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Cardiovascular Disease

Chest pain

M.I.

Heart failure

A F

HTN

ARF

Q. Name some common cardiac emergencies you have seen in our ward.

Ans.

M I

Acute left ventricular failure

Acute coronary syndrome

Q. Name some cardiac disease you have seen in our ward.

Ans.

Coronary artery disease → M I, angina

Heart failure

HTN

Acute rheumatic fever

Valvular heart disease→ MS

Arrhythmia → AF

Q. Name some coronary artery disease.

Ans.

Stable angina

Unstable angina

MI

Heart failure

Q. Name some causes of chest pain.

Ans.

Cardiac or central causes

Peripheral or non cardiac

Myocardial ischemia / Angina

Lung

Myocardial infarction

Pneumonia (pleuritis)

Pericarditis

Pneumothorax

Myocarditis

Pulmonary embolism/ infarction

Aortic dissetion

Malignancy

Aortic aneurysm

Musculoskeletal pain

Osteoarthritis

Rib fracture

Muscle pain

Herpes zoster

1

Q. How will you differentiate between cardiac chest pain from non cardiac chest pain?

Ans:

Trait

Cardiac chest pain

Non cardiac chest pain

1)

Site

Central

Peripheral

2)

Character

Choking, tighting, squeezing

Sharp, stabbing

3)

Aggravating factor

Exertion, heavy meal, cold exposure

Not so

4)

Relieving factor

Rest , Nitrate

Not so

5)

Radiate to

Left shoulder blade, arm, jaw

Not so

Q. How will you differentiate between pain of MI and angina?

Ans.

Pain of MI

Pain of angina

Sudden, more severe

Less severe

Not relieved by rest or nitrate

Relieved by rest or nitrate

Associated with

Not so

Sweating

Vomiting

Cold calmy skin

Hypotension

Q. Define acute coronary syndrome.

Ans. Prolonged and sever chest pain may be due to unstable angina , STE MI or non-STE MI

(non Q wave MI) are collectively called acute coronary syndrome.

Pain

ECG

Toponin I

Diagnosis

Cardiac chest pain

ST elevation

+++

STE MI

Cardiac chest pain

ST depression

++

Non STE MI or non Q wave MI

T inversion

Cardiac chest pain

Transient ECG change or normal ECG

-

Unstable angina

Q. Define unstable angina.

Ans. Unstable angina is characterized by newly onset of rapidly worsening angina or angina on minimal exertion or angina on rest in absence of myocardial damage.

Q. A 40 years old male came to you with severe chest pain with sweating, cold calmy skin,

vomiting and BP 90/62 mm of Hg. What is your diagnosis? Ans. Acute myocardial infarction.

Q. In which ward you will suggest to admit the patient? Ans. CCU [ some of you mistakenly answer ICU. So be careful]

2

Q. Assume, you are in CCU. What will you do to manage the patient?

Ans. First I shall give high flow o 2 . Then I shall do ECG.

Q. What do you expect in ECG?

Ans. ST-elevation, →then `Q’ inversion →then `T’ inversion

Q. What other investigation you will do?/ Do we measure any enzyme level?

Ans. Toponin I.

Q. What treatment you will do?

Ans.

O 2 inhalation

For pain: Inj. Morphin [ I.V. ,5-10 mg]

Injectable anti-emetic [Metochlorpromide]

Tab. Aspirin,300mg (crush the tablet and give it )

Tab. Clopidogrel, 300mg

Glycerine trinitrate spray- 2 puff stat ,sublingually.

Q. In which condition Morphin cannot be given?

Ans. Bronchial asthma, COPD.

Q. Then what will you do?

Ans. Then I shall institute reperfusion therapy: Inj. Streptokinase.

Q. When you will administer streptokinase?

Ans. If the patient comes with ST elevation and within 12 hours of chest pain.

Q. How streptokinase is administered?

Ans. 1.5 million unit in 100ml of NS: 60 drops/min or over one hour.

Q. In which route streptokinase is administered: I.V. or I.M.?

Ans. I.V. in drip.

Q. What are the complications of streptokinase?

Ans. a) hypotension

b) bleeding manifestation

Q. What are the follow up you will give after administration of streptokinase?

ans. I shall regularly measure the B.P. to see hypotension.

3

Q. What are the contraindications of thrombolytic therapy or streptokinase?

Ans.

Active internal bleeding

Previous sub-arachnoid haemorrhage/ Intracerebral haemorrhage.

Uncontrolled hypertension

Recent surgery

Active peptic ulcer disease

Pregnancy

Q. How will you understand that streptokinase is working?

Ans. By seeing the ECG- reperfusion arrhythmia.

Q. A patient was administered streptokinase 2 years back. Now he developed M I. Can he take

streptokinase again? Ans. No. Because, as he took streptokinase before, there is developed antibody against

streptokinase.

Q. Then what drug he will take now?

Ans. Now he will take Alteplase [tissue plasminogen activator].

Q. For how long the antibody persist?

Ans. Up to 5 years.

Q. If this patient of MI goes to higher center, what could be done?/ What are the interventions in

MI?

Ans. In higher center, we can do:

PCI [primary percutaneus coronary intervention]

CABG [ coronary artery bypass grafting]

Q. In CABG which artery is used?

Ans. Internal mammary artery or great saphenous vein

Q. What will you give if a patient comes 12 hours later of MI or have no ST elevation or non Q

wave MI? Ans. Here we give low molecular weight heparin. Name Enoxaparin (1unit/kg), [trade name claxene].

Q. How it is given?

Ans. It is given subcutaneously, 12 hourly for 5-7 days.

Q. What is the most dangerous complication of MI?

Ans. Ventricular fibrillation (VF).

Q. What are the immediate causes of death after MI?

Ans. VF, Cardiac arrest/ asystole.

4

Q.

Mention the complications of MI.

Ans.

1)

Arrhythmia (tell the names of every arrhythmia)

VF

Ventricular tachycardia

Ventricular ectopic

AF

Atrial flutter

SVT

A-V block

Complete heart block

2)

Cardiogenic shock

3)

Heart failure

4)

Pericarditis

5)

Late complications:

Rupture of papillary muscles

Rupture of interventricular septum

Ventricular aneurysm

Q. What do you mean by Dressler’s syndrome? Ans. Persistent fever, pericarditis, pleurisy occur few week after MI.

Q. Mention the secondary prophylaxis of MI.

Ans.

Aspirin 75mg daily

Clopedogrel 75mg daily

β- blocker

ACE inhibitor

Management of hyperlipidaemia→ statin →Atorvastin

Stop smoking.

Q. Which MI is worse- anterior MI or inferior MI?

Ans. Anterior MI is worse. Because it causes arrhythmia. Inferior MI causes only bradycardia.

Heart failure

Q. A patient came to you with sudden, sever respiratiory distress. What are the differential

diagnosis?

Ans. First say,

Acute LVF with pulmonary edema

Tension pneumothorax

Next you may say,

Acute severe asthma

Acute exaggerations of COPD

5

Q. What are the causes of left ventricular failure?

Ans.

