1. Hepatitis C after treatment
   • SVR assessment and post-treatment monitoring
   • Who still needs HCC surveillance
   • Reinfection versus relapse
2. Elastography
   • Principles, interpretation, liver stiffness cutoffs and limitations
   • Uses in fibrosis, portal hypertension, and follow-up
3. Recompensation in cirrhosis
   • Baveno VII definition and criteria
   • Prognostic significance and management implications
4. Acute versus chronic pancreatitis
   • Symptoms, causes, complications
   • Diagnostic criteria, labs, imaging choices
   • Acute management and chronic pancreatitis treatment
5. Septic shock
   • Definitions/stages and recognition
   • Initial resuscitation, fluid choice and amount
   • Vasopressors, antibiotics, monitoring, and source control
6. Hypogammaglobulinemia
   • Primary versus secondary causes
   • Clinical features, evaluation, and IVIG indications
7. Sepsis in a young patient without diabetes
   • Predisposing conditions and immune-deficiency workup
   • Key history, examination, labs, and causes not to miss
8. Neutropenic sepsis
   • Likely organisms by source and risk
   • Empiric antibiotic selection, escalation, antifungal therapy, and duration

Topic map

1. Hepatitis C after treatment
   • SVR12, relapse versus reinfection
   • Post-SVR LFT/HCV RNA monitoring
   • Cirrhosis, variceal and HCC surveillance
2. Elastography
   • Transient elastography, shear-wave elastography, MRE
   • Interpretation, indications, false elevation of liver stiffness
   • Portal hypertension and treatment response
3. Recompensation in cirrhosis
   • Baveno VII definition
   • Required clinical criteria
   • Implications for transplant referral and HCC surveillance
4. Acute vs chronic pancreatitis
   • Causes, symptoms, diagnostic criteria, laboratory tests
   • CT, MRCP, EUS indications
   • Resuscitation and feeding in acute pancreatitis
   • Pain, enzymes, diabetes and nutritional care in chronic pancreatitis
5. Septic shock
   • Sepsis-3 definition, clinical phases, lactate
   • First-hour bundle, balanced crystalloid dosing
   • Norepinephrine, vasopressin, hydrocortisone, source control
6. Hypogammaglobulinemia
   • Primary versus secondary causes
   • Investigations including vaccine antibody responses and lymphocyte subsets
   • IVIG/SCIG indications and infection prevention
7. Sepsis in a young person without diabetes
   • Primary immunodeficiencies, HIV, hematologic malignancy, drugs, anatomical defects, asplenia
   • Focused history, examination and baseline immune workup
8. Neutropenic sepsis
   • Definitions and risk stratification
   • Organisms and source-directed considerations
   • Empiric antipseudomonal beta-lactams, when to add vancomycin, antifungal treatment, G-CSF

1. Hepatitis C post-treatment monitoring
2. Elastography
3. Recompensation in cirrhosis
4. Acute vs chronic pancreatitis
5. Septic shock, stages and fluids
6. Hypogammaglobulinemia
7. Why a young non-diabetic patient gets sepsis
8. Neutropenic sepsis: organisms and antibiotics

• FCPS viva opening answer
• Definition and classification
• Clinical features
• Investigations
• Management with key doses where applicable
• Common viva questions with short model answers
• Examiner pitfalls and differentiating points

FCPS Part II Internal Medicine: Concise Viva Notes

1. Hepatitis C monitoring after treatment

Viva opening

At end of therapy / 12 weeks later

• Do quantitative HCV RNA and liver function tests at 12 weeks or later after treatment.
• Undetectable HCV RNA = virologic cure.
• If ALT/AST remain high despite SVR, look for another liver disease:
  • MASLD
  • Alcohol-related liver disease
  • HBV/HIV coinfection
  • Autoimmune hepatitis
  • Drug-induced liver injury
  • Hemochromatosis, etc.

Follow-up after SVR

• No routine liver-related follow-up required.
• Counsel alcohol abstinence or avoidance of excess alcohol.
• If ongoing exposure risk, do HCV RNA, not anti-HCV antibody, annually and whenever unexplained ALT elevation occurs.

• HCC surveillance: liver ultrasound with or without AFP every 6 months.
• Continue surveillance for portal hypertension/varices according to cirrhosis guidance.
• Continue routine cirrhosis care, including assessment for decompensation and transplant referral if indicated.

