

Ambiasis, dx is dysentery, and you treat with Metronidiazole and the bug is Entamoeba histolytica.

26-What is the MOA of Acyclovir?
Acyclovir blocks viral DNA polymerase when phosphorylated by viral thymidine kinase.

27-A baby come to your clinic with loud cough that resembles the barking of a seal, difficulty breathing, and a grunting noise or wheezing during breathing. What is the dx? And the secondary question they WILL ask is is it enveloped and what is the structure?

Dx is Croup!
It Has an envelope, has single strand, nonsegmented.

28-Case: Cilia lack ability to move, so your patient is sterile, no sperm, and he has ongoing sinus inflammation. What is syndrome and the protein that is lacking?

Kartagener's Syndrome, due to dynein arm defect!

29-Case: Child with multiple fractures and BLUE sclera. The two secondaries are? What is specific defect? What is the inheritance pattern?

Osteogenesis Imperfecta, with abnormal collagen type I, and inheritance pattern is autosomal dominant!

30-A child has defect in EUSTACHIAN tube and MIDDLE ear, which pharyngeal pouch is defective?

The first pouch!!!!!!!!!!!!!

31-A patient with probs. with his circadian rhythms and autonomic regulation and a DETAILED diagram with arrows of brain pops up, which nucleus is affected?????

The suprachiasmatic nucleus of the hypothalamus!

32-Which one of the following is responsible for PERIPHERAL myelin production?
(Choices: Ependymal cells, Oligodenroglia, Astrocytes, Microglia, Schwann cells)

Schwann cells! Remember that Oligodendroglia are CENTRAL myelin production!

33-Case: A patient with a defect in apo C-II and Lipoprotein Lipase. How will her labs look like? I.E. What is her disease?


hyperlipidemia type I is associated with :
Uncontrolled diabetes mellitus, obesity, and sedentary habits, all of which are more prevalent in industrialized societies than in developing nations. In both epidemiologic and interventional studies, high TG is a risk factor for coronary disease.

Two rare genetic causes of hTG (lipoprotein lipase [LPL] deficiency and apolipoprotein [apo] C-II deficiency) lead to triglyceride (TG) elevations

Consequence: cardio disease!

34-ACUTE INTERMITTENT PORPHIRIA!!!What is the deficient enzyme? And What substances accumulate in the urine? AND what two amino acid begin this synthesis of porphrin molecule? AND what metallic ion cofactor is required?

Deficient enzyme: uroporphyrinogen 1 synthetase
Porphobilinogen and aminolevulinic acid accumulate in urine
Glycine and Succinyl CoA are precursors of porphrin
Metallic ion is Fe!

35-Wernicke-Korsakoff syndrome!!What vitamin is missing AND what DOES THIS VIT DO?

Vitamine B1 (thiamine), it functions as a cofactor for OXIDATIVE DECARBOXYLATION OF PYRUVATE and is involved in the crucial HMP shunt!

REMEMBER...thiamine and the word DECARBOXYLATION RXN!!!

36-Folic Acid!!A slide with macrocytic megaloblatic anemia, what is missing vitamin (but it could also be Vit B12 but without Neuro sym)What IS the EXACT function of it, and type of reaction?

Methylation reactions and it is an enzyme for the all important one carbon transfers.
Folic acid=METHYLATION reactions

37-Case:::Pt with meowing catlike cry and later is mentally retarded. But always it is the SECONDARY QUESTION, so what is the disease, the genetic defect, and the organ that is primarily affected and how?

Cri-du chat syndrome!
Chromosome 5's short arm is deleted AND pt has cardiac defects primarily VSD and ASD!!!

38-Case: A college student comes into your clinic with fever, hepatosplenomegaly, lymphadenopathy and + heterophil Ab test. What is the "bug" and most crucial, is it? SS or DS? (single stand or double strand)
Envelope or no envelope?Linear or circular?

Pt has Mono, and it is Epstein Barr Virus. Herpesvirus family, DS, linear, and it has an envelope.

39-Older patient comes to you with bone pain, Visual inspection may reveal bony deformities, such as an enlarged skull, spinal kyphosis, and bowing of the long bones of the extremities. Localized pain and tenderness may be elicited with manual palpation. Labs: elevated alk phos.
What is this common disease and drug Rx?

Paget's Disease, treat with bisphosphonates, physical therapy, could have viral etiology!!

40-Could you point to EXACTLY where the T-cells are housed on a histo slide?
PARACORTEX, where the T-cells are housed!! Where B-CELLs are housed, that would be the germinal centers or follicles, (they are seen on the outside part)!!!

Consequences of ischemia:
(1) Atrophy (reduction in cell/tissue mass)
(2) Infarction of tissue (localized area of tissue necrosis)
(3) Organ dysfunction (e.g., heart failure

Diffusion defect: interstitial fibrosis, pulmonary edema
Anemia: normal Pao2 and Sao2
Methemoglobinemia:Methemoglobin (metHb) is Hb with oxidized heme groups (Fe3+).

Causes: Oxidant stresses
Examples-nitrite- and sulfur-containing drugs, sepsis, local anesthetics (e.g., benzocaine)
(b) Congenital deficiency of cytochrome b5 reductase
(3) Pathogenesis of hypoxia
(a) Fe3+ cannot bind O2

Treat with methylene Blue, I.V.

41-case: skin manifestations include peripheral nerve involvement with fibromas and plexiform neurofibromas; the iris, with Lisch nodules; optic nerve gliomas; pheochromocytomas in some patients; skeletal abnormalities, including craniofacial dysplasia. What is this disease? What is inheritance pattern?

Neurofibromatosis, AD (Don't confuse with McCune Albright which is assoc with girls and precocious puberty)

42-Pt appears healthy at birth. Diagnosis is usually made in infants aged 6-24 months. Inguinal and umbilical hernias are commonly seen at birth. On physical examination, these patients are observed to have corneal clouding, hepatosplenomegaly, skeletal deformities (dysostosis multiplex), coarse facial features, large tongue. What is the missing enzyme?

Hurler's Syndrome and you are having a deficiency of alpha L-iduronidase

43-We know that an ammonium ion comes in into the mitochondria with carbamoyl phosphate, BUT urea has TWO nitrogens, which compound provides the second nitrogen?

Answer is aspartate feeds it in!

NOBODY, but NONE of US will give up. We will ALL succeed and become doctors. Let's let none of us give up and be left behind with their dreams.

44-Pt with right sided ataxia, loss of pain temp of right face and left upper and lower extremities, hoarseness, dysphagia, loss of taste of right tongue, with vertigo and nystagmus.

P.I.C.A. Posterior Inferior Cerebellar Artery stroke!!

45-Pt, older gentleman with visual field defects from a Circle of Willis hemorrhage.

This is a case of anterior communicating artery stroke, the most common circle of Willis aneurysm!

46-Niacin, Melatonin and serotonin are derived from what amino acid? Think hard first before looking!


47-Case: a child come to your clinic with symptoms of hypopituitarism. Where is the lesion? What is the dx?

This is a classic question of a craniopharyngioma which is the most common cause of hypopituitarism in children and it compresses the optic chiasm and hypothalamus.

48-A man comes in with bilateral and multicentric retinal angiomas, central nervous system (CNS) hemangioblastomas; renal cell carcinomas; pheochromocytomas; islet cell tumors of the pancreas; endolymphatic sac tumors; and renal, pancreatic, and epididymal cysts. CNS hemangioblastoma is the most commonly recognized manifestation of and occurs in 40% of patients. What is the dx?

Von Hippel Lindau Disease!!!!! There can be a MRI of a brain with a cyst in the cerebellum from a hemangioblastoma.

49-A patient presents with recurrent viral infections from T-cell deficiency and symptoms pointing to hypocalcemia. Can you tell me disease (dx) and what failed to develop?

Faulty development of 3rd and 4th POUCH caused DiGeorge's syndrome and Thymic hypoplasia and hypocalcemia.

50-What is the precursor for heme, which aa?

Glycine. don't forget!

Thank you TOMMY for your great contribution!!! Where ever you are I wish you are doing well.

51-Dysplastic nevus= What is the associated neoplasm, is it benign or not?

It predisposes to malignant melanoma!!!

52-A color photo of a hyperpigmented skin lesion in the axillary area on an obese person that you have nailed as acanthosis nigricans (as an aside KNOW THAT THIS LESION IS MORE COMMON WITH DARKER SKINNED INDIVIDUALS). Say they ask you the most notable associated malignancy, what will you say?

Commonly associated with cases with dark skinned obese individuals, you must be wary that they may get GASTRIC adenocarcinoma!!!

53-There is a young person who comes in with mild tachypnia because of acidosis, he has enlarged liver, is slightly to moderately icteric; accompanying hypoglycemia (watch for seizures). What is the MISSING ENZYME?

