dowjunk
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u r rite bioguy! I totally agree, altho in my first go i did it wrong. but its the age 72 that is the key here. The BP is fine considering the age and LVH..i mean acceptable. Ppl who say that seek the key word...is what we all can do i guess to reach the target!
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| dowjunk
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bioguy wrote:dowjunk wrote:
A 25-year-old previously healthy woman dies suddenly and unexpectedly. She had complained only of a slight headache for 3 days before her demise. At autopsy, the medical examiner finds an enlarged, dilated 410 gm heart with only minimal coronary atherosclerosis and normal cardiac valves. Microscopically, the myocardium on both the right and the left ventricles demonstrates infiltration by small lymphocytes, with focal myocyte necrosis. Which of the following infectious agents is most likely to have caused these findings?
A Coxsackie B virus
B Candida albicans
C Aspergillus fumigatus
D Streptococcus, viridans group
E Staphylococcus aureus
F Cytomegalovirus
G Streptococcus, group A
Is there any association of these bugs with CVS except for Staph aureus - IVDA tricuspid endocarditis Strep - RF Strep viridans - Endocarditis after prosthetic valve or dental procedures how about candida, aspergillus and CMV?
Candida and CMV in immunocompromised patients only, very rare!
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| dowjunk
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bioguy wrote:
Cyanosis
Troponin
Calcification
Coxsackie
Calcific aortic stenosis (doubtful)
Rheumatic fever
Granulation tissue
Mitral valve stenosis
Pericardial tamponade
Fibrillin
All are correct but granulation has issues?. Here Goljan and kaplan differ. I supported goljan earlier, but now i agree e kaplan: day1-4 necrotic/neutrophilic acc to kaplan, while 4-7day macrophages....while 7-28 is granulation tissue!
acc to goljan before day 7 we have early phase granulation while post-day-7 we have developed granulation tissue!
So I have deicided to call pre7day a macrophage/necrosis/neutrophil stage and the post7day as a granulation phase!!!
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| dowjunk
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bioguy wrote:dowjunk wrote:
I am sure u guys know this one:
A 19-year-old woman has had increasing malaise for the past 5 months. On physical examination she has a cardiac murmur characterized by a mid systolic click. An echocardiogram demonstrates mitral insufficiency with upward displacement of one leaflet. There is aortic root dilation to 4 cm. She has a dislocated right ocular crystalline lens. A year later she dies suddenly and unexpectedly. The medical examiner finds a prolapsed mitral valve with elongation, thinning, and rupture of chordae tendineae. A mutation involving which of the following genes is most likely to be present in this patient?
A Beta-myosin
B CFTR
C FGFR
D Fibrillin
E Spectrin
F Dystrophin
A Beta-myosin - Hypertrophic cardiomyopathy B CFTR - Cystic Fibrosis C FGFR --???? whats this (Fibroblast Growth Factor Receptor???) significance? D Fibrillin - Marfans E Spectrin - Hereditary Spherocytosis F Dystrophin - Duchenne's
Kool going bioguy.....i will add to it: FGFR, u r rite, if theres gene mutation of FGFR, the pt will have skeletal dysplasias................and beta myosin is dilated cardiac myopathy, not hypertrophic i recall?
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| dowjunk
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dowjunk wrote:
I'll start my Qs from tomorrow isA. I am drained for tonite.
But just wanted you guys to explain the changes in heart and CVS due to left to right shunt? like RVH, LVH, heart dilatation, if yes then why?
will the left or right side become dilated in R-L shunt?
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| dowjunk
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bioguy wrote:dowjunk wrote:
Thx match2010....yup will write the answers for sure ....
Ok can any1 tell me why do we have SOB in tetralogy of Fallot?
ok, extremely wild guess. i think the SOB is due to respiratory center being stimulated and not because of local pulmonary cause.
Yes your guess supports my search: Its the low O2 that causes shortness of breath; child exercising will have SOB and if severe will lead to tetralogy spell and unconciousness!