Relapse vs reinfection

• Relapse: same infection returns after end of therapy, usually soon after therapy and uncommon with DAAs.
• Reinfection: a new infection after SVR, especially with injecting-drug use or high-risk sexual exposure.
• Differentiate with risk history and, where needed, genotype/viral sequencing.

Common viva questions

2. Elastography and its uses

Definition

Types

1. Transient elastography: FibroScan, measures liver stiffness in kPa.
2. Point shear-wave elastography
3. Two-dimensional shear-wave elastography
4. Magnetic resonance elastography (MRE): most accurate but expensive and less available.

Principle

Main uses

• Noninvasive staging of liver fibrosis in:
  • Chronic HCV
  • Chronic HBV
  • MASLD
  • Alcohol-related liver disease
  • Autoimmune hepatitis and cholestatic liver disease
• Identification of advanced fibrosis/cirrhosis.
• Risk stratification for clinically significant portal hypertension.
• Monitoring change in stiffness after treatment or lifestyle intervention.
• Reducing the need for liver biopsy.

Interpretation

• Results are reported in kPa.
• Cutoffs differ according to etiology, machine, probe and clinical context.
• Low stiffness makes advanced fibrosis unlikely.
• Higher values suggest advanced fibrosis or cirrhosis, but are not diagnostic alone.

Causes of falsely high stiffness

• Acute hepatitis or high ALT
• Cholestasis
• Hepatic congestion/right heart failure
• Recent meal, hence fasting for about 3 hours is preferred
• Severe steatosis, obesity, technical failure
• Liver infiltrative disorders

Limitations

• Less reliable in ascites for transient elastography.
• Obesity can cause failed measurements, use XL probe if available.
• Cannot reliably distinguish inflammation from fibrosis during acute hepatic injury.
• Biopsy may still be needed if diagnosis is uncertain or competing liver diseases are suspected.

Common viva questions

3. Recompensation in cirrhosis

Definition

• HCV cure
• HBV suppression
• Alcohol abstinence
• Autoimmune hepatitis control
• Treatment of metabolic cause

Baveno VII clinical criteria

1. Removal, suppression or cure of the underlying cause
2. Sustained absence of decompensating events for at least 12 months, specifically:
   • No ascites, without diuretics
   • No hepatic encephalopathy, without lactulose/rifaximin
   • No recurrent variceal bleeding
3. Improved liver function, shown by improvement in bilirubin, INR and albumin.

Important point

• Improvement of ascites just because the patient is taking diuretics is not recompensation.
• Absence of encephalopathy while taking lactulose/rifaximin is not recompensation.
• A fall in MELD or Child-Pugh score alone is insufficient.

Clinical significance

• Better prognosis than persistent decompensation.
• But the patient still has cirrhosis:
  • Continue HCC surveillance every 6 months.
  • Assess portal hypertension.
  • Continue specialist follow-up.
  • Do not automatically delist from transplant pathway. Individualize based on portal hypertension, MELD, frailty and prior disease severity.

Common viva questions

4. Acute versus chronic pancreatitis

Acute pancreatitis: diagnosis

1. Typical acute epigastric pain
2. Serum lipase or amylase more than 3 times upper limit of normal
3. Imaging characteristic of acute pancreatitis

Acute pancreatitis: investigations

• CBC, hematocrit, urea/creatinine, electrolytes, glucose, calcium
• LFTs, especially ALT for biliary cause
• Serum triglycerides
• CRP at 48 hours for severity support
• ABG/VBG and lactate if severe
• Ultrasound for gallstones/biliary obstruction
• Contrast CT if diagnosis uncertain, severe disease, failure to improve, or suspected necrosis/complication. Do not routinely do early CT in straightforward cases.
• MRCP or EUS if choledocholithiasis is suspected but unclear.

Acute pancreatitis: treatment

• ABCDE, oxygen if hypoxemic, opioid analgesia and antiemetic.
• Balanced crystalloid, preferably Ringer lactate, with frequent reassessment.
• Start oral feeding early when tolerated. If unable to eat, enteral NG/NJ feeding is preferred to parenteral nutrition.
• Antibiotics are not prophylactic for sterile necrosis.
• Give antibiotics only for cholangitis, infected necrosis, pneumonia, UTI, bacteremia or another established/suspected infection.
• ERCP urgently if acute biliary pancreatitis with cholangitis; also consider for persistent biliary obstruction.
• Cholecystectomy during same admission in mild gallstone pancreatitis, after recovery.