This is a classic presentation of Aldolase B deficiency. They may want you to know it is autosomal recessive inheritance and you must terminate BOTH fructose and sucrose in the diet.

54-Case: Visual field defect of homonymous hemianopsia. Where exactly is the lesion?


Nerves behind the optic chiasm contralateral.

55-Case: There is a older man with signs of LOWER (not upper) GI bleeding. What is the most common disease (hint, neoplasm is not the answer), secondaries are What area of the bowel is affected and what drug can be given if surgery is not indicted?

This is classic diverticulosis/itis of the lower descending colon and sigmoid (all proximal to the ligament of Treitz). You can give vasopressin as a drug.

Watch for distractor answer choices like Meckel's Diverticulum and Intususception and IBD, these are found in children and adolescents more often. Always always first consider your age and gender and ethnicity and travel and meds of your patients!

in addition to vasopressin you have to give metronidiazole....and some also give Ciprofloxacin.

56-Patient is older gentleman and had a history of lytic lesions and M protein spike and now present w/ lesion in the kidney, lesion was stained w/Congo Red? What is the dx and the name of the tissue stained (condition)?

Multiple Myeloma and the stain is amyloidosis.

57-Case: You are given a clinical case where the gene that is active is c-myc (this is a oncogene, not TSG), what is the related tumor and specific gene translocation?

This is Burkitt's lymphoma AND is a t8;14 gene translocation.

58-Case: A clinical presentation of MENI and or MENII (review this quick), then you have to pick the oncogene that is activated. What will you chose?

ret oncogene!!!

59-you are given a blood smear photo (medium quality) that you know to be follicular lymphomas. But of course, the answer is a secondary. What is the oncogene responsible?

It is bcl-2 which block apoptosis.

60-A clinical presentation is given where a pupil constricts with accommodation and is not reactive to light. What is the treatment? The bug? The name of the syndrome? AND give me the method to visualize the bug!

Penicillin G = Tx

Bug = Syphillis, T. Pallidum

Syndrome = Argyll-Robertson pupil

Visualized by = dark field microscopy

61-Case: One of your patients is in childhood with hepatosplenomegaly, pancytopenia, and crippling skeletal disease. He is Jewish and a liver biopsy shows glycolipid laden cells. What is the disease name and the enzyme deficiency given 5 choices that are agonizingly difficult?

This is Gaucher's Disease and the enzyme def. is B-glucocerebrosidase!

KNOW that Gaucher's like most other enzyme deficiencies are AUTOSOMAL RECESSIVE!!!!!!!!!!

62-A baby patient of yours has loss of sensation around the jaw, and suppose the answer choices ask which brachial arch is defective? What will you answer?

Answer is Brachial arch 1,

Cranial nerve V3 is affected along with all the "m" muscles (e.g. Muscles of mastication, masseter, medial pterygoid), Malleus, and a couple of others.

63-Mechanism of RESISTENCE of bacteria to norfloxacin or ciprofloxacin and then asks you also the side effects?

Resistence comes from a mutational change of the bacterial DNA gyrase. This drug is eliminated renally so don't give to renal compromised patients. A scary side effect of this is inflammation of tendons and cartilage damage.

NOTE: These Quinolones have NO EFFECT on anaerobes!

64-diagram of th Cardiac Cycle/EKG. And you are asked what valve corresponds with the END of the first heart sound (Arrow is pointing there) and is it closing or opening? What do you say?

The Aortic Valve OPENS at the end of the first heart sound!!

65-Arrow points to the place where the S2 STARTS. What valve is opening or closing?

The Aortic Valve closes at the beginning of the 2nd heart sound.

66-What is the MOA of Cyclosporine?

Inhibits IL-2

67-Case: You are given a classic presentation of an older man with Benign Prostatic Hypertrophy (this disease is everywhere). What is the drug of choice and what is the mech of action?

finasteride, a 5 alpha reductase inhibitor.

68-An obese woman with infertility, acne, alopecia, hirsuite. Now, I must ask you what is the hormonal abnormality and the drug of choice? You could also be asked what cancer is she most at risk of?

This is a case of PCOS. There is elevated LH/FSH ratio, and the LH stimulates testosterone. The lack of progesterone predisposes the woman to endometrial cancer.
Treat with Oral Contraceptive Pills or an anti androgen like Spironolactone!

69-Case: Older gentleman with urinary control problems and complaints include back and hip pain as well as other symptoms such as fatigue, malaise, and weight loss. There may also be a history of bone fractures. What is the disease, and the drug of choice

This is sadly prostate cancer with mets to spinal cord. You need to aim to stop testosterone production. Although castration is best (seriously), the choice most men opt for is Lupron or generic name Leuprolide (A LHRH agonist) or Flutamide.

70-You will get a case of a patient with ptosis and inability to turn the eye up, down, or inward. At rest, the eye is deviated down and temporally, and the iris sphincter may be involved or spared. He has a history of an aneurysm, and his eye does not constrict. Two secondaries: What nerve is lesioned, AND if you are given a picture of the circle of Willis and a bunch of arrows, which artery will you pick?!

This is an aneurysm of the posterior communicating artery which is causing CN III to be affected!

Mas informacion gracias a TOMMY!

71-I present you with a patient who has angina at rest with atherosclerosis, is this:
Prinzmetal angina, Stable angina, Unstable angina or MI?

UNstable angina,

KNOW if you get a version asking Prinzmetal's, you see ST elevation on stress ECG and ST depression with exertional/stable angina!!!

72-Case: A 15 year old soccer player named Goober comes into your clinic because of acute, serious throbbing pain in the right knee and is limping. He was "clipped" on his lateral right side of the knee. What three structures are affected?

The triad of anterior cruciate ligament, medical meniscus, and medial collateral ligament. (Think in abbreviations, ACL, MM, MCL)!!

73-If I give you a case with a lumbar puncture (w/ a pic), and ask with arrows where do I get CSF from, can you tell me?

(Choices: Dural, Subdural, Subarachnoid, Arachnoid)

Also asked is between what two spaces is CSF taken?

IT is Subarachnoid, the most common wrong answer is arachnoid or pia mater.

Between L4 and L5!

74-Some patient comes with a history of arrhythmias and is on a med and she presents with antinuclear antibodies, arthralgias, rash. What med is she on?

Procainamide, KNOW that this and HYDRALAZINE gives SLE like symptoms (drug induced)

75-Where does Zafirlukast acts?

Where Leukotrienes are in!!

76-A pt complains to you about his skin thinning and mild osteoporosis and saying his esophagus burns. What med is he on that causes this? (Very popular point)

He is on a Glucocortoicoid, notice that I did not say "buffalo hump", or central obesity. The boards avoids "clicker" words.

En este caso puede ser que se describa la Prednisona.

77-Case: If I present a sideways angiogram of the head, choose the arrow pointing exactly to the sigmoid sinus AND, can you point to the cavernous sinus?

The cavernous sinus is right behind the eyes and the sigmoid floats along the back.

78-Case: What is the proposed mech of action of Lithium, and does your patient have hyper or hypothyroidism? What about poly- or oligouria? A MUST KNOW

You bipolar patient has hypothyroidism and polyuria, Li blocks PIP cascade.

79-Case: A 27 yo AID patient has pulmonary complications. Exam of tissue shows yeast-like with capsules. What does he have? Secondary seen is how do you treat? Very tricky.

He has Cryptococcus Neoformans, NOT Pnemocystis carinii due to ID of the capsule. Treat Cryptococcus with Amphotericin B. KNOW Cryptococcus usually causes meningitis, BUT, it also easily hits the lungs.

80-Case: 32 yo male has demonstrated AIDS and you see cysts containing sporozoites can be seen with silver-stained preparations in the lungs, and he is rather asymptomatic. X-ray shows interstitial infiltrates. What now are you thinking and what drug will you grab!

He has PCP, the most common disease of the AIDS, treat with TMP-SMX!!!!!

81-Case that you nailed as Influenza...secondaries seen are where does it replicate? Pick among answer choices does it have envelope? Linear or NOT?

It along with HIV are the only RNA viruses to replicate in the NUCLEUS, and.... it has an envelope and is linear single strranded!!!!!!!!!!!!!!!!!

82-A pt or question defining the subject of DOPAMINE (A million dollar concept). Which dopamine receptors are excitatory, which are inhibitory, and is the second messenger cAMP or Ca? This concept alone will let you answer a thousand questions, seriously...

D1 and D5 which are excitatory which rev up kidney perfusion in shock, AND

D2, 3, 4 are inhibitory. Most schizophrenic drugs work on the D2 receptor which is inhibitory!!!! Wow, I feel great!

Finally, dopamine works on G-protein coupled cAMP second messengers...