1 st cause- Systemic hypertension

MI -2 nd cause

AS (aortic stenosis )

Q. What are the cardinals sings of LVF?

Ans.

Pulsus alternus/ Tachycardia

Gallop rhythm

Bilateral basal creps

Q. What will be the management?

Ans. Frist say the following three:

Propped up position

High flow O 2 inhalation

Diuretic: Inj. Frusemide ,I.V. up to 160mg (1 amp Lasix= 20mg, Tab. Lasix=40mg)

If sir wants to know more, then say the followings

Glycerinetrinitrate

ACE inhibitor

In some cases, opiate or morphin.

Q. What are the causes of right heart failure/ CCF?

Ans.

PHTN

Cor pulmonale

VSD/ASD

Anaemia

MS

Q. What are the cardinal features of CCF/ right heart failure?

Ans.

Raised JVP

Tender hapatomegaly

Dependent edema

Q. What is the management of right heart failure?

Ans.

Propped up position

Low flow O 2

Injectable diuretic

Q. What are the complications of heart failure?

Ans. To remember (RATE )

R-Renal failure

A-Arrhythmia

T-Thromboembolism

E--Electrolyte imbalance: hyponatramia, hypokalaemia, hyperkalaemia.

Impaired liver function

6

Q. What is systolic heart failure and what is diastolic heart failure?

Ans.

systolic heart failure

diastolic heart failure

When heart fails in systole, that means reduced

When heart fails to dilate Or poor diastolic filling

contractility

e.g.- M I, cardiomyopathy

e.g. constrictive pericarditis, restrictive cardiomyopahty.

To remember the causes of heart failure, you may see the chart, but do not write in the exam

paper.

 

Pressure overload

Volume

Muscle,

Type of heart failure

overload

Usually biventricular

Visible pressure Due to valve stenosis

Invisible pressure due to HTN

LV

AS

Sys. HTN

MR, AR

Cardiomyopathy

MI

/IHD

RV

PS

P. HTN

PR, TR

Cardiomyopathy

(uncommon)

MI

/IHD

VSD, ASD,

 

anaemia,

pregnancy,

thyrotoxicosis

Volume overload occurs to that chamber of the heart which is weaker. LH is stronger than RH due to more pressure. So in case of VSD, ASD, anaemia, pregnancy- there is right heart failure.

Q. In systemic hypertension, which type of heart failure occurs?

Ans. LHF

Q. In aortic stenosis, which type of heart failure occurs?

Ans. LHF

Q. In VSD, ASD, anaemia which type of heart failure occurs?

Ans. RHF

Q. In mitral stenosis, which type of heart failure occurs?

Ans. RHF (you will fail if you tell LHF in MS).

Q. Define dyspnea.

Ans. Dyspnoea can be defined as an unpleasant subjective awareness of sensation of breathing.

7

Q. Define orthopnea.

Ans. Dyspnea in lying position

Q. Define PND.

Ans. It is a sudden severe breathlessness which wakes the patient form sleep.

Q. What are the causes of sudden death?

Ans.

M I

AS

Hypertrophic cardiomyopathy

DCM

Atrial fibrillation

Q. What are the causes of atrial fibrillation? Ans. Mnemonic: MITHA

M- mitral stenosis

I- IHD

T- thyrotoxicosis

H- hypertension

A- alone (lone atrial fibrillation)

Q. What are the causes of irregularly irregular pulse?

Ans.

AF

Atrial flutter with variable block

Multiple ventricular ectopics Then sir may ask question from AF

Q. What are the treatment of AF?

Ans.

Rate control

Rhythm control

Restoration sinus rhythm

Q. What are the drugs used in AF?

ans. Mnemonic: ABCD

A- amidarone

B- β-blocker

C- calcium channel blocker: verapamil, diltiazem.

D- digoxin

Q. which drug commonly used?

Ans. β-blocker

Q. which drug used in a patient with MS?

Ans. Digoxin

Q. which drug used in a patient with bronchial asthma ?

Ans. Diltiazem (Ca- channel blocker).

8

Q. What are the complications of AF?

Ans. 1.Thromboembolism 2.Heart failure/ acute pulmonary edema

Q. A patient with AF came to you with unconsciousness or right sided hemiparesis. What is your

diagnosis? Ans. AF with stroke due to thromboembolism.

Q. A patient with AF came to you with dyspnoea. What is your diagnosis?

Ans. acute pulmonary edema.

Q. What is pulsus deficit?

Ans. In atrial fibrillation, heart rate is more than pulse rate. This is called pulsus deficit.

Q how will u see it ?

Ans. Simultaneously you have to see pulse and heart rate

Q. What will be your approach to a patient of AF?

Ans. A patient with AF , following things must be seen:

Pulse: irregular/ pulsus deficit

BP: HTN- cause of AF

Look for: thyroid gland and features of thyrotoxicosis

Auscultate: For murmur- MS & variable heart sound

Chest pain- IHD

Hypertension

Q.

In your chamber, you found a patient with BP 190/95 mm of Hg. What will be the approach

to

this patient?

Ans. Sir, I shall take some history, do some clinical examination and suggest some investigations

to find out etiology, co-morbid conditions and to see complications (target organ damage).

History: Age, family history, Drug- steroid, in female- OCP

Appearance: Cushing syndrome (to exclude 2ndaries)

Anaemia: present in CRF

Xanthalesma:

Pulse: radio-femoral delay→ coarcation of aorta

Apex beat: heaving due to HTN

Heart sound: loud 2 nd heart sound, murmur

Gallop rhythm and basal crep: LVF

Abdomen: Palpable kidney→ PKD, Renal bruit → renal artery stenosis

Oedema: Renal failure

Funduscopy: to see retinopathy

Investigations: given below.

9

Q. A patient of 15 years age came to you and you found his BP 150/100 mm of Hg. What will be

the cause? Ans. Here answers will be the secondary causes: AGN and other causes.

Q. A newly married female patient came to you and you found her BP 160/90 mm of Hg. What

may be the causes? Ans. May be due to OCP.

Q. Classify HTN.

Ans.

1)

2)

Primary or essential: 95% Secondary: 5%

Q. Name some secondary causes of hypertension.

Ans.

Renal

Drug

Endocrine (all the endocrine disease except Addison’s disease)

other

AGN Polycystic kidney disease Renal artery stenosis

Steroid

Cushing syndrome Conn’s disease Acromegaly Thyrotoxicosis Phaeochromocytoma Hypothyroidism

Renal artery

OPC

stenosis

Q. Mention the grading of BP.

Ans.

Category

Systolic Blood pressure

Diastolic Blood pressure

(

mm of Hg)

(

mm of Hg)

Normal

<140

 

<90

Hypertension

Grade 1

140-159 (to remember: add 20)

90-99 (to remember: add 10)

Grade 2

160-179

100-109

Grade 3

≥ 180

≥ 110

Q. What do you mean by isolated systolic hypertension?

Ans. When systolic BP >140 mm of Hg, but diastolic BP <90 mm of Hg.

Category

Systolic Blood pressure

Diastolic Blood pressure

(

mm of Hg)

(

mm of Hg)

Grade 1

140-159

 

<90

Grade 2

≥ 160

 

<90

10

Q. What do you mean by White coat hypertension?

Ans. When a patient’s BP becomes elevated when he goes to the doctor, but otherwise, his BP is normal, this incident is called White coat hypertension.

