Category Archives: INTERNIST

Cor pulmonale

How copd leads to cor pulmonale
Hypoxic pulmonary VC
pulmonary vascular remodelling
Lung hyperinflation– compresses the capillaries ( alveolar wall stretches)

REVISION CARDIO

Copied from wallnote.
For revision purposes
Cardiology Question
1) Give the mechanism and clinical significance of pulsus paradoxus?
2) Mechanism and clinical significance of 3rd heart sound to the left of the sternum?
3) Central cyanosis, its mechanism and clinical significance?
4) Clinical features of infective endocarditis?***
portal of entry:
majority unknown, dental, urethral,pelvic,cardiac surgery, strep bovis, iv drugs,
hosp acq
onset: insiduous+fever+malaise
neglected: “syndrome” 8
fever,anemia,tender sternum, tender splenomegaly, cardiac murmur, microscopic hematuria, skin petichae,clubbing
cardiac:
murmur: new or intensified
heart failure: intractable/laceration or perforation of valve
coronary emboli
mycotic aneurysm
extracardiac:(1neuro to sternum,4skin,1spleen,1urine)
neurological complication
tender sternum
skin petichae: conj,mouth, roths spot,janeway
osler nodule
splinter hge
clubbing
splenomegaly
proteinuria/mic hematuria
5) Enumerate causes and the pathogenesis of myocardial ischemia?
6) Clincal features & management of left ventricular failure**
7) Discuss investigation needed for diagnosis of pericardial effusion?***
CXR–>flusk shaped heart/water bottle heart
Echo–>increase pericardial space
ECG–>low amplitude QRS complex
pericardiocentesis (Echo guided)–>to relieve symptoms, C&S
8) Give brief treatment of paroxysmal atrial tachycardia?
9) Etiology and pathogensis of persistent dyspnea in the left heart failure?**
10) Clinical manifestation of cardiac temponade?*****
symptom : Dyspnea, tachycardia, tachypnea
sign : KEPp YB
kussmaul sign
Ewart sign
pulsus paradoxus
the y descent
Beck triad
11) Give treatment of infective endocarditis****
prophylaxic: dental hygiene
oral,oral,, respiratory, esophagus: amoxacillin 2gm PO 1hr b4
GU,GI: high risk–>amox/ampi 2gm IV+gentamycin1.5gm IV 1hr b4->ampi/amox 1gm PO aftr 6hr
mod risk–> ampi/amox 2gm IV b4
active medical: bactericidal,IV, min 4wks
Penicillin G iv 12-20mill U/24hr for 4weeks+-gentamycin 3mg/kg/24hr for 2 weeks
resistant: Vancomycin+gentamycin for 6 weeks
MRSA: native: vancomycin 15 mg/kg iv for 4-6 wks
PVE: VGR (6-2-6 wks)
culture -ve n complicated: Native: Vancomycin+gentamycin
PVE : VGR
12) Discuss briefly the etiology and pathogenesis of congested nect vein?
13) Give etiology and possible mechanism of heart failure?
14) Give etiology and possible mechanism of bradycardias?
15) Clinical features of dissecting aortic aneurysm
16) Treatment of acute myocardial infarction?**
a) AHA guideline if suspect MI–> Morphine, O2, Nitroglycerine, Aspirin
b) General Rx–>hosp, CCU, MONA, clopidogrel&statin, ACEI, B-blocker,LMWH
c) Specific Rx–> if w/in 30min: tPA/streptokinase/urokinase
if w/in 90min: PCI
17) Give clinical picture and complication of aortic valve insufficiency?
18) Etiology, clinical picture and management of left ventricular failure?*****
19) Give etiology and mechanism of angina pain?
20) Clinical picture and complication of constrictive pericarditis?**
CP: symptom
Gradual onset
dypsnea, fatigue, orthopnea
LL edema, abd swelling, discomfort
congestive symp : nausea vomiting
: rt upper quadrant pain
sign: KEPP YA
1) kusmaul sign 5) the y descent
2) Elevated jugular venous pressure 6) Apical impulse impalpable
3) pulsus paradoxus
4) pericardial knock
21) Investigations for ischemic heart disease?
22) Treatment acute rheumatic carditis?
23) Etiology,pathology, clinical manifestation, and treatment for infective endocarditis?
24) Give etiology and mechanism of basal systolic murmurs?
25) Clinical pictures of the acute rheumatic carditis?
26) Investigation for fever in cardiac patient?
27) Investigation needed for hypertension on young age?**
28) How to investigate hypertension?
29) Medical treatment for paroxysmal supraventricular tachycardia?
30) Cardiogenic shock ( ccu )
31) Discuss treatment of atrial fibrillation***
32) Clinical picture, diagnosis and management of acute myocardial infarction?**
33) Enumerate complication of acute myocardial infarction
34) 4 factors that may indicate bad prognosis in acute myocardial infarction?
35) Give short notes on treatment of congestive heart failure?****
36) Causes of hypertension?
37) Mention subacute bacterial endocarditis?
38) Causes & Diagnosis of co pulmonale?**
39) Treatment of acute heart failure?
40) Factor precipitating or aggravating heart failure?
41) Outline complication of mitral valve stenosis?
42) Investigation required in atrial fibrillation?
43) Medical treatment left ventricular failure?
———————————————————
GIVE THE ETIOLOGY & PATHOGENESIS OF:
l-Left ventricular failure
2-Pulmonary hypertension
3-Parenchymal cor pulmonale
4-Rheumatic fever
5-2ry hypertension
6-Renal hypertension
7 -Congested neck veins
8-Diastolic murmur on apex
9.Pulsus paradoxus
10-Continuous dyspnea
11-Bradycardias
12-Basal systolic murmur
13-Basal diastolic murmur
14-Tachycardias
15-Anginal pain
GIVE THE CLINICAL PICTURE OF:
1-Left ventricular failure
2-Anaphylactic shock
3-Pulmonary hypertension
4-Rheumatic fever
5-Mitral stenosis
6-Mitral incompetence
7 -Aortic stenosis
8-Aortic incompetence
9-Infective endocarditis
10-Myocardial infarction
11-Cardiac tamponade
12-Dissecting aortic Aneurysm
13-Constrictive pericarditis
14-Adhesive pericarditis