Chronic pancreatitis: diagnosis

• CT pancreas: calcifications, ductal dilation, atrophy, pseudocysts.
• MRCP, preferably secretin-MRCP where available, for ductal anatomy.
• EUS detects early chronic pancreatitis and excludes malignancy.
• Fecal elastase supports exocrine pancreatic insufficiency.
• Check nutrition: albumin, fat-soluble vitamins A, D, E, K, B12, magnesium and bone density where indicated.

Chronic pancreatitis: treatment

• Strict alcohol cessation and smoking cessation.
• Stepwise analgesia. Consider neuropathic-pain agents such as pregabalin where appropriate.
• Pancreatic enzyme replacement for steatorrhea/malabsorption:
  • Start with approximately 40,000-50,000 units of lipase with each main meal and half the dose with snacks.
  • Take during meals.
  • Add PPI if response is incomplete.
• Nutritional support and vitamin replacement.
• Treat diabetes, recognizing high hypoglycemia risk due to loss of glucagon response.
• Endoscopic therapy for duct stones/strictures or pseudocysts in selected patients.
• Surgical drainage/resection for obstructive disease or refractory pain after multidisciplinary assessment.
• Always exclude pancreatic cancer in a new change of pain, weight loss, progressive jaundice or new diabetes.

Common viva questions

5. Septic shock: stages, treatment and fluids

Definitions

• Sepsis: life-threatening organ dysfunction due to a dysregulated host response to infection.
• Septic shock: sepsis with persistent hypotension requiring vasopressors to maintain MAP at least 65 mmHg, and lactate more than 2 mmol/L, despite adequate fluid resuscitation.

Clinical phases often asked in viva

1. Early warm shock
   • Fever, tachycardia, warm peripheries, bounding pulse
   • Vasodilatation, high or normal cardiac output, low SVR
2. Late cold shock
   • Cool mottled peripheries, weak pulse, oliguria, altered sensorium
   • Myocardial depression, low output, worsening tissue hypoperfusion
3. Refractory shock
   • Persistent hypoperfusion despite fluids, vasopressors and source control
   • Multiorgan dysfunction, severe lactic acidosis

First-hour approach

• ABCDE, call senior/ICU help.
• Measure lactate and repeat if initially elevated.
• Take blood cultures and appropriate source cultures before antibiotics if this does not delay treatment.
• Start broad-spectrum IV antimicrobials immediately, ideally within 1 hour in shock.
• Identify and control source urgently:
  • Drain abscess
  • Remove infected line
  • Relieve obstructed urinary system
  • Debride necrotizing infection
  • ERCP for cholangitis
  • Surgery for perforation/peritonitis

Fluids

• Give at least 30 mL/kg IV crystalloid within the first 3 hours for septic shock/sepsis-induced hypoperfusion, then reassess repeatedly.
• Prefer a balanced crystalloid, such as Ringer lactate or Plasma-Lyte.
• Use smaller boluses and more frequent reassessment in heart failure, advanced CKD, cirrhosis or obvious fluid overload.
• Use dynamic assessment of fluid responsiveness:
  • Passive leg raise with stroke volume/cardiac output response
  • Bedside echocardiography
  • Stroke-volume variation or pulse-pressure variation in appropriate ventilated patients
• Do not use hydroxyethyl starch.
• Consider albumin only if very large crystalloid amounts are needed.

Vasopressors

1. Norepinephrine first-line, start early if hypotension persists or while fluid is being given.
2. Target MAP ≥65 mmHg initially.
3. Add vasopressin 0.03 units/min if norepinephrine requirement is rising.
4. Add epinephrine if MAP remains inadequate.
5. If cardiac dysfunction with persistent hypoperfusion despite adequate MAP/volume status, consider dobutamine.

Other measures

• Hydrocortisone 200 mg/day IV, for vasopressor-dependent shock despite adequate fluid and vasopressor therapy. Example: 50 mg IV every 6 hours.
• Maintain glucose generally around 140-180 mg/dL in ICU.
• DVT prophylaxis, stress-ulcer prophylaxis when indicated, renal support if needed.
• De-escalate antibiotics using culture data and clinical response.

