BAYONETO, JULLIANNE MARIE C.

FREQUENTLY ASKED QUESTIONS DURING CONSULTANT AND RESIDENT ROUNDS

CARDIOLOGY:
1. How is heart failure classified?
○ Heart failure is classified based on the measured ejection fraction.
i. Heart failure with preserved ejection fraction (EF > 50%)
ii. Heart failure with mildly reduced ejection fraction (EF 40-49%)
iii. Heart failure with reduced ejection fraction (<40%)
2. What are the 4 Pillars of heart Failure (HFrEF) management?
● Angiotensin receptor neprilysin inhibitor
● Beta-blockers
● Mineralocorticoid receptor antagonist
● Sodium glucose cotransporter 2 inhibitor
3. What are the causes of high output cardiac failure?
● Obesity
● Liver disease
● Arteriovenous shunts
● Lung disease
● Myeloproliferative disorder
4. How to differentiate Stable angina from Acute Coronary Syndrome?
● Stable angina can be differentiated from acute coronary syndrome by checking for cardiac markers,
troponin I is elevated in cases of acute coronary syndromes while in unstable angina, it is within the
normal range. Acute coronary syndromes usually present upon exertion while unstable angina may
happen even at rest.
5. How to differentiate the different Acute Coronary Syndromes?
○ Acute coronary syndromes may be differentiated by its presentation in ECG wherein in STEMI,
there is a widely visible ST segment elevation while in NSTEMI, there can be non specific ST
segment elevations. It is also characterized based on the degree of ischemia noted where STEMI
would have transmural necrosis due to severe occlusion while NSTEMI will present with area of
necrosis due to decreased perfusion.
6. What medications comprise the ACS Regimen? How is it given? What are the loading doses? Maintenance
doses? Why are high dose statins given?
○ Oral antiplatelet therapy
i. Aspirin- initial loading dose of 165- 325 mg in non enteric form, chewed; 80-162 mg OD
maintenance
ii. Clopidogrel- loading dose of 300-600mg; followed by 75mg/dl OD x 1 year
○ Anticoagulant therapy
i. Unfractionated heparin- initial dose 60 U/kg IV bolus (max 4000U); 12 U/kg in 48 hrs or
until PCI is done
ii. Enoxaparin: 30mg IV loading dose; 1mg/kg SC q12 for duration of hospitalization or until
PCI is performed
○ High dose statin
i. Atorvastatin 40-80mg OD PO
○ High dose statins are given due to its mechanism of action of inhibition of HMG-coA reductase
which prevents further cholesterol synthesis. It lowers the chance of thrombus formation due to
plaque.
7. Why are nitrates contraindicated in Right ventricular wall infarction?
○ Nitrates can decrease preload leading to decreased cardiac output. Intake of nitrates can lead to
significant hypotension on patients with right ventricular wall infarction.
8. What are the 3 different reperfusion strategies?
○ Percutaneous intervention
○ Angioplasty
○ Fibrinolysis
9. What is the recommended Door to ECG, Door to Needle, Door to Balloon time (primary and non-primary
PCI capable hospital) in the management of STEMI
○ Door to ECG: within 10 mins
○ Door to needle: < 30 mins
○ Door to balloon time: 90 mins
10. What are the 4 Malignant arrhythmias? What are the shockable rhythms? Non-shockable rhythms?
 4 Malignant Arrhythmia
● Ventricular fibrillation.
● Ventricular tachycardia.
● Premature ventricular beats (PVCs)
● Torsades de pointes
Shockable rhythms
● ventricular fibrillation (VF)
● pulseless ventricular tachycardia (VT)
Non-shockable rhythms
● Sinus rhythm (SR)
● Supraventricular tachycardia (SVT)
● Premature ventricular contraction (PVC)
● Atrial fibrillation (AF)
11. Drug of choice and dose for stable supraventricular tachycardia? For unstable SVT? (See algorithm)
○ Adenosine is the primary drug used in the treatment of stable narrow-complex SVT
(Supraventricular Tachycardia). Now, adenosine can also be used for regular monomorphic wide-
complex tachycardia.
When given as a rapid IV bolus, adenosine slows cardiac conduction particularly affecting
conduction through the AV node. The rapid bolus of adenosine also interrupts reentry (SVT
causing) pathways through the AV node and restores sinus rhythm in patients with SVT.
○ Amiodarone- for unstable SVT

12. Drug of choice for symptomatic bradycardia?

○ Atropine
13. How are Heart murmurs graded?