Q. Mention the grading of hypertensive retinopathy.

Ans. Mnemonic: SAC in Prem (prem means --love)

Grade 1 [S]

Silver wiring

Grade 2 [A]

Arteriovenus nipping

Grade 3 [C]

Cotton wool exudates + flamed / blot haemorrhage

Grade 4 [Prem]

Papilloedema

Q. How will you differentiate between diabetic and hypertensive retinopathy?

Ans.

Diabetic retinopathy

Hypertensive retinopathy

Dot haemorrhage

Arteriovenus nipping

Hard exudates

Cotton wool exudates + flamed / blot haemorrhage

Neovasculization

Papilloedema

Q. what are the target organs of hypertension?

Ans.

Brain

Retina

Heart

Kidney

Blood vessel

Q. What are the complications of hypertension?

ans.

Brain: stroke

Retina: Retinopathy

Heart: Coronary artery disease, AF, LVH

Kidney: Renal failure

Blood vessel: atherosclerosis

Q. What investigations you want to do?

Ans. To see complications:

ECG: Left ventricular hypertrophy

Echocardiography: Left ventricular hypertrophy / LVF

CXR: Left ventricular type cardiomegaly

Urine RME→ Protein, to see nephropathy

Serum creatinine , to see nephropathy

Others:

Urinary catecholamine→ pheochromocytoma

11

Renal USG: to diagnose PKD

RBS and lipid profile

Some 1 st choice of antihypertensive drugs in following conditions:

DM: ACE inhibitor/ receptor blocker

CRF: ACE inhibitor + then calcium channel blocker+ vasodialator

MI, Stroke: ACE inhibitor

Heart failure: ACE inhibitor + diuretic

IHD: β- blocker.

Antihypertensive drug

A- ACE inhibitor-

Ramipril Captopril A-Angiotensive receptor blocker losartan valsartan

B-Beta blocker Cardioselective Metoprolol Atenolol Combined β- and α-adrenoceptor antagonists . Carvedilol Nonselective propranolol used in anxiety, palpitatinon and portal HTN

C-Ca channel bIocker- dihydropyridines Amlodipine (vasa-selective) Rate-limiting calcium antagonists Diltiazem (intermediate)- Verapamil ( cardioselective ) -use in SVT

D- Diuretic Thiazide -Indepamide

D- Vasodilator α-blocker Prazosin

12

Commonly asked questions

Which ant HTN drug given in DM?

ACE I/ ANG.BLOCKER

Which ant HTN drug given in HEART FAILURE?

ACE I/ ANG. BLOCKER Ramipril plus DIURETIC

Which ant HTN drug given in IHD?

BETA BLOCKER

Which ant HTN drug given in CRF?

ACE I/ ANG.BLOCKER next Ca CHANNEL BLOCKER next Alpha BLOCKER next WITH DIURETIC AT LAST BETA BLOCKER

Which ant HTN drug given in STROKE I CVD

ACE I/ ANG.BLOCKER Ramipril

Which ant HTN drug given in isolated systolic HTN

Ca CHANNEL BLOCKER Amlodipine DIURETIC

which ant HTN drug given in COPD

Ca CHANNEL BLOCKER

ACE inhibitor I Angiotensin receptor blocker

 

indication

contraindication

DM CKD CVD HEART FAILURE LV dysfunction / hypertrophy /DCM POST MI

 

Hyperkalaemia Oligouria or ARF In hypovolaemic patient Pregnancy and Renal artery stenosis CLD COPD

SIDE EFFECT

Dry cough

Postural hyopotension- to avoid it, give first dose at night

BETA BLOCKER

Indications

Contraindications

Myocardial infarction Angina Heart failure stable--only carvedilol Atrial fibrillation

Bronchial asthma/ COPD Heart block /if pulse less than 60 DM Psoriasis PVD Heart failure (can be used in Carvedilol compensated heart failure)

Why beta blocker is not used In DM:

it will mask the sign +symptoms hypoglycaemia (tremor I tachycardia I sweating )

13

Before giving beta blocker see following:

H/O DM, COPD. asthma, heart failure, Auscultate lung for spasm and pulse for bradycardia

Ca channel blocker

Indications

Contraindications

Amlodipin-

Heart block

Any patient/Elderly patient without heart failure

Heart failure

Isolated systolic HTN

Complications

CRF

Amlodipin

COPD/ Bronchial asthma Verapamil (240 mg daily)

Can be useful when hypertension coexists with angina

Flushing of face, headache

Palpitation

Fluid retention Verapamil

Verapamil used in SVT

Constipation

Diltiazem

Bradycardia

Hypertensive crisis

Hypertensive emergency

Hypertensive urgency

Hypertensive emergency

Severe elevation of BP > 180 /120 mm of Hg complicated by evidence impending or progressive target organ damage.

They require immediate reduction of BP ( not necessarily to normal )

Example of hypertensive emergency

HTN Encephalopathy

Intracerebral haemorrhage

Acute MI

Acute LVF

Acute pulmonary edema

Unstable angina

Eclampsia

Management of hypertensive emergency

Treatment in ICU with monitor

Parental administration of Anti- HTN drugs.

Goal of therapy is to ↓BP not more than 25 % in 1st hour.

Then target BP→ 160/110 mm Hg in next 6 hrs

Sudden fall may cause Cerebral ischemia

14

Renal ischemia Coronary ischemia

Then reduction of BP to normal in next 24-48 hours.

Hypertensive urgency Severe elevation of BP with target organ damage Upper level of stage ii with

Severe headache

Epistaxis

Dyspnea

Severe anxiety

Acute rheumatic fever

Q: scenario: A 13years old boy comes with fever & multiple joint pain & swelling (polyarthritis). What is your diagnosis? A: Acute rheumatic fever.

Q: Mention the diagnostic criteria. A:

Major criteria:

Migratory polyarthritis(75%)

Carditis

Sydenham’s chorea

Subcutaneous nodule

Erythema marginatum

Minor criteria:

Fever

Arthralgia

Elevated acute phase reactants (e.g. high ESR,CRP)

Prolonged P-R interval

Evidence of group A streptococcal infection

Raised ASO titre

Positive throat swab culture

Recent scarlet fever

The diagnosis of acute rheumatic fever is made when there is

2 major criteria or,

1 major +2 minor +

Supporting evidence of group A streptococcal infection

15

Q: Which organism is responsible for RF? A: Group A βhaemolyticus streptococcus (S.pyogens)

Q: How many days are required for development of RF? A: 2-3weeks (pt. has a H/O of sore throat i.e; pharyngitis)

Q: Why 2-3weeks are required after sore throat? A: For antibody formation.

Q: What type of hypersensitivity reaction is it? A: Type -2.

Q: What do you mean by migratory polyarthritis? A: It means a joint is involved, when it resolved another joint is involved.