83-PIC: HISTO of muscle fiber. Can you do these if arrows are everywhere?
1) Point to myosin fibers
2) Point exactly where ATP works/acts in EM.
3) To what does Ca bind to (answer is diff for smooth and skeletal muscle)

1) Myosin are the middle lines/area (Look up Histo atlas)

2) ATP is bound to myosin on the Head

3) Ca binds to troponin in skeletal muscle and CALMODULIN (which activates MLCK)

84-Patient complain of gradually worsening shortness of breath, progressive exercise intolerance, and fatigue, and swollen feet. He is an older man with amyloid deposits everywhere? From 4-6 answer choices of -myopathies, what does he have? (Hint: Loud diastolic S3 heard)

He has the rather rare but often quizzed Restrictive Cardiomyopathy (myocardium is stiff)

85-Young child with clinical triad of mental retardation, epilepsy, and facial angiofibromas. What associated cancer is common?

CNS hamartomas and cardiac rhabdomyomas You will see skin lesions so don't pick neurofibromatosis as the answer choice for the pre cancerous condition.

86-You are given a case and asked to quickly calculate the ejection fraction. What's the equation?

Stroke vol/ EDV

87-You will be asked questions about Down Syn. Tell me:
What is the organ most commonly affected (although Down's hits all systems)?
What cancer is associated?
What hormone do you often treat them with?
Is alpha feto protein low or high at 14 week gest?

Cardiac (e.g. VSD)
Cancer is ALL
Hormone is thyroid hormone
Alpha fetoprotein is low in testing

88-A pic with B1 receptor, which neurotransmitter acts here (Epi, norepi, Ach, Dopamine)?
Now you see a pic of Lung with B2 receptors. Does same neurotransmitter act there?

Norepinephrine acts on B1 receptors but NOT B2 receptors (epi does though)

89-LOBAR Pneumonia. Histo shows encapsulated orgs. Then you see myriads of bact/fungi/viruses as possibilities. What is your first choice?

Strep Pneumoniae!

90-Slide with megaloblastic anemia, pt looks like a B12 def. Intrinsic factor administered. Patient improves. What disease did he have? (Pick between terminal ileum deficiency and atrophic gastritis) Also, could there be a bug involved? Which one

He has atrophic gastritis fr. H. Pylori.

Si no haz podido contestar estas preguntas es hora de darle duro a los libros. Anotar y ahcer resumenes de lo leido es lo ideal. Si conoces los temas pero no pasaste el ENARM, significa que tienes buenas bases asi que practica muchas preguntas y mas que nada de los ENARM previos.
Claro lo mismo aplica para el USMLE!! Aprender bien los conceptos es lo ideal.

Universidad : Universidad Autonoma de Guadalajara
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91-What is the term for the most appearing number amongst a given series of number values?

It is called the MODE.

92-The ABCs or name three anaerobes and what is name of enzyme lacking which makes them vulnerable to oxidative damage?




They are missing catalase. Treat with Clinda above the diaphragm and Metronidazole below the diaphragm!!!

93-You are given a case with a druggie and he has Hepatitis C. Choose if it is RNA/DNA/SS/DS/Helical/Square.

RNA, SS, LINEAR (remember that all RNA viruses are single stranded except Reovirus, AND the letter PCR denote the NON-ENVELOPED VIRUSES or P-Picorna, C-Calic, R-Reo).

94-A man comes into your office acting very strange, sticking out his swollen tongue, and complaining of numbness and prickling. He is a vegetarian. What two crucial reactions cannot occur because of the missing diet cofactor?

This is classic triad for Vit B12 deficiency. Homocysteine METHYlation and Methyl malonyl CoA step into TCA cycle is blocked! Ain't that awesome, I mean the knowledge, I feel sorry for the patient though.

95-Your patient goes for plastic surgery to look like Michael Jackson and he is given succinylcholine (muscle relaxant). He suffered prolonged respiratory paralysis and muscle paralysis afterwards! What enzyme or mineral is defective? (Hypomagnesium, Hypokalemia, Pseudocholinesterase def)

It is pseudocholinesterase deficiency. Many causes, but pregnancy, neonates, elderly, burn victims, pesticide poisoning, can be presented by the Boards.

96-A patient presents with epigastric symptoms and melena.. You should pick PUD or peptic ulcer disease (this disease is everywhere, like air), BUT there is a secondary! Labs rule out H.Pylori (most common). What is the next HUGE cause?

Chronic NSAID use. Man, I had to do so many anal exams for this (checking for bleeding with those little Heme cards). They call it the M-3 student consult.

97-You have a patient with a description of allergic rhinitis, and he is taking steroids, antihistamines, and pseudoephedrine. He is depressed and wants anti depressants. You pick one from 5 choices, which one did you pick that is a no-no?

MAO inhibitors cause hypertensive crisis.

98-You have a young patient with a gene defective in making myeloperoxidase, thus the cause of his recurrent infections. What cells are weakened, what is the MECHANISM LOST, what is the metal ion in MPO?

(You will see this case, or DiGeorge's, SCID, etc.)

The ability of the immune cells to engage in respiratory burst is cut off. Myeloperoxidase, MPO, catalyzes the conversion of hydrogen peroxide and chloride ions (Cl) into hypochlorous acid. Hypochlorous acid is 50 times more potent in microbial killing than hydrogen peroxide.

Neutrophils are weakened which contain Fe.

99-Case: You get another child just like the previous case with bacterial infections. BUT, this time you discover there is a defect in microtubules and phagocytics. You see severe gingivitis and oral mucosal ulceration PLUS albinism on the skin. Secondaries: What is the disease, what two bugs eat at you, and what is the first drug you reach for?

Is Chediak-Higashi disease (not too common). But you get strep and staph infections and you treat with Acyclovir. The KEY to this diagnosis is the mouth stuff and hypopigmentation!

You start with Acyclovir THEN give the missing globulins through IV because Chediak Higashi is an IMMUNE DISEASE and Acyclovir boosts the recovery while fighting the viruses. The globins you transfuse will address the Staph and Strep.

100-Patient comes in with recurrent bronchpulmonary, bacterial, neurologic disease, thymus aplasia, telangiectasias, growth retardation, and impaired organ mutation, and is walking funny and waddling. What are you looking at NOW?

Ataxia telangiectasia, where both the T and B cells are busted. The alpha fetoprotein levels are always elevated, and they key finding is ATAXIA!

101-A child, younger this time, 2 years old walks in, again with recurrent bacterial, fungal, infections. His mom say he suffers often from candida. And you note he has IL-2 def, poss. reticular or ZAP-70 gene def. He will suffer from PCP and Herpes. You to write a prescription for .... ???? What disease? What med?

This unfortunate child has Severe combined immunodeficiency or SCID. They usually die by age 2 from PCP. You must prophylaxis with TMP-Sulfmethoxazole. Consider IV globin transfusion if counts stay low.

102-ANOTHER CHILD comes into your peds clinic with an immune def. But this time, the child is hyperreflexic on exam, has abnormal facies, congenital heart disease, hypocalcemia on labs, and increased susceptibility to infections. A radiograph shows he has no thymus! What do you prescribe?

This child has DiGeorge's Disease or thymic aplasia. His 3rd and 4th arch failed to develop. Including considering marrow transfusion, you must prescribe Calcium salts and Vit D!!!!

103-ANOTHER child walks in with his mom with another immune deficiency. Here he is 4 years old, with recurrent otitis media, eczema, and thrombocytopenia from Strep pneumoniae. AND, he bleeds a lot. His IgM is low. Your attending and chief are wondering if you are able to distinguish all these immune def. diseases. Name disease? What will you treat with? What is mech that is broken?

He has X-LINKED Wiskott-Aldrich syndrome. This is often confused with the others and Bruton's on exams. But remember the tendency to get attacks from capule bugs like Strep, with otitis, eczema , and BLEEDING. The key is LOW IgM, High IgA,and the bleeding. IgM response curtailed. He is not nearly as bad as SCID case, and you must give him amoxicillin (there are a lot of options here, like you can give ceftriaxone too) plus globins.


104-This boy has low IgG and presents like WAS syndrome with continued bacterial infections, diarrhea. And you find out this is X-linked too! In the absence of functional Btk, mature B cells expressing surface immunoglobulin and the marker CD19 are few to absent. What disease?

Bruton's agammaglobulinemia

Here is the first immune def. described by Dr. Bruton. So similar to WAS syndrome, but WAS boys will BLEED!!

105-A GIRL, comes in with OF COURSE, an immune deficiency with bacterial and fungal infections. note that all the immune def. choices are mixing but you see her presenting with lymphadenopathy, hepatosplenomegaly, growth failure, and stigmata of chronic skin infections. Something about def. w/ phagocytes. TWO distinct hints. AND culture comes back and she has Aspergillus. Diagnosis?

This is Chronic Granulomatous Disease. This is marked by the granulomas (skin stuff) and key words phagocyte def. and Aspergillus infection.

106-A patient has immune def. with recurrent bacterial sinopulmonary infections.The patient is OLDER, LESS SYMPTOMATIC (i.e. less severe disease), and complains of GI symptoms too like diarrhea. What is the diagnosis?