Common viva questions

6. Hypogammaglobulinemia

Definition

Clinical clues

• Recurrent bacterial sinopulmonary infections
• Recurrent otitis, sinusitis, pneumonia, bronchiectasis
• Infection with encapsulated bacteria:
  • Streptococcus pneumoniae
  • Haemophilus influenzae
• Chronic giardiasis
• Chronic diarrhea/malabsorption
• Poor response to vaccines
• Autoimmune disease, lymphadenopathy or splenomegaly in CVID
• Recurrent severe viral infections may suggest combined immune deficiency

Causes

• X-linked agammaglobulinemia/Bruton disease
• Common variable immunodeficiency, CVID
• Selective IgA deficiency
• Hyper-IgM syndromes
• Combined immunodeficiency
• WHIM syndrome: warts, hypogammaglobulinemia, infections, myelokathexis

• CLL, lymphoma, multiple myeloma
• Rituximab and other B-cell-depleting therapy
• Steroids, immunosuppressants, chemotherapy
• Nephrotic syndrome
• Protein-losing enteropathy
• Severe burns
• Malnutrition
• HIV and other immunodeficiency states

Evaluation

• CBC with differential and peripheral smear
• Quantitative IgG, IgA, IgM
• Serum protein electrophoresis and immunofixation
• HIV test
• Renal function, urinalysis/proteinuria
• LFT, albumin and stool evaluation if protein-losing enteropathy suspected
• Lymphocyte subsets: B, T and NK cells
• B-cell phenotyping, including memory B cells if available
• Specific antibody response to vaccines:
  • Pneumococcal polysaccharide
  • Tetanus/diphtheria
• HRCT chest if recurrent infections/bronchiectasis
• Evaluate CLL/lymphoma/myeloma if appropriate

Management

• Treat active infection promptly and culture where possible.
• Vaccinate appropriately, but avoid live vaccines in significant combined immunodeficiency.
• Regular airway clearance and management of bronchiectasis.
• Antibiotic prophylaxis in selected recurrent-infection cases.
• Immunoglobulin replacement when there is low IgG plus recurrent/severe infections or poor specific antibody response:
  • IVIG commonly 400-600 mg/kg every 3-4 weeks, individualized to infections and trough IgG.
  • SCIG is an alternative.
• Treat the secondary cause where possible.

Common viva questions

7. Young patient with sepsis without diabetes: why?

Viva opening

Causes to consider

A. Immunodeficiency

• HIV
• Primary antibody deficiency, such as CVID or X-linked agammaglobulinemia
• Complement deficiency, especially recurrent invasive meningococcal disease
• Asplenia or functional hyposplenism:
  • Previous splenectomy
  • Sickle-cell disease
• Neutrophil disorders:
  • Congenital neutropenia
  • Cyclic neutropenia
  • Chronic granulomatous disease
• T-cell/combined immunodeficiency
• Immunosuppressive drugs:
  • Steroids
  • Biologics, especially anti-TNF agents
  • Rituximab
  • Chemotherapy
• Malnutrition and alcohol/substance use

B. Hematologic and malignant disease

• Acute leukemia
• Lymphoma
• Aplastic anemia
• Neutropenia due to drugs or viral illness

C. Anatomic/device-related source

• Obstructed urinary tract or stones
• Congenital urinary tract abnormality
• IV line, dialysis access or prosthetic device
• Endocarditis related to IV drug use
• Bronchiectasis, CSF leak or recurrent aspiration
• Skin/soft tissue infection, perianal abscess

D. Specific infection/exposure

• Meningococcemia in complement deficiency/asplenia
• Severe pneumococcal sepsis in asplenia or antibody deficiency
• Staphylococcal toxic shock
• Malaria, dengue, leptospirosis, enteric fever according to geography and exposure
• Tuberculosis or fungal infection in immunodeficiency