Q: What type of carditis is it? A: pancarditis (all the 3layers is involved)

Q: What are the features of pancarditis? A:

Endocarditis: murmur due to valvular involvement

Myocarditis : conduction defect, cardiomegaly (HF), tachycardia

Pericarditis: pericardial effusion & rub , pain

Q.

how will understand pericarditis ? pain & rub

Q.

How will understand myocarditis ? Feature of heart failure and tachycardia

Q.

How will understand endocarditis ? feature of changing murmur

Q: What is Carey Coombs murmur? A: It is a soft mid-diastolic murmur due to vulvulitis.

Q: What is the common age of RF? A: 5-15years.

Q: Causes of HF in ARF? A:

o

Myocarditis

o

Vulvular causes (MR, AR)

16

Q: R x of ARF? A:

Bed-rest (Next Q: How many days? > The duration should be guided by symptoms along with temperature, leucocyte count & ESR. It should be continued until these have settled)

Aspirin 60-100mg/kg BW/day in 6 divided dose. Continue until ESR falls and then taper gradually.

Steroid (If severe arthritis or carditis): Tab. Prednisolone 1-2mg/kg BW/day

Antibiotic (to eliminate residual streptococca l infection)

Inj. Benzathine pencillin 1.2million unit 1ampule I/M stat. or,

Tab. Phenoxymethyle penicillin 250mg, 6hourly for 10days

Q: Which should be done before administration of Benzathine penicillin? A: skin sensitivity test should be performed to prevent Hypersensitivity/anaphylactic reaction.

Q: Complications of Aspirin. A: Nausea, vomiting, tinnitus, deafness and metabolic acidosis*.

NB: if pain is not subsided within 24hours, then it suggests that it is not due to RF.

Q: What should be done for secondary prevention? A:

Inj. Benzathine penicillin 1.2million U 1amp I/M monthly. Or,

Phenoxymethyl penicillin 250mg 1+0+1.

Next Q: How many days? A:

If RF without residual heart disease → upto 5years last attack or until 21 years whichever is longer.

If RF with residual heart disease → continue upto 10years of last attack or until 40years or lifelong.

NB: If there is penicillin allergy, erythromycin can be used.

Q: What are the complications of RF? A:

Acute: HF

Chronic: MS, MR or aortic Valvular disease.

17

Q: What is the mechanism of development of MS? A: Repeated RF cause progressive fibrosis & thereby cause MS. Q. scenario : 15 yr old male comes to u with fever and increased ASO titer will u start anti- rheumatic fever treatment or prophylaxis ? Ans. No I will not started anti-Rheumatic drug . I look for major criteria and minor criteria if it fulfilled then only start drug . Q: What is the pathognomic feature of RF? A: Aschoff nodules (multinucleated Giant cell surrounded by macrophage & T-lymphocytes)

Important

Name of

Pulse

Apex

Heart sound

Murmur

murmur

beat

MS

Normal /as

Tapping

 

Mid-diastolic in mitral area, which is low-pitched, localized, rough, rumbling (LLRR), best heard with bell of stethoscope, if left lateral position breath hold after expiration, with presystolic accentuation.

like AF

Loud 1 st HS , opening snap

MR

Normal

Thursting

Soft 1 st HS

Low blowing pansystolic murmur best heard at apex & radiate to left axilla

AS

Slow rising

Heaving

Soft 2 nd HS

Harsh high pitched ejection systolic murmur best heard in aortic area sitting & leaning forward with breath hold expiration & radiate to right side of neck.

AR

Collapsing

Thursting

 

High pitch blowing ejection systolic murmur best heard at left parasternal area sitting & leaning forward with breath hold expiration.

18

Infective endocarditis

Q: Scenario: A pt. comes to you with fever for 2weeks. On examination there is clubbing, rash, splinter haemorrhage, there is also changing murmur & splenomegaly. What is your diagnosis?

A:

Infective endocarditis. R x : according to culture report.

Q: What investigation you want to do? A: Blood culture & echocardiography.

Q: Name some organisms that cause infective endocarditis? A:

Staphylococcus aureus

Streptococcus viridians

Streptococcus epidermidis

HACEK ( H aemophilus, A ctinobacillus, A ctinomycosis, C ardiobacterium hominis, E ikenella spp. , K ingella kingae)

Q: Cause of complete heart block? A:

Complete heart block

Acute MI (inferior)

Drug ( mnemonic- BAD: β-blocker, amiodarone, digoxin)

Cardiomyopathy

Q: Clinical feature:

A:

Symptom: Blackout, Syncope and Dizziness Pulse: Regular but bradycardia

JVP: Cannon wave Complications: Stoke Adam’s attack

R x : -If Bradycardia - Inj.Atropin -Temporary pacing followed by permanent pacing

Q: Scenario:A pt. comes to you with sudden loss of consciousness & fall. On examination pulse is 30-35beats/minutes. What is your Diagnosis? A: Complete heart block with Stoke Adam’s attack.

19

Q: What is the R x of 1& 2heart block? A:

1 HB & 2 HB Type-1 → No need of R x

2 HB Type-2 →

o

If due to Inferior MI:

-Asymptomatic: No R x -Symptomatic: Inj. Atropine

o

If due to Acute Anterior MI: Temporary pacing followed by permanent pacing.

Q: Sequele of 2HB. A: mnemonic--HSC

a. C-Complete HB

b. S-Stoke Adam’s attack

c. H-Heart failure

Q: Name some cyanotic heart diseases? A: Tetrology of Fallot, transposition of great vessel, tricuspid atresia with pulmonary atresia, Ebstein anomaly.

Q: What are the components of tetrology of Fallot? A: mnemonic: PROVed

Pulmonary stenosis

Right ventricular hypertrophy

Over riding of aorta

Ventricular septal defect.

Q: What is the presentation of TOF?

A:

Clubbing

Cyanotic spell /Fallot’s spell (pt. becomes cyanosed after crying or feeding and may become apnoeic or unconscious & relief by squatting position)

Q: VSD/ASD- cyanotic / acyanotic heart disease? A: acyanotic.

NEXT Q: Can they be cyanotic?? A: Yes, they may develop cyanotic heart disease if associated with reverse shunt (Rt →Lt) [Eissenmenger Syndrome]

Please see the following topics from short case

MS

Tachycardia & bradycardia

Heart sound

Venous & arterial pulsation

20

Q: What are the causes of acute pericarditis? A: In our country: TB Foreign: Viral Then: MI, Uraemia, Malignancy, Connective tissue

Q: Clinical features of Pericarditis. A: Pain & pericardial rub

If there is effusion:

o

Apex beat non palpable

o

↑ Area of cardiac dullness

o

Heart sound-muffle

o

↑ JVP

Q: What is the X-ray finding of pericardial effusion? A: Globular / Pear shaped heart with oligaemic lung field

ECG : low voltage ECG

Echo : confirmatory

Q: What do you mean by Cardiac tamponade? A: It is a term used to describe acute heart failure due to compression of heart by large or rapidly developing pericardial effusion. R x : Pericardial aspiration.

Q: What R x should be given for the following cases? A:

Pericardial effusion with TB : - Anti TB - Steroid ( 3 months)

Pericardial effusion with uraemia: dialysis.

Q: What is the indication of use Steroid in pericardial effusion?