Bioguy may I kiss your hands buddy! ur extreme wild guess is on the mark!!!
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| bioguy
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I was wrong about MI morphology question -
1-3 days - Coagulation necrosis, Neutrophil infiltrate
3-7 days - Early phagocytosis by Macrophages, Dying neutrophils
7-10 days - Well developed phagocytosis, Early granulation tissue at margins
10-14 - Well-established granulation tissue
Ref: Robbins
All I remembered was that neutrophils act very early and they are gone by day 3. This stuff is all gray. I have to be careful about this.
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| bioguy
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dowjunk wrote:
So I have deicided to call pre7day a macrophage/necrosis/neutrophil stage and the post7day as a granulation phase!!!
Excellent, dude! Great idea to make things easy to remember.
Will there be questions specific about which cells predominate in the pre-7 day period - for example neutrophils until day 3 and macrophages after day 3?
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| bioguy
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dowjunk wrote:
Yes your guess supports my search: Its the low O2 that causes shortness of breath; child exercising will have SOB and if severe will lead to tetralogy spell and unconciousness!
Bioguy may I kiss your hands buddy! ur extreme wild guess is on the mark!!!
hey hey hey! don't flatter me so much. i am just sitting idle and going to great extremes of imagination. this won't happen in the actual test where i will be PIMP (peeing in my pants)
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| bioguy
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dowjunk wrote:
Kool going bioguy.....i will add to it: FGFR, u r rite, if theres gene mutation of FGFR, the pt will have skeletal dysplasias................and beta myosin is dilated cardiac myopathy, not hypertrophic i recall?
Both dilated and hypertrophic types can be caused by mutations in beta myosin. Check the image below (from Robbins) if you are interested -
"Some forms of dilated cardiomyopathy (others are caused by myocarditis, alcohol, and other toxic injury or the peripartum state) and virtually all forms of hypertrophic cardiomyopathy are genetic in origin. The genetic causes of dilated cardiomyopathy involve mutations in any of a wide variety of proteins, predominantly of the cytoskeleton, but also the sarcomere, mitochondria, and nuclear envelope. In contrast, the mutated genes that cause hypertrophic cardiomyopathy encode proteins of the sarcomere. Although these two forms of cardiomyopathy differ greatly in subcellular basis and morphologic phenotypes, they share a common pathway of clinical complications."
Not that Robbins is my primary book . I stick to Goljan RR , but in case of conflict I resort to Robbins.
Attached Files:
CMP.jpg (128 KB, 1 downloads)
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| bioguy
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Interesting that even Dystrophin mutations cause Dilated cardiomyopathy. If you go back to your question, that was one of the choices , irrelavent to the question though.
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| bioguy
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dowjunk wrote:dowjunk wrote:
I'll start my Qs from tomorrow isA. I am drained for tonite.
But just wanted you guys to explain the changes in heart and CVS due to left to right shunt? like RVH, LVH, heart dilatation, if yes then why?
will the left or right side become dilated in R-L shunt?
I think its complicated and depends on whats causing the R to L shunt.
As an outline, its early cyanotic - TOF, TGA, TA, TA .
Or it could be Eisenmenger's complex - late cyanotic
its might be different in each case.
TOF - RVH (obviously)
TGA - RV hypertrophy because it has to pump to aorta against systemic pressure
Truncus arteriosus - probably RV hypertrophy due to Pulmonary-HTN
Tricuspid atresia - hypoplastic RV
In eisenmenger's complex - RV hypertrophy due to L to R shunt in the beginning, and then failure due to Pulm-HTN and R-L shunt.
wo!! when i started writing this refering to Robbins, i thought it will be different for each case. but except for T-atresia rest all seem same.
