Tommyk's concepts: 601-650

[Anonymous]

601.
Case: Everyone in clinics and from all the USMLE tests are saying some of the versions heavily quiz physio and graphs and major homeostasis concepts. So...if you have any patient with V. cholera infection and they present with dehydration, OR if you have a patient with Diabetes IDDM with ketoacidosis, what will you initially do? Guess first before peeking at the answer!

A) Replace fluid and electrolytes first.

602.
Case: For the patients with dehydration, do a careful history to find out just why they are ill. Give me two classic findings on PE suggestive of dehydration.

A) Oliguria, (low urine output), and acute weight loss!

603.
Case: Regarding homeostasis and water balance, tell me some major causes that are CHRONIC which present with dehydration!

A) We already discussed diabetes, but also think of congenital adrenal hyperplasia, diabetes INSIPIDUS, severe sore throat (which prevents desire to swallow), cystic fibrosis. Did you get any of these?

604.
Case: As a patient of yours continues to LOSE fluid balance, he will present first with tachycardia, then his or her respiration will speed up. Why is this?

A) Often metabolic acidosis ensues, so you have compensatory respiratory alkalosis!

605.
Case: What is the most common form of dehydration (hyponatremic, hypernatremic, or isotonic)?

A) ISOtonic!! So this means that water losses roughly equal sodium losses.

606.
Case: You have a patient with severe fluid loss...what will the PE present like regarding his skin?

A) When you press his fingertips, capillary refill will be greater than 3 secs. Also, his or her mucous membranes will be dry (open their mouths and LOOK). If it is a baby, the fontanelles will be sunken!

607.
Case: Again, your patient is water deprived for a long time...what will the Urine osmolarity and specific gravity look like?

A) Both values will be severely ELEVATED. think why...and so will the BUN/Creatine ratio.

608.
Case: Again, lumpin along, what will your water deprived patient show on his PE for the bicarb level?

A) Secondary to acidosis, his bicarbonate will be decreased! BUT, KNOW that if he is VOMITING all the time, his body will face metabolic ALKALOSIS.

609.
Case: This concept is SO CRITICAL...tell me some differences between INCREASED vs. DECREASED anion gap! Be specific!

A) Increased anion gap includes: Hyperphosphatemia, HYPOkalemia, HYPOcalcemia, HYPOmagnesemia. Massive diarrhea, lactic acidosis, DKA, aspirin overdose, chronic kidney failure.

DECREASED anion gap includes: HYPERkalemia, HYPERcalcemia, HYPERmagnesemia, low albumin, Li overdose.

610.
Case: Say I give you a case study and tell you this is a prerenal failure. What exact LAB value threshold will you like to see to confirm this?

A) A BUN/Creatinine ratio over 20.

611.
Case: Lumpin...let's say I present a case to you and the patient has a capillary finger refill of 1 sec and is very mildly dehydrated after a tough rugby match. Should I give him IV boluses?

A) No, for mild cases, just do ORT or oral rehydration therapy. Kinda sorta like giving GATORADE juice, you need to give approx. a solution with 90 mEq/L Na, 20 mEq/L of K, and 20 g/L of glucose. DO NOT give or pick just free water to rehydrate!

612.
Case: You have a patient with EDEMA from CHF. You do recall our discussion of the MOA (Mech. of Action)?

A) The CHF results in decreased renal blood flow. Thus, you retain Na and water, resulting in EDEMA


613.
Case: Lumpin along....another patient of yours comes in with EDEMA. He or she has LIVER DISEASE. What is the MOA?

A) Decreased albumin synthesis from liver dx results in edema here from decreased oncotic pressure.

614.
Case: Lumpin still. Another pt. with edema comes in with associated protein malabsorption syndromes. What is the MOA?

A) So much protein malabsorption results again in decreased plasma albumin...thus lower oncotic pressure...and ensuing EDEMA!

615.
Case: Another EDEMATOUS individual. This time he/she has one of the NEPHROTIC syndromes. What is the MOA of edema?

A) The loss of albumin and protein clotting factors results in again lowered albumin in the blood, thus lowered oncotic pressure...and thus EDEMA!

616.
Case: A sexually active female walks into your office. She has a lot of edema. What is the main thing you are thinking of?