A: Pericardial effusion due to TB. (Advantage of use:

1)

Early absoption

2)

Prevent adhesion)

Q: What is constrictive pericarditis? A: It is the condition where pericardium became progressively thickened, fibrosed & calcified. So the heart encased in a solid shell & can’t fill properly.

C/F of constrictive pericarditis /Cardiac tamponade:

o

Low volume pulse

o

Raised JVP

o

Kussmaul sign ( Paradoxic raised of JVP in inspiration )

o

Hepatomegaly

21

o

Ascites

o

Pulsus paradoxus ( excessive fall of BP during inspiration)

o

Oedema

Q: Scenario: A pt. comes to you & on examination you get early diastolic murmur in left lower sterna area with high volume pulse, what is your diagnosis? A: AR

Q: Scenario: A pt. comes to you & on examination you get ejection systolic / a systolic murmur murmur in aortic area with radiation to neck and low volume pulse, what is your diagnosis? A: As

Q: Scenario: A pt. comes to you & on examination you get diastolic murmur in mitral area with loud first heart sound , what is your diagnosis? A: MS

Q: Scenario: A pt. comes to you & on examination you get systolic murmur in mitral area with radiation to axilla , what is your diagnosis? A: MR

22

GIT and Pancreatic Disease

Q: 30 years old man come to you with haematomesis and malaena. How will you approach?

A:

First, I will resuscitated the patient.

See- Pulse, B.P, Urine output.

Then open I.V. Channel,

Blood grouping and cross matching and give one unit of fresh blood ,

inj. P.P.I,

Tab.Sucralfate(1+1+1+1)

Q: What are the causes of upper GIT Bleeding / Haematomesis?

A:

1.Peptic ulcer disease

2.gastric erosion

3.Carcinoma of stomach

4. esophageal varies

5.esophagytis

Q: what is the most important one investigation for Upper GIT Bleeding?

A: Upper GIT endoscopy

Q:What is the Definition of malaenae?

A: Black tarry offensive stool.

Q: what are the causes of haematocrazia?

A:

hemorrhoids

Anal fissure

Diverticulitis

Cancinoma rectum

Polyps

23

Q: a patient with CLD comes with haematomesis and melaena. What wiil you do?

A:

Initial Rx- resuscitation, see pulse , blood pressure , urine output

-I.V. fluid

-Blood grouping and Cross matching

-Give one unit of blood

-Do emergency endoscopy

. sclerosis therapy

.band and ligation

.balloon tamponade

Medical Rx

Vesopress- such as terlipressin

-give antibiotic to prevent SBP

What is the definite treatment ?

TiPSS- Transjugular intrahepatic Protosystemic Slent Shunnting

Q. 30 years old female comes to you with epigestric pain . what will be the diffential; diagnosis?\

A: Acute exaggeration od PUD

Acute cholecyctitis

Acute pancreatitis

Q: how will you approach the patient?

PUD- epigestric pain, recurrent episodic pain; if relief by food-in duodenum, if increase by food- in Gastric

Duodenal point is tender

Acute cholecystitis- in epigastric and right hypochondrium region, Murphy’s sign present

Acute pancreatitis- severe pain, pain radiate to back, patient in knee-elbow position.

24

Q What Investigation for patients:

1 st USG of whole abdomen- acute cholecystitis or acute pancreatitis.

Q. If normal then,

Do upper GIT endoscopy

Q .If u suspect perforation or intestinal obstruction ,

Do plain X-ray of abdomen in erect position

Q. If u suspect pancreatitis , do Serum amylase with in 24 hours(24 to 48 hours)

Q.If patient comes after 24 hours, do urinary amylase

Other investigation- USG of whole abdomen,

Q. if can not be diagnosed by that or for more specific test- CT scan

And to see complication-RBC,CBC, S.calcium, S.Creatinin

Q: how will you see the prognosis or severity of this patien?

A: By CRP

Q. what will be the treatment?

A. diet-nothing per oral

-NG Feeding

-I.V. fluid (3 liter in adult)

-injection. Broad spectrum antibiotic (ceftriaxon/cefuroxime/imipenem)

-Analgesic (inj.pathedin/ opiate analgesic)

-Inj. PPI

-I/O chart

Q. what are the causes of pancreatitis

A G-. gall-stone

I-idiopathic

A-alcohol

ERCP--post ERCP (to remember:GIA-ERCP)

25

Q. Complication of acute pancreatitis?

a. 1.Systemic Inflammatory Response Syndrome(Sirs)

2. Hypoxia

3. hypo-albominia

4. hypo-calcaemia

5. hyperglycemia

Local- N-Necrosis,A-- Abscess, P--pseudocyst, A--ascitis(NAPA)

(For remember: Sirs, 3 hypos, 1 hyper, NAPA)

GIT complication-

V--Variceal bleeding

E-Erosion of colon

D--Duodenal obstruction

I--Upper GIT Bleeding

O-Obstructive jaundice

(For remember: VEDIO)

Q. what are the non-abdominal causes of that patient?

A. MI

Right lower lob pneumonia

Q. What are the causes of hyperglycaemia with abdominal pain?

A.Pencreatitis

DKA

Q. When Pencreatic Pseudocyst need surgical removal?

A. If it become more than 6 cm

Rx- Drainage in stomach , duodenum, after 6 weeks(because pseudo capsule takes 6 week to be matured)

26

Q.

when ERCP is needed?

A.

if pancreatitis is associated with jaundice

Q.

who many days after pancreatitis, cholecystitis can be done?

A.

2 weeks later

q. A patient comes to you with recurrent upper bdominal pain with diarrhea specially after falts good. And the patien is cachectic. What will be you diagnosis?

A.

chronic pancreatitis

Q.

what are the causes of chronic pancreatitis?

A.

C-Hypercalcemia

O-Obstruction/ obstructive(ductal adenocarcinoma or pancrease division or spheiler oddislener)

C-CRF

A-Alcoholism

(to remember: COCA)

Q.

what are the clinical features?

A.

-Patient is cachectic and lean &thin

-recurrent upper abdominal pain

-Malabsorption- Stealorrhoea(bulks of pale and offensive stool, which float in the toilet, due to fat malabsorption)

-Patient may have DM

Pain relief by Alcohol consumption.

Write down the treatment ?

Fat free diet and stop alcohol

Enzyme supplementation(pancreatic enzyme)

Pain killer: NSAIDs, Antispasmodic

PPI(because it optimizes duodenal pH for pancreatic enzyme)

27

Q.

what are the investigations for the diagnosis of chronic pancreatitis?

A.

 

USG

CT

Plain X-ray of abdomen to see stone

MRCP

Q.

a patient comes to you with different lump in region. What are the causes?

A.

if epigastric region-

Carcinoma stomach

Ca- left lobe of liver

Pancreatic pseudocyst

Ca transverse colon

If hypochondrium region-

Right lobe of liver

Palpable gall bladder

If right iliac fossa-

Appebdicullar lump

Ileo-caecal TB

Caecal carcinoma

If left iliac fossa-

Ca sigmoid colon

Viverticular mass

Stool/ impaoted stool

Q.

what are the most common types of Peptic ulcer disease?