GIVE THE INVESTIGATIONS NEEDED FOR: u
1-Myocardial infarction
2-Infective endocarditis
3-Rheumatic fever
4-Left ventricular failure 5-Atrial fibrillation
6-Recurrent syncope
7- Hypertension in young
8- Pericardial effusion
GIVE THE TREATMENT O.F:
1-Acute left ventricular failure
2-Atrial fibrillation
3-Infective endocarditis
4-Rheumatic carditis
5-Acute myocardial infarction
6-Acute pulmonary edema
7 -Angina pectoris
8-Paroxysmal Atrial tachycardia
LONG QUESTIONS:
1-Give the etiology, pathophysiology, c/p, and management
of shock
2-Give account on: diagnosis and management of infective endocarditis
3-2ry Hypertension: Cause”s & Diagnostic features of 3 of them
4-Causes, clinical picture, investigations of Rt. & Lt. ventricular failure
5-Give an account on atrial fibrillation (causes, diagnosis & Rx)
6-Pulmonary hypertension (definition, causes, CP & investigations)
Definition: Right ventricular hypertrophy and dilatation secondary to pulmonary hypertension due to disease in the lung vessel and parenchyma and not due to left heart
causes: 1) Increase resistace to flow : large pulmonary artery
a) uni absence/stenosis
b) thromboembolism
: pulmonary vascular bed
a)
7-Mitral stenosis (pathophysiology, CP, complications & investigation)
8-Aortic stenosis (pathophysiology, CP, complications & investigation)
9-Aortic incompetence (pathophysiology, CP, complications & Ix) .’
10-Myocardial infarction (causes, CP, investigations & Rx)
11-Pericardial effusion (causes, CP, investigations & Rx)
12-Clubbing (Causes, grades & pathology) 13-Edema (Causes, mechanism & Diagnosis)

REVISION DIABETES

Past year questions

DIABETIC

1-Lines of treatment hyperTGdemia in diabetic pt (06,08)
2-Give short account on indication of insulin theraphy in type 2 DM
3-Mechanism in neuropathy in DM (95)
4-Cp of hypoglycemic coma (95)
5-Rx of DI (95)
6-Causes and pathogenesis of DKA (96,00)
7-Etiology and phatogenesis if hypoglycemia (02,05,07)
8-Rx of type-2 DM
9-Cardiovascular complication of DM (03)
10-Rx of DKA (03,08)
11-Skin changes in DM (03)
12-Enumerate 6 oral anti-diabetic agents (04,08)
13-Rx of diabetic microalbunuria (05)
14-Medical nutrition theraphy in DM (07)
15- Dx of gestational DM (07)
16-Approach to hyperglycemia pt (08)
17-Discuss non-pharma Mx of DM (08)
18-Features of Diabetic dyslipidemia (08)

Ecg, ami

There is always confusion around the terms third-degree heart block and AV dissociation. Dr. Chou makes a clear distinction in his book (see Additional Readings section): “The term complete AV block is used when the atrial rate is faster than the ventricular rate, whereas the reverse is true in AV dissociation. In AV block, there is a failure of impulse conduction even though the ventricles are receptive. In AV dissociation, there is an increase in the automaticity of the subsidiary pacemaker, which renders the ventricles functionally refractory to the slower atrial impulses.” These are the definitions we have used in this book.

Look at V1, which is usually the best place to see P waves

Myoglobin levels rise within 1-4 h fr onset of chest pain!!!! The earliest!!