This IgA D or Immunoglobulin A def. Many stay asymptomatic, IgG and Neutrophil levels could be normal. Give antibiotics.

107-Fraternal triplets THEY ALL HAVE systemic symptoms such as weakness, fatigue, malaise, and fever low-grade, two have neck pain, one does not. Physical exam shows hypothyroidism. But here is the concept that comes again again again again:

Child A has hypothyroidism, neck pain, and fever chills and dysphagia.

Child A has ACUTE THYROIDITIS (bacterial) so you must manage aggressively with antibiotics (penicillin G is DOC)

Child B has SUBACUTE THYROIDITIS (viral) so you just give aspirin and return visit. (KEY!!, HYPER, then HYPOthyroid features)

Child C has AUTOIMMUNE THYROIDITIS. This is bad because it is a life-long condition. Treat with levothyroxine.

108-What MAJOR MAJOR drug other than trimethoprim blocks the loved enzyme dihydrofolate reductase?


KNOW you often use it for rheumatoid arthritis, hydatiform mole, leukemias and it works its magic in the synthesis phase, stopping thymidine (thymidineless death) and blocks protein synthesis.

(Information:IL-5 revs UP IgA and IL-6 (like IL-1) revs up the acute phase response.)

109-Patient comes into the office and he has vertigo and remarks that he has difficulty with taste and swallowing. Before you give a prescription for antivert, is this a dysfunction of the vestibular apparatus of the inner ear? Or is it a brain stem issue? If it is a brain stem issue, what two nuclei and nerves are involved?

Tricky case. Because vertigo has many causes, note the DIFFICULTY with taste and swallowing. This pushes up the suspicion of a lesion to the nucleus solitarius and ambiguus with nerves 7,9, and 10 also lesioned. AND for the cherry, we see that all the time with a POSTERIOR INFERIOR CEREBELLAR ARTERY stroke which supplies that area! See?

110-if a patient has no pupillary reaction to light shined on the right side but there is a reaction to light in both eyes, when light is shined on the left. The lesion is what? NOW I change the patient so there is pupil rxn to light on only the right side, when light is shined in either eye. NOW, where is the lesion?

For the first patient, the lesion is the right CN2. For the second, the lesion is left CN3.

[b]Gracias TOMMYK!! Honor a quien honor se merece! Este residente hace un par de a~os escribio estos apuntes y gracias a la manera en que los escribio, me ayudo a aprenderme conceptos de medicina que me fueron utiles para el ENARM. Claro originalmente fueron escritos por el para el USMLE 1,2, y 3 pero la manera en que escribio sus notas me inspiro a hacer lo mismo y asi ayudarme a continuar recordando lo que he aprendido. Hoy en dia no se sabe que paso con este autor, solo que fue diagnosticado con una enfermedad de la cual estuvo grave. No se sabe que paso con el, si aun vive o a fallecido. Gracias TommyK!

111-Say your pt comes in and you touch both her corneas one at a time with a q-tip, and you note that ONLY the LEFT eye blinks, then which cranial nerve is activated?

Right CN7 (NOT THE LEFT ONE, common mistake)

112-Patient A has a stroke in motor cortex that lesions UMN tract to central facial n.

Patient B went on a camping trip and has a lesion to the LMN CN VII.

Tell me how each patient will present on physical exams...

Patient A will have CONTRALATERAL, and LOWER QUADRANT paralysis.

Patient B will have same side Bell's Palsy features (can't smile and may drool on affected side)

113-A nurse brings in a 15 year old boy with "fatty" thick calf muscles. The child trips on a toy and strangely uses his proximal muscles to assist in standing....Is not Duchenne's!!

What is the disease and what is the defective protein? And what are the labs?What is the only drug with known effectiveness for his condition?????

The disease is Becker's, a milder form of progressive muscular dystrophy.
The defective protein is DYSTROPHIN!
The labs show elevated CPK!
The ONLY drug with current known effectiveness is prednisolone.

114-You see a female with a blood smear with RBCs small n'round, physical is anemia, hyperbilirubinemia, and abnormal results on the osmotic fragility test. OK OK she has hereditary spherocytosis (so common in clinics).
1) What protein is defective?
2) What is the inheritance pattern?
3) What are the main two complications?
4) Surgical treatment?
5) What do you prescribe to them?

1) spectrin
2) AD inheritance
3) cholecystitis and aplastic anemia
4) Splenectomy
5) They need folic acid!

115-Another patient comes in weak with signs pointing to anemia. You take a blood smear and whoa! cytopenia...blast cells, reticulocytes, sparse RBCs. And you know this is not autoimmune because it is recent. Hold it...she mentions she had a gonorrheal infection and is on a med. OH YES! OK, so what is the disease, name of the med she is on AND what will be the name of the med you give her as you transfuse bone marrow!?!?!

Chloramphenicol is the drug she is on that caused aplastic anemia. AND you can give cyclosporine or a steroid along with her transfusion. REMEMBER, aplastic anemia has many causes so be careful. Benzene, pregnancy, CMV, HIV, EBV, and autoimmune causes are all to be considered!

116-An African American male comes into your office with signs of very very mild anemia, almost no symptoms, a little jaundice. His main complaint--a UTI. Your senior hints this is the most common enzyme pathology. A smear shows Heinz bodies (review please). Now your senior starts a pimping away.

1) What is his disease?

2) Why is it so prevalent?

3) What does the enzyme catalyze? What is the end product?

4) You grab some sulfamide and nitrofurantoin to treat his Urinary Tract Infection and your attending smacks you on the other side of the face that she missed before. Why was she so upset with you?


1) G6PD Deficiency

2) It confers protection against malaria

3) The G6PD enzyme catalyzes the oxidation of glucose-6-phosphate to 6-phosphogluconate while concomitantly reducing the oxidized form of nicotinamide adenine dinucleotide phosphate (NADP+) to nicotinamide adenine dinucleotide phosphate (NADPH). NADPH, a required cofactor in many biosynthetic reactions, maintains glutathione in its reduced form. RBCs need NADPH to protect itself against oxidative stresses. (Long winded explanation, but you have to know it., sorry).

4) You cannot give an oxidizing agent like primaquine, choroquine, or a sulfa drug, or nitrofurantoin to a patient with G6PD def. Their RBC will hemolyse and you will lose your license and your attending will lose her's and your hospital will close and turn into an apartment complex.

117-Case: an elderly psych patient of yours complains of arrhymias, what drug is she on? (amitriptyline or thioridazine or lithium or olanzapine?)

she's on amitrypyline, a tri cyclic antidepressant. (OTHER tricyclics are imipramine and nortriptyline.

Bad side effect: arrhythmias. Review MOA.

118-Another elderly psych patient comes to your office with complaints of colds and a peripheral smear shows low WBCs, what drug caused this? MOST LIKELY one..Secondaries: which two receptors does it block.?

Clozapine, blocks 5HT-2 and dopamine. Causes leukopenia.

119-Yet another elderly psych patient comes into your office this time with constipation and rigid muscles and (hint other antimuscarinic sym). He was given a med FOR an ACUTE psych episode where he shouted and hit others. What is the drug? 2nd: Receptor/MOA? And Name at least two other drugs in this family.

Answer: He is on Haloperidol (used for Positive symp, in ACUTE cases), the drug blocks D2 receptors, and fluphenazine and thioridazine are within this family named NEUROLEPTICS,

Assoc. of course to tardive dyskinesia!
(these are different from the atypicals, make sure you know the atypicals are risperidone, but also clozapine and olanzapine--neg symptoms controlled more, diff receptors involved)

120-Woman walks in with chronically sore right knee. She is neg. on labs for rheumatoid factor. Under microscope, you see crystals appearing shorter and often rhomboidal. Under a polarizing filter, crystals do not change color depending upon their alignment relative to the direction of the red compensator.

Diagnosis? Name of the crystals deposited?

Answer: IS NOT rheumatoid arthritis or gout, BUT, the answer is pseudogout, and you see calcium pyrophosphate crystals as oppossed to birefringent needle crystals in gout! P=Pseudo=Positively birefringent

People keep missing Goodpasture's and Wegner's, you know, the diseases with BOTH kidney damage and Lung damage. Can't discern.

121-A child enters your clinic with chronic diarrhea and fatty stools. Does he have Cystic Fibrosis, Giardia, or Ulcerative Colitis, or Chron's? But, YOU go further and order labs. They come back with weird D-xylose test, anti-IgA antibodies, B-cells in the lamina propia

You know:
1) Disease
2) Etiology (viral/immune/etc)
3) is there a specific substance or drug he should take or avoid?