A.

duodenal ulcer

gastric ulcer

28

Q. what is the difference between ulcer and erosion?

A. Ulcer involved the muscularis mucosa but erosion not involves

Q.Causes of PUD?

A.

H.Pylori

NSAID

Smoking

Q. causes of erosion?

A. NSAID

Q.Difference between gastric ulcer and duodenal ulcer

A.

Gastric ulcer

Duodenal ulcer

Usually single

multiple

Turns into melignancy

Not so

Pain increases after food taking

Pain relives after food taking

Q.

which one is worse?

A.

Gastric ulcer, because there is a chance of malignancy.

Q.

when we need to take biopsy during endoscopy?

A.

Gastric ulcer

Q.

what are the investigation?

A.Upper GIT Endoscopy

Q.what is h. pylori?

A.

gram negative bacteria

Q.

h.pylori is responsible for which malignancy?

A.

MALToma, Gastric lymphoma

29

Q.

what are the complication of PUD?

A.

Haemorrhage(Haematomesis , malaena)

Gastric ulcer(Carcinoma)

Perforation

Gastric outlet obstruction

Q. what are the treatment?

A. Eradication of H. pylori

Triple therapy one strip on the morning and one strip at night

One strip contains the following (Tab. Amoxicillin 1 gm, Cap. Clarithrimycin 500mg, Cap. PPI 20 mg)

Q Duration of triple therapy ?

For 7 days

Q Then what will u give after 7 days , ?

Cap.PPI for 2 months

Q.

what are the complication of h. pylori therapy?

A.

D-Diarrhoea

R-Rash

C-Clostrideum difficle associate colitis

A-Abdominal pain/cramp

N-Nausea, vomiting

(to remember- DR.CAN)

Q.

Name some indication of h.pylori treatment ?

A.

PUD

H.pylori paritive dyspepsia

MALToma

30

Q. What are the investigations for diagnosis?

A. non-invensive

Urea breath test

Serology test

Invasive

Rapid urease test

Histology

Microbiological culture

Q. What is Zolliger-Ellison syndrome?

A. it is a disorder characterized by severe peptic ulcer, gastric acid hyper secretion ann non-beta

cell eslet tumour of the pancrease(gastrioma)

Q.

name some functional bowel disorder?\

A.

 

IBS

Pshychogenia dysphagia

Volumia nervosa

Anorexia nervosa

Q.

what are the causes of chronic diarrhea?

A .

IBD

IBS

Chronic pancreatitis

Celiac disease

Malsbsorption

Colonic neoplasm

A 20 years female comes to you with history of frequent loose stool proceed by abdominal pain without nocturnal symptom? What is your diagnosis?

A. IBS

31

Q.

what are the clinical features of IBS?

A.

 

Abdominal pain/cramp/colic

Pain relief by Defecation

Alternation of bowel habit

More on day and nocturnal symptom free.

What are the Alarming sign?

Age>50 years

Weight loss

Fever

Anaemia

Rectal bleeding

D/D- IBD,Neoplasm of colon, Malabsorption

Q. what will be the investigation?

A. no investigation is needed .do only exclude malignancy

ESR---normal

Colonoscopynormal

Q. what will be the treatment?

A. treatment

Diarrohoea predominant

Constipation predominant

Reassurance

Reassurance

Diet: Avoid fiber diet, wheat free, milk and milk product

Diet: increase fibers and increase water taking

For pain: anti-spasmodic-mebeverine

Anti-spasmodic-mebeverine

For diarrohea loperamid 2-8 mg daily

For constipation- lactilose, ispaghula

TCA-tab. Amitriptyline(10 mg) at night

TCA-tab. Amitriptyline(10 mg) at night

Q. name of IBD?

A. Inflammatory bowel disease-1.ulaerative colitis, 2.chronn’s disease

Q. how will you differentiate ulaerative colitis and chronn’s disease?

32

A. Difference between ulaerative colitis and chronn’s disease

traits

 

ulaerative colitis

chronn’s disease

 

1.

involvment

Only colon

From mouth to anus(mainly recto-segmoid junctiom)

2.nature of lesion

continuous

Skip lesion

 

3.Ulcer

Superficial ulcer

Deep ulcer , crypt abscess

4.

smoking relation

Non smoker

smoker

5.

treatment

Masalazin. corticosteroid

MTx, steroid, Azathioprine

Q.

What is the skin manifestation of IBD?

A.

Erythama nodusum

Q.

how will you differentiate the colonic carcinoma left side to right side?

A.

 

in case of right sided colon: anaemia due to malaena , alternation of bowel habit

In case of left sided colon: obstruction and fresh blood

Q.

how will you approach to a patient with dysphagia? How will you differentiate these?

A.

 

traits

Neurological dysphagia

Mechanical dysphagia

Type of food

Initially liquid

Initially solid

onset

Acute

Gradual

timing

Difficulties in initiating swallowing

Food sticking at a specific sit / certain point

Association

Associated with chocking or nasal regurgitation

Not so

Q.

what are the causes of neurological dysphagia?

 

A.

Bulbar pulsy

Pseudobalbar pulsy

Myasthenia graves

33

Q.

Name some causes of mechanical dysphagia?

A.

Inside lumen

Ca. aesophagus

Stricture aesophagus

External: enlarge thymus, enlarge thyroid

Q. what is GERD?

A. Gastro esophageal reflex disease

Factors responsible for GERD:

Increased extra abdominal pressure

Decreased tone of lower esophageal sphincter

Diet-choclate, coffee, alcohol

Hiatus hernia

Obesity

Delayed emptying of gastric content

Pregnancy

Q .How will u diagnose this?

Diagnosis by-

1. Upper GIT endoscopy

Othe investigation

2. 24 hour intraluminal pH monitoring of the esophagus.

3. Esophageal manometry.

What are the complication ?

Esophagitis

Barrett’s esophagus

Treatment of GERD:

Avoid precipitating factor

Cessation of smoking,

loss of weight

Avoid alcohol, fatty meals & drugs e.g. nitrates.

Avoid heavy meals especially before sleep.

Raising the head of the bed at night.

should not go to bed within 2 hours of taking foods

Avoid any other precipitating factor.

Drugs-PPI 20 mg (1+0+1)

Domperidone 10 mg(2+2+2)

Endoscopy. to confirm the presence of esophagitis.

Q. write down the difference between Hematemesis & Hemoptysis:

 

Hematemesis

Hemoptysis

Def

Hematemesis is the vomiting of blood

Hemoptysis means coughing out of blood

Source

GIT tract stomach and duodenum

From respiratory tract

Color

dark red or brown or coffee ground due to action of gastric acid

Bright red

pH

Acidic pH

Alkaline pH

Mixed

Mixed with food

Mixed with mucous

Associated

Abdominal pain , nausea

Cough , chest pain , resp. distress

Investigation

Upper GIT endoscopy

Bronchoscopy

35

Define jaundice?

Hepato billiary

Jaundice refers to the yellow appearance of the skin, sclerae and mucous membranes resulting from an increased bilirubin concentration in the body fluids.

Normal bilirubin level

?