Focused work-up

• Detailed history:
  • Previous severe/recurrent infections
  • Childhood infection history
  • Family history/consanguinity
  • Splenectomy, sickle-cell disease
  • Drug/biologic use, IV drug use
  • Weight loss, night sweats, lymphadenopathy
  • Sexual history/HIV risk
  • Travel, animal, water and occupational exposure
• Examination:
  • Splenectomy scar, lymph nodes, hepatosplenomegaly
  • Skin lesions, injection marks
  • Heart murmur/endocarditis signs
  • Perianal and line examination
• Investigations:
  • CBC with differential and smear
  • HIV Ag/Ab
  • HbA1c despite no known diabetes
  • Immunoglobulins
  • Lymphocyte subsets
  • Complement screen: CH50/AH50 if recurrent Neisseria
  • Blood/urine/sputum cultures, imaging for source
  • Echocardiography if endocarditis suspected
  • Peripheral smear/hematology assessment if cytopenias

Common viva questions

8. Neutropenic sepsis: organisms and antibiotic choice

Definitions

• Neutropenia: ANC <1500 cells/mm³.
• Severe neutropenia: ANC <500 cells/mm³.
• Profound neutropenia: ANC <100 cells/mm³.
• Febrile neutropenia: single oral temperature ≥38.3°C, or ≥38.0°C sustained for 1 hour, with ANC <500 or expected to fall below 500.

Likely organisms

• Pseudomonas aeruginosa
• E. coli
• Klebsiella
• Enterobacter species
• Acinetobacter in hospital-acquired disease
• ESBL-producing Enterobacterales depending on local epidemiology

• Coagulase-negative staphylococci, particularly central-line related
• Staphylococcus aureus, including MRSA where prevalent
• Viridans streptococci, particularly with mucositis
• Enterococcus

• Candida
• Aspergillus, especially prolonged neutropenia, steroid exposure, hematologic malignancy, or persistent fever despite antibiotics

• HSV and VZV with mucositis/vesicular lesions
• Respiratory viruses
• Anaerobes in typhlitis, perianal sepsis or abdominal source

Immediate assessment

• ABCDE and sepsis screen.
• Cultures: at least two blood cultures, preferably peripheral plus each central-line lumen, plus cultures from relevant source.
• CBC/differential, renal/liver function, CRP, lactate.
• Urine tests/culture if indicated.
• CXR if respiratory symptoms. CT chest if persistent fever or suspicion for fungal disease.
• Examine oral cavity, skin, line sites, lungs, abdomen and perianal region. Avoid rectal examination and rectal thermometers because of mucosal injury risk.

Empiric antibiotics: high-risk/inpatient

• Piperacillin-tazobactam 4.5 g IV every 6-8 hours, according to local protocol and renal function
  or
• Cefepime 2 g IV every 8 hours
  or
• Meropenem 1 g IV every 8 hours if unstable, previous ESBL/resistant gram-negative infection or high local resistance.

When to add vancomycin or alternative anti-MRSA therapy

• Hemodynamic instability/septic shock
• Suspected catheter-related infection
• Skin/soft tissue infection
• Pneumonia
• Known MRSA colonization/infection
• Severe mucositis with likely viridans streptococcal infection in a patient exposed to fluoroquinolone prophylaxis
• Positive gram-positive blood culture pending identification

Special clinical situations

• Typhlitis/neutropenic enterocolitis: piperacillin-tazobactam or carbapenem provides anaerobic cover. If cefepime used, add metronidazole.
• Perianal infection: ensure gram-negative and anaerobic coverage; early surgical consultation.
• Suspected line infection: add vancomycin and assess line removal.
• Persistent fever after 4-7 days of appropriate antibiotics with prolonged neutropenia: evaluate for invasive fungal infection. Start empiric/pre-emptive antifungal treatment based on risk and imaging:
  • Echinocandin for suspected candidiasis
  • Voriconazole or liposomal amphotericin B if invasive aspergillosis is suspected, depending on context.

Low-risk outpatient patients

• Oral ciprofloxacin plus amoxicillin-clavulanate is one recognized regimen.
• Do not use this if prior fluoroquinolone prophylaxis, instability, pneumonia, abdominal syndrome, central-line concern, major comorbidity or inability to return urgently.

G-CSF

• Not routinely used as treatment for every febrile-neutropenia episode.
• Consider in high-risk patients, such as profound/prolonged neutropenia, age >65, uncontrolled infection, pneumonia, hypotension/multiorgan dysfunction, invasive fungal infection, or anticipated delayed marrow recovery.
• More important role is primary prophylaxis when chemotherapy regimen risk of febrile neutropenia is high.

Common viva questions