1) He has Celiac sprue
2) Autoimmune/hereditary/Europe
3) Avoid gliadin wheat in diet

122-You have a older African American male who comes in with chronic CHF and began a new medication. But he suddenly one morning found his left foot joints swollen and so tender even the weight of the bedsheets are so painful! (BIG HINT COMING). Labs come back and you see crystals with needle shapes (shown a pic), (-) birefring...

1) Tell me the likely med he was on and at least two other meds which could cause this condition.
2) What is the short term and LONG term treatment?
3) MOA (Mech of Action) of disease?
4) What compound builds up?
5) What foods should he avoid?
6) Bonus Biggie: He had a great grandfather who had similar symptoms but was mildly retarded and scratched himself like crazy! Dx?


1) Thiazide diuretics, Cyclosporine, Nicotinic Acid and a LONG LONG list can do this.
2) Colchicine short term/and Indomethacin and Allopurinol long term
3) Uric acid precipitates from supersaturated extracellular (ie, synovial) fluid. The resulting crystals stimulate phagocytosis by neutrophils and initiation of the inflammatory cascade. OUCH.
5) (Purine rich foods (especially of anchovies, sardines, sweetbread, kidney, liver, meat extracts)
6) Lesch-Nyhan syndrome.

123-Case; Pt comes in and says she has: Inability to eat dry food, such as crackers, which sticks on the roof the mouth Tongue sticking to the roof of the mouth She always has to be putting a glass of water on their bed stand to drink at night. She has difficulty speaking for long periods of time, and her eyes are dry and her right wrist is starting to hurt.

1) Disease?
2) Which HLA is involved?
3) Drug of Choice (DOC)?
4) What dx, is she at increased risk for?


1) Sjogren's syndrome (they'll give choices like Reiter's, PSS, etc.)
2) HLA 3
3) Pilocarpine to stim. secretions! And eye drops!
4) a lymphoproliferative disorder

124-A male patient comes in with myalgias and low back pain. He also has reddish (infection like) tinge on his left eye. You think is Ankylosing spondylitis or Rheum. Arthritis!. But not so fast! You note that labs came back positive for HLA B27, BUT so did chlamydia culture!!!!!

You scold your med student.

1 Why? Because he had picked the wrong disease, the right one is?

1.. Reiter's syndrome!
Reiter's= male Sjogren's=female

The KEY finding is the Chlamydia or could be Salmonella and urethral connections. The closing of the triad is the conjunctivitis. Don't be tricked my brothers and sisters!

125-Another male patient comes in with myalgias and low back pain! He also has a reddish (infection like) tinge on his left eye. HLA-B27+! You are about to say that you have another case of Reiter's, but you note his labs reveal cardiac anomalies.


This one is ankylosing spondylitis, compare carefully with Reiter's. One triad has the heart, the other has the urethra!

126-Another patient comes with lower back pain and the usual suspects. But she says her arthritis often comes with a fever and is WORSE IN THE MORNING! You know this dx of course, you know it is NOT osteoarthritis, which has osteophytes, but what if I presented a pic of the hands with arrows to all joints. WHICH ONE(S) OF THE THREE JOINTS ARE AFFECTED (DIP, MCP, PIP)? Besides NSAIDS, what other three drugs are often tried?

She has rheumatoid arthritis, + rheumatoid factor. This autoimmune dx has systemic symptoms like her fever and malaise.
MCP and PIP joints OSTEOarthritis has DIP joint inflammation.

127-A young girl comes into your office with a fever and history of weakness, infections, cardiac flow murmur and petechaie. You order a CBC and find that her smear shows what looks like immature leukocytes...but you cannot seem to distinguish between ALL and AML (THIS IS A MAJOR TEACHING POINT, BECAUSE THE SMEARS CAN LOOK VERY VERY SIMILAR AND THERE WILL BE BOTH ON THE ANSWER CHOICES, SO LOOK IT UP IN A HISTO ATLAS!). You suddenly see thin stick like features in some of the cells, then you see some spotty nulear chromatin and more nucleoli. You think you nailed the diagnosis: but see this:

1) What is it?
2) What is the most common sub-classification?
3) What were those thin stick like bodies?
4) What enzymatic test NAILS the diff between ALL and AML?

Markers are CD3 is T-cell so think ALL and CD19 is B-cell so think AML.Most ALL is of, B cell origin ( a few , of T cell origin resemble lymphoblastic lymphoma. So, both CD3 and Cd19 can be markers for ALL. On the other hand, AML's origin is NOT LYMPHOID, BUT G-M.


1) This is AML, the myeloblasts have delicate nuclear chromatin, strong nuceoli, LOOK FOR GRANULES in cytoplasm
2) M2 is the largest incidence
3) Auer Bodies
4) Myeloperoxidase - positive test

128-A 40 yr old gentleman middle aged enters your clinic with a complaint of fatigue, weight loss, splenomegaly. A lot of newspapers report that doctors are missing leukemias thinking the disease is a common cold. Big mistake and big problems. The gentleman's blood smear looks distinct with a lot of mature neutrophils (twisting nuclei) (CML, ok I gave it away) is very distinct from ALL, AML and CLL on slides, it has a lot of mature neutrophils. But of course you need the secondaries....

1) What is the chromosome that is definitive of CML? Definitely will be asked.

2) The translocation results in the formation of what gene?

1) Key is the Ph or Philadelphia chromosome
2) You will see bcr-c-abl fusion gene

129-You see an elderly male come into the office with vague symptoms of anemia but is very stable over years. His peripheral smear is distinct and shows a whole bunch of lymphcytes (you need to see the slide, it is very distinct). But here is the questions you will encounter:

1) In this rather insolent disease, what is the CD marker?
2) Is CLL mostly B or T cells?
3) What main leukemia is CLL associated with?


1) CD5
2) B-cells most than 95%
3) small lymphocytic lymphoma

130-Myeloid leukemia where you will see a bunch of monoblasts on a smear. You are asked, which FAB classification is this? (This is NOT TOO MUCH DETAIL)

You are looking at M5 type.

131-Differentiate Multiple Myeloma and Waldenstrom's macroglobinemia on questions. What is the difference?

Multiple Myeloma has an M spike of IgG while..
Waldenstrom's macroglobinemia's M spike is IgM

132-Which of the Hodgkin's lymphomas has the best prognosis?

Nodular sclerosing type has the best prognosis and is also most common with few Reed Sternberg cells.

133-You have a case that confuses you about leukemias and you are lost, but you see DIC (Disseminated Intravascular Coag) as an answer choice. Now you know that is the answer because there is a clue that the patient is a woman giving birth...What key finding nails the diagnosis and is often asked?

The key is they must and will give you lab findings where aPTT, PT is elevated for DIC, and KEY is low platlets and POSITIVE D-Dimer test.

134-A case of anemia symptoms and you have to know the differences between:
H.U.S. (Hemolytic Uremic Syndrome)
von Willebrand's disease

They can all present so similar with the same signs like bleeding problems, microhemorrhages, etc. You need to know the keys to differentiate! Especially confusing is choosing between HUS and TTP (TTP and ITP are easier because TTP will have neuro findings). How do you tell HUS and TTP and Hemophilias and von Willebrand's apart on a test?

Answer: Thrombotic thrombocytopenic purpura (TTP) is a life-threatening multisystem disorder of unknown etiology, first described by Moschcowitz in 1924. TTP and hemolytic uremic syndrome (HUS) are both thrombotic microangiopathies characterized by microvascular lesions with platelet aggregation.
TTP and HUS share the same pathophysiological etiology and may be varied expressions of the same underlying disease process. They both have abnormal bleeding times due to low platlets.

KNOW that HUS is more common in children and is characterized by prominent renal involvement. TTP is more common in adults and is associated with pregnancy; diseases such as HIV, cancer, bacterial infection, and vasculitis; bone marrow transplantation; and drugs.

Between HUS and TTP, you may be asked to know that TTP has SCHISTOCYTES visible on a smear.
TTP and HUS have abnormal bleeding times and NORMAL aPTT and PT. Contrast with Hemophilias which have labs with prolonged aPTT and PT and NORMAL bleeding times!!!! (Another popular secondary is Hemophilia A=factor VIII, Hemo B=factor IX).

YOU WILL KNOW to pick vonWillebrand's because it has abnormal aPTT AND prolonged bleeding times.


135-A CLEAR CASE OF SICKLE CELL ANEMIA. This is easier to diagnosis for obvious reasons. The important secondaries will be:

1) What is the newest drug for treatment (NOT PAIN MEDS)?
2) What is the mechanism of disease?
3) Which bug causes an osteomyelitis?
4) Very important: What can trigger an onset of the sickling?


1) Hydroxyurea!
2) There is a substitution of valine for glutamic acid at the sixth position of the Beta chain.!!!! KNOW THIS!
3) Often Salmonella, maybe Staph
4) Any kind of hypoxemia or disturbance of core body temperature!!!!!!!!!!!!!!!!!!!!! Look for respiratory causes!