When will jaundice detectable clinically?

it is usually detectable clinically when the plasma bilirubin l > 3 mg/dl) or 50 μmol/

Classify jaundice?

Prehepatic or Haemolytic jaundice

Hepatocellular

Post Hepatic or Obstructive jaundice

Mention the cause of haemolytic jaundice?

Haemolysis.

Gilbert's disease.

Dubin-Johnson syndrome.

Rotor syndrome.

Mention the cause of hepatocellular jaundice?

Acute viral hepatitis,

Alcoholic,

Autoimmune,

Drug-induced

Cirrhosis

Mention the cause of obstructive

jaundice?

Causes of cholestatic jaundice

Extrahepatic

Choledocholithiasis

Carcinoma

Ampullary

Pancreatic

Bile duct (cholangiocarcinoma)

Secondary

Parasitic infection

36

Intrahepatic

Viral hepatitis

Primary biliary cirrhosis

Primary sclerosing cholangitis

Alcohol

Drugs

Autoimmune hepatitis

Pregnancy

How will u differentiate these three types of jaundice?

 

Haemolytic

Hepatocellular

obstructive

jaundice

less

moderate to severe

severe

anemia

more marked

absent

absent

hepatospleno

present

absent

absent

megaly

stool

pale

normal color

normal color

itching

absent

usually not

present

viral prodome nausea , Malaise

absent

present

absent

 

investigation

Bilirubin

unconjugated

mixed

conjugated

SGPT/ ALT

 

>6 times

 

Alk.phosphatate

   

> 2.5 times

Name some causes of viral hepatitis?

Common causes:

Hepatitis A

Hepatitis B ± hepatitis D

Hepatitis C

Hepatitis E Uncommon causes:

Cytomegalovirus

Epstein-Barr virus

Herpes simplex

Yellow fever

37

Route of transfusion?

Oro-faecal route ---A & E

parental route ----B & C

D-virus how transmit?

IF only B infected patient

How does hepatitis D spread along ?

The hepatitis D virus (HDV) is an RNA-defective virus which has no independent existence; it requires HBV for replication . it infected people only in presence of HBV infection which virus is more spread via IV drugs User ?

HCV mainly spread between IV drugs user which one is DNA virus ?

Hepatitis B

which virus have chronic form ?

Hepatitis B & hepatitis C

What investigation you want of do?

Liver function test

SGPT (ALT)

Alkaline phosphatase

S. Blirubin

Prothrobin time Viral marker

HBs Ag

Anti HAV

Anti HEV

Anti HCV

USG of hepato billiary system

What will be the finding of liver function test in viral hepatitis?

SGPT/ ALT >6 times

Alk.phosphatate <

2.5 times

38

What are the complications of viral hepatitis?

Acute liver failure.

Cholestatic hepatitis.

Aplastic anaemia.

Chronic liver disease and cirrhosis (hepatitis B and C).

Relapsing hepatitis .

What is fate of viral hepatitis ?

In Most of viral hepatitis the fate is complete resolution.

Plus above complication.

What is the most dangerous complications of viral hepatitis ?

Acute liver failure

Which one has more chance of turn in to chronic viral hepatitis between B @C?

or which form of viral hepatic needs treatment ?

Acute B viral hepatitis no needs of treatment --- 95 % resolve spontaneously

Acute C viral hepatitis needs of treatment ----- 95 % turn into chronic

What is the mechanism of jaundice viral hepatitis A, B, E ?

HAV , HBV cause viral hepatitis by immunological mechanism

HEV ---Here jaundice occur due to direct cell destruction that why it is cytopathic

Why jaundice is more severe / deep acute viral hepatitis than CLD ?

In CLD jaundice less because here hepatocyte are fibrosed

Mention the route of transfusion of HBV?

parental

Transfusion of blood and blood product

Sexual exposure

IV drug user Vertically from mother to child

39

A patient comes to you with deep jaundice for 1 ½

It may be due to hepatitis E virus

month what may be the cause?

Which viral hepatitis is dangerous in pregnancy and at which trimester

?

hepatitis E and at last trimester

Classification of acute hepatic failure

Hyperacute

< 7 days

Acute

8-28 days

Subacute

29 days-12 weeks

What do u mean by Non-A, non-B, non-C (NANBNC) or non-A-E hepatitis ?

Non-A-E hepatitis is the term used to describe hepatitis thought to be due to a virus that is not HAV, HBV, HCV or HEV.

Mention the anti viral therapy in hepatitis B virus ?

acute ---no antiviral therapy

chronic carrier -- no antiviral therapy and observe only

chronic active hepatitis anti viral therapy

Mention the criteria of and will be the treatment of carrier ?

Criteria for carrier

1. HBs Ag positive > 6months

2. ALT normal

3. HBV-DNA level undetectable

4. Biopsy: minimal hepatitis ( Knodal score )

5. anti- HBc ( + )

if all these are positive than it is carrier

What treat u will give the patient?

No treatment is needed Do the following

Patient will do normal activity

Stop smoking and alcohol consumption as it aggravate CLD

Do not donate blood

40

Sexual partner should be vaccinated

Breast feeding allowed

When will u tell chronic active hepatitis?

Chronic active hepatitis

1. HBs Ag positive > 6months

2. ALT > 2 times (persistent / intermittent )

3. HB e Ag +

4. HBV-DNA level > 10 5 copies

5. Biopsy: moderate / bridging hepatitis ( Knodal score )

A single test to diagnosed

Anti-HBC I g G

chronic viral hepatitis?

Name some anti-viral drug use in chronic hepatitis B virus?

Dug use in HBV

Interferons/ Pegylated interferons

Adefovir

Lamivudine

What will u do A patient comes to u with HBs Ag positive and wants to go foreign?

Or patient with HBs Ag positive and want to make it negative?

No , He cannot go to foreign as there is no chance of spontaneous Removal of HBs Ag( chance of spontaneous recovery 0.5% year )

Interferon can clear the virus 10 % per year , no role of oral anti viral therapy

Come to 6 month later and Repeat HBs Ag if positive then look for whether it carrier and chronic Active hepatitis

If doctors get needle is stick injury what

Will u do?

First see he is vaccinated or not

If not

o give immunoglobulin ( Ig G )

o Followed by active immunization

If doctors is immunized then see triter Do accordingly level of triter

41

what advise u will give to wife of HBsAg positive husband

Wife of HBs Ag + husband

Do HBs Ag of wife

Immunized her if negative

Until

If she become positive do not immunized her.

developing immunization ( 36 mon) pl. use

barrier contraceptic method

What will u do A HBs Ag + mother give birth a child?

Within

Both active and passive immunization should be done after delivery

24 hr s of Delivery give Ig G

What is cirrhosis?

Cirrhosis is defined pathologically as a diffuse liver abnormality characterized by fibrosis and abnormal regenerating nodules

Micronodular cirrhosis ---nodules about 1 mm in diameter (seen in alcoholic cirrhosis.)

Macronodular cirrhosis nodules is about > 1 mm in diameter

Mixed --- Both micro and macro nodular

What are causes of cirrhosis or CLD?