A) PREGNANCY or OCPs!

617.
Case: Lumpin still...your physio prof comes in and tells you your edematous patient has a cardiac origin. HOW will his PE present?

A) SOB, cyanosis, sweating with eating suggest a congential cardiac origin to the edema.

618.
Case: True or False: Can a severe allergic reaction mimick other forms of edema?

A) True or Yes...

619.
Case: Speaking of edema, there is a famous often tested disease that presents as a patient young or old that comes in with a deep rash that started on the buttocks or lower legs. There is edema on the hands and feet. About half of the patients initially presented with Upper Respiratory Infections. What is the pathophys of this disease that we once spoke of? What meds should you give? (Hint: name starts with H... and is named after someone.)

A) This is Henoch Schonlein Purpura. About half the cases were preceded by a upper respiratory infection. The etiology of HSP involves the vascular deposition of IgA immune complexes. More specifically, the immune complexes are composed of IgA1 and IgA2 and are produced by peripheral B lymphocytes. The circulating complexes become insoluble, are deposited in the walls of small vessels (arteries, capillaries, venules), and activate complement, most likely by the alternative pathway. Thus, group A streptococci, varicella, hepatitis B, Epstein-Barr virus, parvovirus B19, Mycoplasma, Campylobacter, and Yersinia are often picked as inciting factors. Treat against the bug if persistent (after culture), and give prednisone for the inflammation. They also need pain relief like Tylenol or Ibuprofen for some pain.

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620.
Case: For the previously discussed cases of edema, which labs will help you differentiate between a liver, cardiac, renal, etc. source?

A) For the liver, do the liver function tests. For the cardiac, check for cardiomegaly and pulmonary edema on X-***. Renal sources will point to inconsistent serum electrolytes and proteinuria.

621.
Case: We discussed patients with water deprivation from vomiting and diarrhea in a patient. What exact lab value for the Na indicates Hyponatremia?

A) Serum sodium under 130 mEq/L!

622.
Case: Because you will treat dehydrated patients all day long in clinics, you need to know what are the most serious consequences of protracted diarrhea/vomiting? What labs will the USMLE give you to assess the causes?

A) Beware of Hypovolemic shock as the patient's mental status worsens with decreased reflexes. The most serious consequence is seizures and cessation of breathing. Other than BMP, you need blood glucose, liver function tests, protein and lipid levels.

623.
KNOW every kind of hyponatremia and how the little arrows will point with respect to Urine Na, Urine specific gravity, etc. Here, let me ask just ONE question: For hyponatremia due to CHF, what is the value of the Urine Na and Urine specific gravity?

A) In CHF hyponatremia, urine Na is DOWN, and Urine specific gravity is UP. Remember the subtle differences...like KNOW that if you have ADDISON'S dx, the urine Na will be up and the urine specific gravity will be DOWN! Think why!

624.
Case: Since HYPERkalemia is so dangerous, tell me a few of the causes of hyperkalemia!

A) Addison's Disease, Acidosis, Dehydration (severe), Spironolactone drug therapy, and too much K infusion, tubular kidney damage leading to improper K excretion.

625.
Case: Despite warnings, your patient becomes Hyperkalemic. What does his/her EKG look like?

A) You will see T wave elevation, then muting of P waves, then QRS complex widening, and ST segment depression. Deadly V-fib can result!

626.
Hi brothers and sisters,

I need to address a vital question for everyone because it continues to be asked.