Know that B-thalassemia heterozygote is common and you can survive, but A-thalassemia IS DEADLY and will result in fetal hydrops.

Vit B12 has neuro stuff and Folate doesn't but BOTH are macrocytic

136-A child comes into your office and his mom said he was eating paint chips in their OLD apartment building!

What does his smear look like?

This is a classic favorite of lead poisoning and the smear is hypochromic, microcytic. Iron defficiency is also hypochromic and microcytic.

DE farma!!!

137-Pt with tinnitis, headache, can't hear a thing. Patient has a heart condition. What med did this?

Quinidine, a class IA anti arrhythmic.

138-You are in OB GYN in NYC USA and a woman comes in with convulsions. She is on birth control pills!!!!!!!!! BIG POINT!

What vitamin is she going to lack???

She is showing deficiency of vit B (specifically B6 or pyridoxine). This all important vitamin is used in

TRANSAMINATION REACTIONS, SULFUR RXNS, RACEMIC RXNS, AND TRANSAMINATION, and must be in active form of pyridoxal phosphate.

139-You are presented with a LM image of the thyroid with arrows everywhere. In the cell point the exact location on the image where calcitonin is secreted.

Answer: The parafollicular or C-cells secrete calcitonin.

140-Bill who has a testicular tumor, ok it is a Vinca alkaloid. WHAT PROTEIN DOES IT BIND TO AND GIVE MOA?


141-A pt of yours comes in with abd pain after eating raw fish. He looks lk he has cholecytitis. What drug do you give? What is the bug?

Answer:This is a fluke (looked weird like a worm), Bug is CLONORCHIS SINENSIS, treat with PRAZIQUANTEL.

142-A young boy comes to your clinic with diarrhea after eating "mud pies", what is the bug and the tx?

Answer:But is the infamous Strongloides stercoralis, tx. with Thiabendazole!

143-You have a male pt, 30, with epilepsy coming in after eating "raw pork". What is the helminth and the treatment?

Answer:The bug is a tapeworm--Taenia solium and you give Praziquantel and Niclosamide and a steroid to relieve CNS pressure because this bug swims everywhere, even in the CNS!

THE CASE WILL give travel to Southeast Asia or maybe Africa.

144-A traveler comes from Africa (could also be a West Alaskan Indian), and had told you he ate coyote and dog poop as a college dare! He is ASYMPTOMATIC but you see cysts in his lungs on X-ray. What's the bug and TX?

Answer:Albendazole which works by depleting ATP, and the bug if asked is Echinococcus. For this and the other tapeworm, Taenia, the guy could be scratching his rear end a lot so wash your hands!

145-A pt of yours came back from Brazil and has dysuria and nausea. Plus he told you he ate a bunch of snails at a local exotic restaurant. What's the bug and tx?

Answer:He has the famous Schistosoma Haematobium. In US it is rare because they don't usually eat a lot of snails! But know this fluke has many subtypes and can clinically present LIKE ANTHING! One key is it results in granulomas! Treat with Biltricide which has generic name Praziquantel

146-A pt returns to your clinic fr. Latin America with signs of Asthma. But a stool sample shows a round curved worm (slide is given). YOUR ATTENDING TELLS YOU THIS IS THE MOST COMMON HELMINTH INFECTION IN THE WORLD! You are looking at what and will treat with what? AND also seen is what is MOA of the drugs?


147-Don't confuse this with Ascariasis. This nematode is quite prevalent in the US. That will be the give away and so will the fact that your peds patient is scratching his behind. Give me bug and drug?

Answer:Enterobius vermicularis and the case seen is a kid with an itchy "butt".
Treat with Pyrantel pamoate.

148-A woman patient comes to you after sampling raw spiced pork sausage links (classic case). She has myalgias and PERIORBITAL EDEMA. What's the bug and drug and MOA of drug?

Answer:This helminth is the ubiquitous Trichinella. Very common the US.
Treat Trichinella with Thiabendazole!
Again, Trichella is assoc. with pigs if all else fails.

149-You get a patient who came from a trip photographing wild animals in AFRICA (let's say Ethiopia). He comes to your clinic and you see hypopigmented (leopard spot like) lesions on his legs. He photographed from a riverbank (HINT). Give me bug and drug and MOA of drug?


Transmission is by black flies, along riverbeds, mostly all in Africa. Treat with IVERMECTIN, which works and binds selectively with glutamate-gated chloride-ion channels in invertebrate nerve and muscle cells.

150-A post college grad comes to you who came back from the PEACE CORPS. She volunteered her time so well, but this is a crisis. She is thin and athletic, and pretty but sadly one of her legs looks swollen like an ELEPHANT'S. What's the bug and drug you give?

Answer:Very common case of Bancroftian Filariasis or Wuchereria bancrofti where a person is bit by a mosquito and has lymph node swelling everywhere. Common is a foot and/or leg elephantiasis. Treat FAST with Ivermectin or Diethylcarbamazine or she will lose her precious leg!

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Autorepaso......español y en ingles..!! - Página 9 Empty Re: Autorepaso......español y en ingles..!!

el Mar Jun 14, 2011 2:23 pm
Very Happy Esto continua siendo para mi un repaso del material que en un momento llegue hasta casi vivirlo y so~arlo para poder aprenderlo. Parte de lo que voy anotando aqui, viene de apuntes personales, articulos de diferentes fuentes, paginas web, etc. Pero muchos de los apuntes vienen de libros como Robbin's, Harrison, y Goljan. No hay que olvidar que como medicos debemos tener muchas cosas frescas en nuestras cabezas y asi leer y seguir investigando por nuestra propia cuenta todo lo que vemos y leemos. Hoy en dia un paciente puede estar mejor informado de los avanzes que un medico con solo estar pegado a Google. Por lo tanto hoy en dia es un gran reto mantenerse al margen de lo que sale en el mundo de la medicina e investigar con nuestras bases y leer otras fuentes. No estamos en el mundo de antes donde los medicos se les veian como Dioses y todo lo que dijeran era la pura verdad. Algunos medicos hoy en dia viven con esa mentalidad erronea y juzgan sin investigar y solo por que viven en su arrogancia de semi-dioses no se molestan en leer o investigar. Solo como pericos repiten lo que otros medicos comentan y en muchas ocaciones son comentarios sin bases. Aqui sigo anotando lo que seguido voy leyendo y repasando. Pronto tendre que darle una buena leida al Goodman Y Gillman.

Buen dia!!

151-Mebendazole. What is the MOA?

Mebendazole is often used for treatment of eosinophilic enteritis; inhibits microtubule polymerization by binding to cytoplasmic b-tubulin; by affecting parasite's intestinal cells, prevents use of nutrients and essentially starves parasite to death!

152-patient who came back from Puerto Rico (could be other places too). Now, he complained that a month ago he started itching, THEN coughing, THEN having diarrhea! Terrible! He is begging you to diagnose him because he is starting to look anemic!!

What is the bug and drug???????? Oh, also what does his blood smear show?

Answer:Anclostoma or HOOKworm disease which is SO prevalent around the world. You should look for travel history. Another related hookworm is Necator Americans.

When the bug hatches in the intestine, you get IRON DEF. ANEMIA, so blood smear will show microcytic RBCs.

You treat with Albendazole or Mebendazole.

153-In your peds clinic, a kids comes in with vision problems and his mom said he had gotten a couple of new puppies. He also has wheezing urticaria and he lives in Southeast US. What is the bug and drug?

The association of:
puppies=southeast US=eye stuff gives it away easy.

Toxocariasis. You treat with a drug called Diethylcarbamazine but Thiabendazole can be used too. Puppy poop has this. You cannot miss this and accidentally treat with antibiotics thinking you have Pasturella (bacteria).

So how will you KNOW? Remember eosinophilia? It can be as high as 80% with high IgM!!!!!
Differences between bacteria and parasites:
1) You may see a clinical history with stages (first intestines, then lungs, etc. because these guys lay down larvae)
2) You MUST look for the clue for labs and sometimes my students say they completely skip the lab section because they are in a hurry. ONE TWO MILLIMETER SPACE has the info HIGH EOSINOPHILIA! If you miss this, you may treat your patient with antibiotics on your test and get the question wrong.
3) Also, a lot of these bugs are not endemic to the this area. So look for a history of travel.
4) There are only a few drugs here, so please don't forget them.

154-A Japanese family just came to this area 3 months ago and then went straight to your clinic. One of the kids has serious pulmonary signs and was treated for Tuberculosis. HE IS NOT BETTER. Worried parents gave you a history that he was treated by his older grandma in Japan with raw crayfish for health. You are glad they came to you because you know you are not looking at TB but rather....? And you will treat with ???

A finally the drug was what MOA????


doctors mistake this deadly PARASITE with other things like TB or coccidomycosis.
So here you have a big clue about the Japanese ethnicity and the ingestion of crayfish and the lung findings.