CAUSES OF CIRRHOSIS

TO remember ---ABCDEFGHI

A--- Alcohol

B---

o

Biliary

o

Primary biliary cirrhosis

C--- Chronic viral hepatitis (B or C)

D---Drug

E--- Endocrine - Wilson's disease

F--- Non-alcoholic fatty liver disease

Ggenetic- α1-antitrypsin deficiency

H--- Haemochromatosis

I---

o

Autoimmune liver disease/hepatitis

o

Primary sclerosing cholangitis

42

Mention the Complication of CLD?

1. Hepatic encephalopathy.

2. Ascites

3. Spontaneous bacterial peritonitis.

4. Hepatorenal syndrome.

5. Hepatopulmonary syndrome

6. Hepatocellular carcinoma

7. Portal hypertension.

o

Variceal haemorrhages.

o

Portal gastropathy

8. Coagulopathy and feature of hypersplenism

Mention The Factor Predisposing Hepatic Encephalopathy ?

To remember it BCDEF minus TOP

BBleeding from GIT haematemesis @ malaena C--- Constipation D---drug sedative, hypnotic, NSAID, E---electrolyte imbalance, hypokalaemia FFever indicate infection Minus top

T--- Trauma , Ooperation , Pparacentasis

What follow u will give in a patient with CLD in ur ward ?

Level of consciousness orientation & alternation sleep rhythm and

Jaundice

Dehydration

Flapping tremor

Pulse , BP, Cyanosis

Abdomen

o

Abdominal pain

o

Percussion distension

o

Bowel sound

o

Fever / Temp.

o

Constipation / bowel pass

o

Bladder (urine out put )

o

Rebound tenderness

Abdominal girth

Planter extensor

Daily weight

43

What investigation u want to done in case of CLD ?

Liver function test

SGPT------N / ↑

S.Bilirubin --- N / ↑

Prothrombin time— N / ↑

s.ablumin----

AG ratio---- alter Viral marker

HBs Ag

Anti-HBc Ig G

Anti-HCV

Imaging

USG of HBS and pancreasescoarse echo structure ,

o splenomegaly , ascites

Ascitic fluid study Transudative and SAAG > 1 .1

urine copper (Wilson's disease),

Serum ferritin in case of haemochromatosis

Endoscopy of upper GIT --- to see varcies

Write down the Treatment decompensate CLD?

Diet

o Salt restriction

o No fluid restriction until Na< 120 m mol / l

Diuretic

o

o

Paracentesis

o

o

spirolactone

or Combination spirolactone and frusemide

Aspiration of 2-5 L/ d ascitic fluid is safe

If more than 5 L is done in one day then need 6-8 gm albumin for each litre

Syp. Lactulose is given for bowel movement

Treatment of complication such as

SBP

Hepato-renal syndrome

Specific R x -- liver transplantation what is the definite treatment of CLD ?

liver transplantation

44

what is refractory ascites ?

failure to decrease wt loss 0.5 kg/d after 1 wk of max dose of combin diuretic (frusemide 160 ,spirolactone-400 )

How will u differentiate between acute and chronic viral hepatitis?

Acute viral hepatitis

Chronic viral hepatitis

Clinical

Prodrome present (nausea / vomiting /anorexia )

No prodome

Short HO < 1 month Jaundice present

Usually absent if present duration is > 3 month

No stigmata of CLD

Stigmata CLD present Ascites , splenomegaly , spider and gynaecomastia , testicular atrophy

Bio-chemical

Prothrombin time increased

Prothrombin time increased in Acute on chronic

Albumin and A:G ratio normal

hypoAlbuminia and A:G ratio alter

Viral marker HBs Ag + < 6 months

Viral marker HBs Ag + > 6 months

Anti-HBC I g G

negative

Anti-HBC I g G

positive

Imaging ( USG )

Shows liver Hypo echoic

Coarse echo structure

Inflammation of gall bladder (Chloe cystitis )

Ascites @ or Spleno-megaly

Normal

45

What the clinical signs are of decompensate CLD?

To remember JEA

Jjaundice

EEncephalopathy

A---Ascites

What is management hepatic encephalopathy? Or A patient with CLD suddenly become

unconscious

What is ur diagnosis?

Hepatic encephalopathy

Treatment of hepatic encephalopathy?

A, B, C

NGfeeding

Based on carbohydrate diet and protein restricted

IV fluid

o glucose containing fluid

injectable antibiotic

o ceftriaxone

H 2 blocker

syp . lactulose

enema simplex

inj. Vitamin K

What is 1 st neurological sign in encephalopathy?

Constructional apraxia (ask to draw star )

If the patient of CLD

develop fever and abdominal pain? what is your diagnosis ?

Spontaneous bacterial peritonitis (SBP)

How many organism is responsible for SBP and what is the organism?

Usually by single organism mostly Escherichia coli

46

Clinical feature is to remember -- BAFAR

BAbsence of bowel sound,

A- ascites,

Ffever,

A abdominal pain,

Rrebound tenderness

What is the treatment Treatment ?

o Broad spectrum antibiotic

o Injectable Cefotaxime or ceftriaxon

what is used for prophylacting

For Prophylactic antibiotic

o Norfloxacin (400 mg daily) or Ciprofloxacin (250 mg daily)

A patient with CLD suddenly comes to u recently appearing lump in the right upper abdomen .what is ur diagnosis ?

Hepatocellular carcinoma

What are sign of hepatic insufficiency?

What are the signs of portal hypertension?

Hepatic faces (sunken eye, Malar prominent)

To remember it keep mind SEA

SSlepnomegaly

Jaundice

EEngorged vein

Flapping tremor

o

Abdomen

Gynaecomastia

o

Esophageal varices

In case of female breast atrophy

AAscites

Spider nevi

Other

Loss of body and pubic hair

o

Fetor hepaticus ,

In hand

o

Hepatic encephalopathy

leukonychia.

 

Dupuytren's contracture

Palmar erythema

Testicular atrophy

47

How the portal vein is formed

It is formed by combination superior mesenteric vein and splenic vein

What is the normal portal pressure?

Normally 2-5 mmHg

Clinical features Developed when portal venous pressures above 12 mmHg What are blood supplies of liver

Liver has dual blood supply

2/3 is supplied by portal vein rich in nutrients

1/3 is supplied by hepatic artery rich in O 2 Oxygen supply of liver

Half of the oxygen supply is met by the portal vein and rest half by the hepatic artery

Complications of portal hypertension

to remember portal HTN HAV HCR

H- Hypersplenism

A- Ascites

V--Variceal bleeding (Oesophageal)

H-- Hepatic encephalopathy

C--Congestive gastropathy

R--Renal failure

Write down the causes of ascites

Exudative cause infection and malignancy

Transudative all causes of edema u look at ward

Infection

Nephrotic syndrome

o

Tuberculosis

CLD

o

Spontaneous bacterial Peritonitis

CCF

Malignancy

Malnutrition

Budd-Chiari syndrome

Protein-losing enteropathy

hepatic venous obstruction

Pancreatitis

Lymphatic obstruction

Hypothyroidism

48

CAUSE of HEPATOMEGALY:

Tender hepatomegaly

Non tender hepatomegaly

o