1) Many are asking about their personal assessments and how to gauge progress. This is an excellent question. This is SO VALUABLE because you will then KNOW if you are making progress or not. There is a LOOSE connection between say QBank performance and the actual exam. But, the material does correlate in the sense that if your QBank score is moving higher slowly and steadily, then you KNOW you are at least retaining some information. But, if you do not have QBank and/or cannot afford it, you can use Q-Book or another popular source. The most important issue is not really what you are getting in the absolute percentage, but whether that number is increasing over a set time. As an aside, I mentioned what I found to be accurate as to QBank scores... Most of the students scoring at least a 50% on QBank passed the exam. Now, the QBank leans heavily on Pathology and Pathophysiology, and asks questions with a slightly different slant than the actual test. So, if you are UNLUCKY and get say series of questions on Embryology and Immunology and you completely skipped these two subjects, then you will find that your 50% on QBank was not relevant. So, that is what a lot of repeat test takers are saying...that their second or third etc. test was ENTIRELY different from the initial ones. Although I am not sure of this since I did not see their tests, I am certain that the NBME will not allow someone to receive the same or similar questions from his/her previous test. So much of the computer based testing is CENTERED on avoiding ANY POSSIBLE shortcuts like this.
Therefore...gauge your progress with weekly question banks like a QBank . Then, as I mentioned before, do the USMLE Sample Questions for ALL THREE STEPS that are found on the NBME website (These are free to download). Then, do the Kaplan Simulated CD that is found EVERYWHERE, your roommate probably has a copy. Also please complete the two NBME self assessment exams found on their website (There a cost to this that the NBME charges, but I think it is worth it to gauge your progress). Also, do the RETIRED NBME Step 1 questions. They can be found everywhere too for free. I think even ValueMD has a copy of it. You definitely WILL benefit from doing this to test yourself. For example, if the RETIRED questions have 100 biochemistry questions, then split them into 4 blocks of 25 questions each. Then do one block every weekend a month before the exam for each subject topic. Then graph your results to see if you are studying effectively. I know the question format is different, but the concepts tested were HIGHLY related to the actual exam in many cases. Also, try to do some of my questions too as a way to gauge your progress. Maybe you can make notecards of them and get a filebox. If you get the flashcard question right, then place the notecard in the end of the file so you will not see it again right away. If you get the item wrong, then place the notecard towards the front of the pack so you will see it again sooner. This is a highly effective way to study, and you need to keep up the repetitions daily. If you start skipping them, you will start forgetting them.

627. Dear Family,
Many are writing that they are suffering under severe anxiety and are asking me for advice. This is again a VERY good question.
1) The first thing to know is that this test is very "coachable" and "doable". Plus, unless you are pushing 50 years of age, you have time! Even if it takes one or two years to pass Step 1, 30 years from now, this event will seem like a distant dream.

But there needs to exist the right circumstances or it just cannot work. Still, many are shouldering the burden of work, family (kids), AND suffering some personal crisis. Then, they mention their test is in a month. My heart and everyone else's breaks upon hearing this, but we must ask God for the right TIME to PASS Step 1. If life events are not going to permit you the time to study, it is like trying to climb Mt. Everest tomorrow without any preparation or running the 26.3 mile marathon in a week. Both tasks are doable, but if you just broke your leg, you cannot run next week. We must all pray to get that necessary block of time required. Some are trying to lift their anxiety with serious alcohol and anti-anxiety and then sleeping all day long instead of studying. Not good. Although a few can use some anti anxiety medication in MODERATION, this often has the effect of putting you to sleep, which will make the anxiety 100 times worse after you awaken and lose a day of studying. Better again to WAIT until the right moment. If you are working and you cannot find anyone like a family member to live with and feed you while you are studying, please reconsider taking the test until the right time presents itself. You will only put more agony onto yourself if you do not pass...

628. Case: Although we glanced over this in Pharm, tell me what is the Rx for a first time HIV patient of yours and tell me the MOA of the drugs. Then, we will next quickly go over the MAIN dx of HIV and the Rx.

A) In clinics, we like to give 2 nucleoside analogs like AZT (Zidovudine) and Lamivudine....PLUS a protease inhibitor like Lopinavir or Rotinavir (These drugs usually end with suffix -avir). Recall that the nucleoside analogs are THYMIDINE analogs which blocks virus replication via REVERSE TRANSCRIPTASE. The protease inhibitors work by blocking the modification of precursor polyproteins responsible for synthesis of reverse transcriptase and HIV-1 protease itself.

629.
Case: The next patient comes in with a positive ELISA and Western Blot for HIV. Do you recall at least TWO VIRAL ANTIGENS in the peripheral blood to also confirm HIV infection?

A) Look for GP41 and P24 antigen.

630.
Quick, what was the MOST COMMON worry you have with HIV patients (i.e. main dx)? What is the Rx? (Hint, this bug hits the lungs and can cause SPONTANEOUS PNEUMOTHORAX!)

A) PCP (Pneumocystis carinii). Give TMP/SMX as the Drug of choice. This can be LUMPED by thinking all have popular 3 letter abbreviations (HIV-PCP-TMP/SMX).