This is pathognomic for....Paragonimiasis.
Please treat with Praziquantel. You must know...
Praziquantel again that it inhibits microtubule polymerization by binding to cytoplasmic b-tubulin; by affecting parasite's intestinal cells, prevents use of nutrients and essentially starves parasite to death.

use some pneumonic because they are kinda hard to distinguish.
Taenia> Sounds like Tan-in-sol (sun) while Praying (praziquantel)
[These are weird pneumonics but I think you need some and personalize them, I can think of Tanning and Praying so I associate Taenia with Praziquantel for the drug treatment]
Strongyloides> "strong thighs" (Thighs sounds like) Thiabendazole
Onchocerca > "On cocaine via IV" (IV for Ivermectin)
Corny, but the parasites need this because their names are weirder.
Again, try not to confuse the parasites and bacteria. Look for Travel, look at labs, and look for symptoms that wax and wane over a month as the parasite goes through larvae stages.

155-THE PREVIOUS case of the 2 year old with Chronic Granulomatous Disease which wAS discovered is REALLY BAD, what is the name of the enzyme that was lacking?



Our phagocyte oxidase system is an NADPH oxidase enzyme complex consisting of 4 component proteins. Membrane-bound gp91 and p22 make up the b and a subunits of the heterodimer cytochrome b558 portion of phox gene.

Remember you might get distractors such as: NADH OXIDASE or NAD+OXIDASE or NADPH REDUCTASE!

156-VDJ recombination: Which chain, the H (Heavy) or L (Light) carries the 3 gene segments? And in CLASS SWITCHING, which antibody, IgM, IgG, IgA, IgD, or IgE is most "primitive"?

know that the Heavy chain has the VDJ and there is DNA rearrangement. Know the L and H chains are made SEPARATELY in the CYTOPLASM by means of DISULFIDE BONDS!!! The LAST step is the addition of the CARBOHYDRATE moiety.

At first, all B lymphocytes carry IgM specific then after undergo class switching to the others.

157-A patient presents with dyspnea, endless differential, but here are the secondaries for ARDS:
1) Pretend you already diagnosed ARDS, a deadly illness, what cell is responsible for the distress?
2) So what are the main causes?)
3) We know there are a lot of causes of Pulmonary Edema, but how can you differentiate ARDS edema and Cardiogenic edema?

ARDS carries a 50% death rate.

1) Neutrophils
2) Ischemic shock/Endotoxic shock/DIC; breathing really hot air; acute pancreatitis (weird, eh?), drug use
3) It is called Pulmonary Capillary Wedge Pressure test (LV) LOW in ARDS, HIGH in CARDIOGENIC!

158-1) Could you pick out the right ratio of T to B cells?

2) YOU know the T cells pass through thymus for thymic education, do the B cells pass thru thymus? If not, where (amongst a series of choices of course)?
3) Which IL type boosts up T helper cells?

2) B cells don't pass thru thymus but the precursors mature in GALT and Peyer's patches.
3) IL-2

159-We know IL-1 and TNF-alpha makes your temperature go up, so
which IL revs up IgA?


160-In helminths. Which IL is most involved?

It is IL-5. You may "memorize" what I just asked, IgA is stimulated by IL-5, but then when I bring up the concept that IL-5 revs up both IgA (intestinal mucosa) and Eosinophils.

161-Which mediator is responsible for endotoxin septic shock and makes you have cachexia (like in cancer)? And then, what is the MECH?

TNF alpha,
1) secreted by MACROPHAGES
2) It causes cachexia by inhibiting lipoprotein lipase in adipose tissue.
KNOW TNF-A also revs up IL-2 and B-cells.

162-A patient of yours is predisposed to TYPE I hypersensitivity. Which IL is mostly responsible?


The answer is IL-4 IL-4 revs up IgE, WHICH THEN is responsible for anaphylactic shock.

Quizas pensaste que seria TNF o IL-1 pero aunque puede ser similar pero no es asi. Recuerda que IL-4 esta relacionada a IgE.

163-Which IL revs up stem cells?

Muchos conceptos que te pueden ayudar tanto en el ENARM y sobre todo el USMLE. Parte de esto en el MIR o quizas en tu examen de Homologacion.
Asi que dale duro a los


Is IL-3!! Quizas en lugar de Stem Cells les pongan medula osea o bone marrow pero recuerden que pueden poner esta pregunta usando cualquier de estas dos regiones.

164-Which IL is part of the acute phase other than IL-1?

Also, which IL does the same as GM-CSF(Granulocyte-Macrophage Colony Stimulating Factor)?


La respuesta es IL-6!!

And IL-3 is like GM-CSF!!!!

165- KNOW MHC I = T=cells
AND MHC II =B-cells (these are loose associations).

Mature MONOCYTES secrete which two cytokines?


Mature monocytes are macrophages and they are the ones that secrete IL-1 and TNF-alpha!!!!!!!!!!!

166-Give a place where macrophages are fixed in tissues and name a mediator that activates them to move!!!!!

Con estos conceptos podras contestar gran parte del USMLE y ENARM!!

Kupffer cells of the LIVER and C5a!!!!

Todo esto esta relacionado a varias patologias las cuales pueden ser preguntadas en cualquier area de el examen.

167-Differentiate NK T-cells with cytotoxic T-cells!!!

Esto es un paso importante de inmuno.!!

NK, or natural killer cells specialize in killing virus infected cells and cancer cells but unlike cytotoxic T cells, THEY ARE ACTIVE WITHOUT PRIOR EXPOSURE TO THE VIRUS, ARE NOT REVVVEEED UP BY CONTACT, AND ARE NOT SPECIFIC!


(You DO know the cytotoxic T-cells have a receptor, NK's don't!)

(NK's don't need MHC to act)

Since NKs activated by IL-2 are being used in cancer research!!!!!

168-Which ILs rev up growth and maturity of B-lymphocytes?

"Rev up" Se puede traducir como estimula o incita!!

The answer is IL-2,4,5!!! Recuerden que es 2!!!!4!!!!5!!!!!

Esta pregunta se puede hacer mostrando una imagen!

169-CD-8 binds to MHC-1, which IL revs it UP????

Tambien se estimula asi misma!!!

IT is IL-2 !!!!!!!!!!!!!!!!!!!!!!!!!!!! Asi que CD-8 se une a MHC-1 debido a la estimulacion por IL-2.

170-All T cells have CD3 , but, what does CD3 do? Importante concepto!!!

Is it using the cAMP pathway?

Answer: CD3 molecules transmit into that the antigen receptor is OCCUPIED!

This works NOT by cAMP but by the IP3 Ca pathway.

Conceptos y areas que pueden traer desde 3 hasta mas de 20 preguntas en el USMLE!!!!!!!!!! Asi que a darle duro a los libros!!! 5 horas como minimo todos los dias y unas 50 preguntas del Kaplan o UW!!!

Si se puede!!!!!!!!!!!!!!!!!!
HY Concept 182,
KNOW COLD that B Cells do not have CD3!!!! AND
B-cells have IgM on the surface BUT T-cells DO NOT!!!

171-Which 3 cytokines bring neutrophils to the scene? Esta pregunta se pueden hacer mostrando una laminilla con un neutrofilo.

Answer:IL-1, IL-6 and TNF-alpha = acute phase response

172-What is different about the T-cells that make IL-3 (vs. others)?

Recuerden que IL-3 estimula la medula osea!!!

Which mediator is used in cancer chemotherapy to rev up some neutrophils to stave off infection?

Answer:IL-3, unlike the others are ACTIVATED first!!!

IL-3 IS SIMILAR TO GM-CSF (colony stim. factor)


173-C3b opsonizes bacteria, but which factor (s) neutralize viruses?

Repasar la cascada!!!!!!

Answer:C1, 2, 3, and 4 neutralizes viruses in the CLASSIC pathway, and complement:

2) IgM and IgG activate complement in the classic pathway,
3) But, Endotoxin and nonspecifics work in the alternative pathway!!!

Lean GRAM-NEGATIVE BACTERIA!! Una pregunta puede incluir varias bacterias gram positivas y solo anotar una gram-negativa!!!

REcuerdedn C3a puede causar anafilaxis!!!! Cual otro complemento puede funcionar como C3a? C5a!!!!!!!!!! Importante aprender la cascada!!!

174-Which complements are part of the membrane attack complex (MAC)?
And, which complement do both pathways meet at?

Si, son mas de complementos por que el USMLE puede tener varias preguntas con relacion a inmuno.!!!

Answer:C5b thru C9 = MAC
And both classic and alternative pathways meet at C5.


175-The system can overreact and destroy our good cells. C1 is an esterase and what factor blocks C1 and what happens if you lack C1?


Answer:Your body has C1 INHIBITOR (rather unoriginal name) to block C1.

176-Human cells have DAF or (decay accelerating factor) to protect themselves. What factor does DAF work on?