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| match2010
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oh yeah i didnt read the 8th question .....dysphagia was a give away and chest radiograph reveals a near-normal left ventricular size with a prominent left atrial border as well ....it sure is mittral stenosis .....
thnx bioguy for the expalanations as well .....guys keeep posting q's here so tht we can help each other
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| dowjunk
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bioguy wrote:Interesting that even Dystrophin mutations cause Dilated cardiomyopathy. If you go back to your question, that was one of the choices , irrelavent to the question though.
shew this is makin me go mad dude!
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| dowjunk
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This ones a siiter:
Which one of the following ECG components varies with heart rate?
a. PR interval
b. QRS duration
c. ST segment
d. QT interval
e. QRS voltage
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| dowjunk
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Which of the following associations is correct?
- a. Hypokalemia: shortened Q
- –T interval–T interval
- b. Hypercalcemia: long Q
- c. Hypercalcemia: flattened T waves
- d. Hypocalcemia: U waves
- e. Hyperkalemia: peaked T waves
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| dowjunk
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216.
[font face="GillSans-Bold" color="#221f1f" size="2"]
[/font]
Which of the following is true regarding right ventricular hypertrophy? -
a. The hypertrophy may result from aortic valve stenosis
-
b. The hypertrophy is characterized by poor R wave progression in leads V
1 to V3
c. The hypertrophy is usually associated with left axis deviation
d. There are no associated ST-T wave changes
e. The hypertrophy is secondary to an atrial septal defect
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| dowjunk
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Any gr8 pnemonics or concepts u guys want to share in?
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| bioguy
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how would FEVER cause myocardial ischemia on a background of partial stenosis of a coronary artery
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| bioguy
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 i am no good in ECG. will read and attempt your questions.
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| dowjunk
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bioguy wrote:
how would FEVER cause myocardial ischemia on a background of partial stenosis of a coronary artery
Fever is a response of hypothalamus against an exo/endo pyretic substance. This response is PGE2................PGE2 will favour an ischemic attack, especially in the presence of platelets: more TXA2 will be formed, as the cor art constricts!
I will be needing your opinion whether its the constriction (more of what i think) in coronary arteries, becuase i am confused as i read somewhere that its the pGE2 influenced reperfusion of myocardial cells thats more threatening?
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| dowjunk
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Respiration for the comin saturday!
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| bioguy
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dowjunk wrote:
Fever is a response of hypothalamus against an exo/endo pyretic substance. This response is PGE2................PGE2 will favour an ischemic attack, especially in the presence of platelets: more TXA2 will be formed, as the cor art constricts!
I will be needing your opinion whether its the constriction (more of what i think) in coronary arteries, becuase i am confused as i read somewhere that its the pGE2 influenced reperfusion of myocardial cells thats more threatening?
I thought PGE2 is a vasodilator. In the case of fever, I was thinking more in terms of hemodynamic changes that demand an increased cardiac output - increasing O2 demand of myocardium - relative ischemia - MI
I am not sure - what are the hemodynamic changes in Fever? (if there are any)
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| GoodGirl
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Hello,
I just read about Tetrallogy of Fallot yesterday, found this in Merck,liked how it's explained, so for anyone who is interested , as addition to Bioguy's great explanation....
Edited by GoodGirl on 04/08/08 - 01:42 PM
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| GoodGirl
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Had a problem with posting , so here it is :
''In some patients with tetralogy of Fallot, sudden episodes of profound cyanosis (“tet spell ) may occur, which may be lethal. A spell may be triggered by any event that slightly decreases O2 saturation (eg, crying, defecating) or that suddenly decreases systemic vascular resistance (eg, playing, kicking legs when awakening) or by sudden onset of tachycardia or hypovolemia. A vicious circle may develop: The initial fall in arterial Po2 stimulates the respiratory center and produces hyperpnea. Hyperpnea increases systemic venous return to the right ventricle by making the negative thoracic pump more efficient. In the presence of a fixed right ventricular outflow obstruction or decreased systemic vascular resistance, the increased systemic venous return to the right ventricle goes out the aorta, further decreasing arterial O2 saturation and thus creating the vicious circle of the hypoxic spell.''
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