631.
Case: Now, the HIV positive person comes in with headaches and fever. A radiograph is shown that has ring lesions and midline shift. He was scratched by a cat last month. What COMMON bug starting with the letter "T" are you thinking of? What is the Rx? What are some side effects? THINK before you look at the answer below!

A) This is Toxoplasmosis gondii, give a folic acid antagonist like Pyrimethamine. Watch for his HTN in intracranium and possible seizure activity!

632.
Case: Now, another HIV positive pt comes with fever, and MILD headaches and a radiograph with hydrocephalus. What COMMON bug starting with the letter "C" am I looking at? What drug or Rx?

A) This is highly confused with PCP and Toxoplasma. The bug I am seeing here is Cryptococcus meningitis. MAKE SURE YOU KNOW THE DIFFERENCES COLD LIKE YOUR NAME, MOTHER'S NAME, etc. Treat with Amphotericin B. (Mneumonic: When you think of a "Crypt" (cemetery relation), think of a crazy band that is obsessed with the DEAD, and likes to play their AMPlified (Amp B) electric guitars inside the scary Crypt.)

633.
Case: Quick, the NEXT RELATED COMMON bug with HIV attacks the eyes, leading to loss of vision and retina detachment. What bug and drug? No hints here...except it starts again with the letter "C". Give morphology of bug...too.

A) This is CMV retinitis. YOU must give GANCICLOVIR! This is part of the HERPESVIRUS family. It is double stranded, linear, enveloped. (My mneumonic....think....CMV stands for California Motorcycle Vehicle GANG) [Think and imagine a CMV gang riding down the highway getting flies stuck in their eyes and slowly losing their eyesight!!!]

634.
Case: Now an ENT doctor refers to you a patient with HIV and oral thrush. What is this super common bug and drug in HIV? Can you identify IT PRECISELY under a microscope? If not, LOOK for it in a Microbiology book/atlas!

A) This is Candida. Treat with an "azole" like Ketoconazole, Clotrimazole or Nystatin.

635.
Case: OK, an HIV patient of yours has really BAD diarrhea. Your acid-fast staining of stool demonstratess red-stained round oocysts against a blue-green background. White and red blood cells should not be seen in the stool. What super common opportunistic bug starting with the letter "C" is here? Rx?

A) This is Cryptosporidiosis. Drug treatment is difficult, but the HAART treatment for HIV is helping a lot. Give them symptomatic treatment with LOPERAMIDE or Kaopectate.

636.
Case: You have a pregnant woman that asks you the difference if any between taking a teratogen in the first trimester or third trimester. What do you say?

A) Taking a teratogen in the first trimester usually damages organogenesis, while taking a teratogen in the third trimester often slams the CNS development and the growth of the baby!

637.
Case: Some pregnant women come to your office and asks what is the MOST COMMON maternal disorder that is teratogenic. What do you say?

A) Diabetes mellitus, one in ten diabetic females' babies have a birth defect.

valuemd.com

638.
Case: A women who is African American with history of benign fibroids is pregnant. She asks if this could hurt the baby. What do you answer?

A) Unfortunately, the fibroids can "squeeze" the baby, and present with abnormal facies, club feet, or abnormal lie/breech presentation.

639.
Case: What is the inheritance pattern for the most common blood coagulation disorder named after a doctor with the name "V"?
A) So so common and heavily tested in clinic and exams, this is Von Willebrand's disease, and is AD or an Autosomal dominant disorder. Recall, you must tell the pt. she has a 50% chance of passing this to her children!

640.
Case: You have a patient with the classic triad of low intelligence, epilepsy, and raised tumorlike angiofibromas on the skin. What is the inheritance pattern of the dx? What is the name of the dx? What is the pathology exactly?

A) AD, this is Tuberous Sclerosis (we mentioned it long ago once), The protein tuberin is dys-regulated, leading to hamartomas and tumors in all organs of the body, notably on the skin.

641.
Case: This can be both autosomal dominant and recessive inheritance, but the common-"ness" of it demands a question. A patient comes in with a history of recurrent episodes of acute pancreatitis and eruptive xanthomas. He is at increased risk of coronary disease. He lives a sedentary life and eats only greasy hamburgers. Name SOME common causes of his condition, both genetic and non-genetic.