Respuesta!!!!DAF blocks C3b thus protecting your cells.

177-La siguiente pregunta esta relacionada a las tres previas!
What diseases arise if the above controls are LOST?

Answer: If C1 inhibitor and/or DAF is gone, your capillaries will weaken!!!! you will get PNH(Paroxysmal Nocturnal Hemoglobinuria) which means you will get hemoglobin in your urine at night. This is also known as Marchiafava-Micheli Syndrome!!!

178-Interferons, because they are DRUG and part your body's defense..

They are GLYCOPROTEINS , and they protect healthy cells and virus replication. KNOW there are alpha, beta, and gamma interferons:

Alpha (fr. WBCs) interferons and beta (fr. fibroblasts) are triggered by viruses and target viral mRNA.

1)NOW, GAMMA interferon are the third interferon, they are produced by?
2) They active what process?
3) Gammas rev up what cells?

Answer: Importante esta area!!!

1) Gammas are made by activated CD4 and CD8 T-cells.
3) This by those NK, macrophages, neutrophils and revs up MHC I and II antigen presentation, which is like a plate of food that attracts the phyagocytes. Finally, Gammas revs up B-cell antibody production.

UNa buena leida a esta area en un buen libro no seria mala idea!!

179- "The basics of activation. IF say an antigen presenting cell (Dendrocyte, B-cell, Macrophage) [T-CELL ARE NOT ANTIGEN PRESENTING!!!!], binds an antigen (virus), then CROSSLINKING occurs and the cell gobbles up antigen and then PRESENTS IT ON THE SURFACE. A lot of you know that, but THEN you must follow the storyline. And lovely young helper T cell comes along and attaches or holds hands with the antigen presenting cell. THEN, the T-helper cell "blushes red" and is so happy she throws out IL-2, IL-4, and IL-5 that stimulate both B-cells and T-cells (IL-2 here). Some of the activated B-cells from what kind of cells in the secondary response and what is the most common surface Ig?"-TommyK

Answer:A few activated B-cells turn INTO MEMORY CELLS (BEFORE, THEY WERE PLASMA CELLS), and they usually have IgG on top of them for rapid response to reexposure.

180-Esta con relacion a el Fab anticuerpo!!
1) Is the Constant Light Chain region part of Fab fragment or Fc fragment?
2) Is the CARBOXY terminal part of the constant or variable region?
(There are ways with arrows to address this, so know this)
3) What kind of bonds KEY PT, holds the chains together?

1) Fab fragment
2) Heavy chain
3) Disulfide bonds, know which drugs can cleave these....




181-Give that famous Y antibody with arrows, where does complement bind (Fc or Fab portion?)?

Fc portion

182-In an image POINT to where CMV virus attaches.

Answer: Both L and H hypervariable regions.

183-Where can I find sugar side chains?

Fc fragment

LIGHT chains only lie in the AMINO TERMINAL and are part of only the Fab fragment!!!!

184-MOst know that babies have IgG from Mom until 6 months of age, can the baby defend itself against syphilis at one month?


YES, the fetus can make IgM.!!

Thank you Tommy K.!!!

185-You see an EM of an Ig that is a dimer. Where in the body is it found and MOA? Does this fix complement?

IgA (also can be monomer). See in saliva, tears, gut, vagina, etc.

186-You see an EM of an Ig pentamer! What's so special here?
IgM is the PRIMARY response, most efficient in agglutination

187-The only Ig to cross the placenta, this dude is most dominant in 2nd response about is what percent of total Ig?


IgG of course - 75% of all

188-You see an Ig in a baby's cord blood that the IMMUNOLOGIST tells you is rather unknown what it does? what is it?



189-You see an EM of an Ig that binds a basophil on a smear! Does this one fix complement? What else is special here?


IgE, anaphylactic allergies DOES NOT FIX COMPLEMENT!!!

190-Delayed hypersenitivity is a function of antibodes, right?

Answer:No,Type IV Delayed is CD4 T-cells!

Gran parte de estas preguntas fueron inspiradas por Tommy K. La manera de anotarlas facilitaba el aprender el material. Continue su manera de anotar solo que aparte de poner puntos importantes en mayusculas, deje que cada quien agregara mas informacion a su estilo de aprender.

Muchas horas de estudio y sobre todo llegar a aprender el material requirio de mas tiempo. Esot para mi sigue siendo una manera mas de seguir aprendiendo medicina y seguir refrescando material que en un momento quise aprender mas en detalle.

Espero les ayude a ustedes para cualquier examen que se preparan!!

Foroenarmita Avanzado
Foroenarmita Avanzado
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el Miér Jun 15, 2011 8:45 pm

Mecanismo de accion de clopidogrel y otros medicamentos usados en la profilaxis de trombosis y antiagregantes plaquetarios... ¿te sabes las diferencias a nivel molecular, del sitio de acción?
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el Miér Jun 15, 2011 10:38 pm

Creo que lo puse anteriormente y precisamente en este post. Pero en si la funcion es inhibiendo la union de ADP con los receptores de baja afinida de las plaquetas. Al inhibir el ADP tambien bloquea o inhibe GPIIb-IIIa complex, la cual es responsable de la agregacion plaquetaria.

Aqui dejo un articulo de oubned que explica un poco mas este proceso pero el enfoque es en el ADP.

Clopidogrel: a review of its mechanism of action.
Savi P, Nurden P, Nurden AT, Levy-Toledano S, Herbert JM.
SourceSanofi Recherche, Haemobiology Research Department, Toulouse, France.

The search for active antiplatelet drugs within the original chemical class of the thienopyridines, led to the discovery of clopidogrel, a novel ADP-selective agent whose antiaggregating properties are several times higher than those of ticlopidine. The antiaggregating properties of this compound are well known and, very recently, new results have clarified its mechanism of action. Clopidogrel is active only after intravenous or oral administration, and no circulating activity has been found in the plasma of treated animals or human volunteers. Experiments in rats have demonstrated that the antiaggregating activity was caused by a shortlasting metabolite generated in the liver by a cytochrome P450-dependent pathway. The antiaggregating property of clopidogrel is caused by an inhibition of the binding of ADP to its platelet receptors, and more specifically to the low affinity receptors, the high affinity binding sites being unaffected by clopidogrel. Several events in the ADP activation process, including adenylyl cyclase down-regulation, protein tyrosine phosphorylation, activation of the GPIIb-IIIa complex, fibrinogen binding, aggregation and release, were inhibited by clopidogrel and indicate their close relationship with the activation of a low affinity receptor by ADP. In contrast, binding of ADP to its high affinity binding sites (clopidogrel-resistant receptors) induced shape change, cytosolic calcium increase and phosphorylations of several other proteins, some events which were clopidogrel-sensitive. Thus, clopidogrel not only constitutes a potent antithrombotic drug in humans but also a good tool to study the effect of ADP on platelets.

PMID: 16793712 [PubMed]

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el Lun Jul 25, 2011 8:27 pm
Abruptio Placenta: painful bleeding, maternal hypertension or cocaine abuse
Placenta Previa: painless bleeding, placenta implantation over cervical os

Rheumatic fever: Type-2 HS (Hyper Sensitivity)
Rheumatoid arthritis: Type-3 HS

Carbomyl phosphate in cytoplasm: pyrimidine synthesis
Carbomyl phosphate in mitochondria: urea cycle [both are different enzymes with
similar name]

Thiazide Diuretics: used in renal stone (hyper calciurea)
Loop Diuretics: used in hyper calcemia

Antibody Dependent Cellular Cytotoxicity (ADCC): IgG + NK cells - use CD
16 molecule (Fc receptor) to identify target cells. (NOT CD 56)
NK cell mediated Cytotoxicity: CD 56 (No antibody involve. e.g. - lysis of
infected RBCs)

de Quarian thyroiditis: (subacute granulomatous): painful, mild hyperthyroidism
Subacute Lymphocytic thyroiditis: painless, mild hyperthyroidism

Berger's disease: hematuria following URTI, IgA deposition in mesangium
Buerger's disease: (thromboangitis obliterates) - Male smoking cigarettes,
involvement of toes

Congenital inguinal hernia: total failure of processus vaginalis to fuse
Hydrocele of spermatic cord: incomplete fusion of processus vaginalis

Pericentral vein zone (zone 3) in liver contains P450 oxidase enzyme system & is
most sensitive to Ischemic injury
Periportal zone (zone 1) in liver is the most sensitive to toxic injury

Pemphigus vulgaris: IgG against desmosomes (intracellular atttachment), (+)
Nikolsky sign, oral lesion
Bullous Pemphigoid: IgG against basement membrane, (-) Nikolsky sign

Cortical necrosis of both kidney sparing medulla - DIC
Sickle cell anemia - Affect medulla most severly - can cause papillary necrosis

Hypokalamia - "U" wave on EKG Hyperkalamia - peaked T wave on EKG

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