Dont give nitrates in RV INFARCT , SHOCK, AORTIC STENOSIS, HYPOTENSION, CARDIOGENIC SHOCK

In 1st dgree heart block there is ONLY PROLONGATION OF PR BUT IN

2nd degree ( mobitz type 1) there is PROGRESSIVE PROLONGATION OF PR.

MOBITZ TYPE II –> there is constant PR BT OCCASIONALLY, THERE IS WITHOUT A QRS!!!
PLLLLLLLZZZZZZ INGAT SYG OIIIIIII

The triad of right vt infarction( hypotension, jugular venous distension, clear lung fields)

Mitral valve prolapse & MS

Mitral valve prolapse is the most common valvular abnormalities. So, take note.

However , the most common symptom is NO SYMPTOMS AT ALL.

So lets say , you detected it in an asymptomatic patients? You jz keep him reassured.

In symptomatic patients, do your investigation( echo) , follow up and if indicated, mitral valve repair.

So listen carefully

Midsystolic click..

Can someone summarize this for me?

Mitral annulus calcification(MAC) can produce both mitral stenosis / mitral regurgitation and the latter is more common.

Causes of MAC? ageing , atherosclerosis association,
read more here

In mitral stenosis , increase in left atrial size leads to increase excitability thus, atrial fibrillation (AF)occurs.

AF causes loss of atrial kick , hence further lowering the cardiac output

Hey guys, finally a proper explanation for tapping apex!
read futher here

20120415-151525.jpg

Tapping apex is…… PALPABLE S1!!!!(mitral area) its just an exaggeration of the normal apex… I think?
Correct me

OPENING SNAP is caused by????
Forceful opening of mitral valve if stenosed.but but why the forceful opening?why doesnt this happen in other valves like aortic stenosis?
From what i have understood, first, we need to know that due to the stenotic mitral valve, this impedes the blood from flowing freely to the left ventricle, creating some sort of pressure gradient.so possibly this forceful opening is due to the high pressure gradient difference whereby the pressure in left atrium is 25 mmhg while in the left ventricle , 5 mmhg ( all of this during diastolic phase).. Normally there is NO PRESSURE GRADIENT.

And also the reason behind this is because of the anatomy of the mitral valve itself.( i dont know exactly why but if someone knows , i beg you to tell me). All i know is it is a bicuspid valve,with the anterior leaflets larger than the posterior one… But in aortic valve, its a tricuspid..and it is more rounded… So???? I dont get it.. I think i know but im not 100% sure.help?

The famous question

Signs of mitral stenosis….( i was asked this lucky question once when i wasnt prepared… By an intelligent professor… I was sort of humiliated in front of a bunch of egyptian guys and its really embarassing since i was alone at that moment, but i took it positively, it spurred me to work harder)

Malar flush
Tapping apex
Signs of pulmonary hypertension- diastolic shock; palpable 2nd heart sound in the pulmonary area, possibly; rt vt hypertrophy with its signs- heaving apex, ejection systolic click
Loud S1
Loud P2( due to phtn)
Mid diastolic rumble(Low pitched- hear it with the bell!!!!!!!!!!) or let him roll to the left to clarify your findings or exercise.
Presystolic accentuation( caused by atrial contraction and lost if atrial fibrillation present)
Jugular venour pressure elevation; due to phtn so–> prominent “a” OR loss of “a”(due to AF in the right that is… Perhaps because of the phtn????)

Systolic Ejection sounds occur shortly after the first heart sound, at the time of ventricular ejection. Normally, the opening of the aortic or pulmonic valves and the onset of ventricular ejection is not audible. In certain cardiac conditions extra sounds are heard shortly after the first heart sound, S1. They are produced by the opening of the aortic or pulmonic valves, either when one of these valves is diseased (valvular) or when ejection is rapid through a normal valve (vascular).
Aortic ejection sounds of valvular origin are heard in patients with coarctation of the aorta usually associated with congenital bicuspid aortic valve, valvular aortic stenosis, aortic insufficiency, or aneurysm of the ascending aorta. Valvular ejection sounds may be heard in clinical conditions associaated with forceful left ventricular ejection, such as thyrotoxicosis, anemia, pregnancy, exercise, high cardiac output states.
Aortic ES is loudest at aortic area and cardiac apex with no respiratory variations.

Pulmonic ejection sounds are associated with dilatation of the main pulmonary artery, including pulmonary hypertension and valvular pulmonary stenosis. Pulmonary ES is best heart at pulmonic area and decreases coincident with inspiration.

Source;here

So theres no SNAP, but theres the CLICK.
The weird thing is Regardless of the stenosis or the regurgitation, it produces the CLICK.( for semilunar valves)

ecg findings of MS
normal OR
P-mitrale- broad notched P wave due to left atrium overload definition
Signs of rt vt hypertrophy( this needs a long explanation)
AF- seen as FIBRILLATORY WAVES

I think thats enough.here. I mean. Further elaboration in books.duh!

This is percutaneous mitral ballon valvotomy

Pssst! Most common cause of MS is rheumatic heart disease!!!!