A) HyperTRIglyceridemia, this is caused by uncontrolled Diabetes and obesity. Two genetic causes of high TG are lipoprotein lipase [LPL] deficiency and apolipoprotein [apo] C-II deficiency leading to triglyceride (TG) elevations that are exceedingly elevated.

642.
OK, OK, you will be asked a lot of inheritance pattern questions. That is because you will have to explain to your patients their risks of passing their dx to their children. So, for all autosomal dominant disorders, we discussed they are STRUCTURAL PROTEIN disorders. They have 50% inheritance patterns.

Also, most autosomal recessive disorders are enzyme and "-emia" (blood stuff) related. Except for three common "-emias", that is: Hereditary spherocytosis, von Willebrand disease, Protein C deficiency (REMEMBER AT LEAST THESE THREE EXCEPTIONS), the enzyme and "-emia" diseases are autosomal recessive. The exceptions to the blood "emia" rule is initials H.P.V. as seen above. This is an abbreviation "mnemonic". AR is 25% passed on.

643.
Case: Anemia, jaundice, and splenomegaly. This class triad is seen with a patient who is young and has that classic palpable spleen. You see a slide which has these round RBCs. What is the disease?

A) We JUST spoke of it. Hereditary spherocytosis presents in this way. Don't forget this NBME/attending/resident favorite!!! Try to recall the MOA of the giant spleen.
644.
Q) I may have asked this long long ago, but what is the problem in Hereditary spherocytosis?

A) Alpha or Beta Spectrin def. (The alpha form is related to AR inheritance.) But know the Beta form is more common as is AD.

645.
Case: A nonsmoking patient of yours comes in and has panacinar emphysema. She also had chronic bronchitis. What protease is malfunctioning? What is the disease and Rx? What is the pathophysiology?

A) This is ALPHA 1 ANTITRYPSIN DEFICIENCY. The genetic defect of alpha 1 antitrypsin deficiency results in a molecule that cannot be released from its production site in hepatocytes. Low serum levels of the protein result in low alveolar concentrations, where the molecule normally would serve as protection against antiproteases. The resulting protease excess destroys alveolar walls and causes emphysema. Give a drug branded called Prolastin to replace the deficiency.

646.
Case: Couple A comes in and you note that the male is achondroplasic (dwarfism/extremely short stature). The female is pregnant, she asks what is the chance her baby is going to be have achondroplasia. What do you say?

A) This is AD, autosomal dominant inheritance, so the male will transmit the gene to half his offspring.

647.
Case: Couple B comes in and you note that BOTH are suffer from achondroplasia (dwarfism). They are asking about the inheritance to their children. What do you say?


A) Again, this is 50% BECAUSE the homozygous form usually does NOT survive to birth. So the 50% HETEROzygous form will have the phenotype of dwarfism, but half will be normal.

648.
Q) We are discussing achondroplasia. What is the MOA of this AD disease?

A) The MOA or pathophys is such that fibroblast growth factors are structurally related proteins affected...and are associated with cell growth, migration, wound healing, and angiogenesis. At the cellular level, their function is mediated by transmembrane tyrosine kinase receptors, known as fibroblast growth factor receptors (FGFR). Mutation in FGFR3 gene is responsible for the achondroplasia, or dwarfism.

649.
Case: You research 100 achondroplasia patients and only 10 had any history of the dx in the family... why???

A) Don't forget the mech. of SPONTANEOUS MUTATION. This disease is noted for 90% new mutations in the lineage.

650.
Case: You see a patient with hypertension, infections, hemorrhage and renal stones. You feel a large mass on one side of the body. What mode of inheritance is this dx? What is the dx?

A) AD inheritance, Adult Polycystic Kidney Disease presents as above with large cysts in the kidneys. Renal failure will usually result by age 60. Radiographs will show large circles or cysts.

[nikki]

from me.

[katwal]

647.
Case: Couple B comes in and you note that BOTH are suffer from achondroplasia (dwarfism). They are asking about the inheritance to their children. What do you say?

in book its written that.... HZ with HZ lead to 75%
i 'm so confuse.. pls explain me.
and thank u very much for assisting us like this.
GOD BLESS YOU!!