○
14. How is JVP Measured?
The technique for examination for CVP (central venous pressure). Assess the vertical distance
between the sternal angle and the top of the pulsation point of the IJV (in healthy
individuals, this should be no greater than 3cm).
1. Patient reclining with head elevated 45 °
○ Measure elevation of neck veins above the sternal angle (Lewis Method).
○ Add 5 cm to measurement since the right atrium is 5 cm below the sternal angle.
2. Normal CVP <= 8 cm H2OLight should be tangential to illuminate highlights and shadows.
3. Neck should not be sharply flexed.
4. Using a centimeter ruler, measure the vertical distance between the angle of Louis (manubrio sternal joint)
and the highest level of jugular vein pulsation. A straight edge intersecting the ruler at a right angle may be
helpful.
○ Note: Ability to measure jugular venous pressure will be difficult if pulse is >100 per minute.
5. If the internal jugular vein is not detectable, use the external jugular vein. The internal jugular vein is the
preferred site.

15. How is cardiac tamponade diagnosed?

○ Echocardiography (TTE or FATE)
16. What comprises the Becks Triad?
● Jugular vein distention
● Hypotension
● Muffled heart sounds
17. What is the difference between Dihydropyridine and non-dihydropyridine calcium channel blockers?
Example of each?
 18. What are the criteria to say that the rhythm is sinus?

PULMONOLOGY:
1. What are the 4 types of respiratory failure?

Type 1: Hypoxemic PaO2 is low (< 50 mmHg)

Respiratory Failure CO2 is not elevated (< 60 mmhg)
Usually from alveolar flooding with intrapulmonary shunting
Alveolar flooding may be a consequence of:
● Pulmonary edema (cardiogenic or non-cardiogenic)
● Pneumonia
 ● Pulmonary (alveolar) hemorrhage
● ARDS

Type 2: Hypercapnic PaO2 is low (< 50 mmHg)

Respiratory Failure CO2 is elevated (> 60 mmhg)
Result of alveolar hypoventilation and leads to the inability to eliminate carbon
dioxide effectively
● Diminished CNS drive to breathe
● Reduced strength of neuromuscular function
● Increased overall load in the respiratory system

Type 3: Pre- FRC fails below closing volume as a result of Atelectasis.

operative Contributing factors: supine posture, Gen. Anesthesia, Depressed cough reflex,
Respiratory Failure Splinting due to pain

Type 4: Shock with Results from hypoperfusion of respiratory muscles in patients in shock
Hypoperfusion (respiratory muscles normally consume <5% of the total cardiac output and O2
delivery)

The proportion of the cardiac output to the respiratory muscles rises by as much
as ten-fold when the work of breathing is high; this can seriously impair coronary
perfusion during shock.

2. What is the criteria in the diagnosis of ARDS? How is ARDS classified?

How to compute the PF Ratio? How to compute the desired FiO2?

PFR = PaO2/FiO2
Desired FiO2 = (current FiO2 x Desired PaO2) / Current PaO2
3. What are the different causes of exudative and transudative pleural effusion? Its mechanism?

PLEURAL EFFUSION:
● Excess quantity of fluid in the pleural space
● Most common cause of pleural effusion is left ventricular failure
 ● Transudative effusion: occurs when systematic factors that influence the absorption of pleural
fluid are altered

● Exudative effusion: occurs when local factors that influence formation and absorption of pleural
fluid are altered
○ Parapneumonic Effusion
■ Bacterial Pneumonia
■ Lung Abscess
■ Bronchiectasis
■ Empyema
○ Effusion secondary to malignancy
○ Effusion secondary to pulmonary embolism
○ Tuberculosis Pleuritis
○ Hemothorax
● Clinical Manifestations of PE:
○ Patients may present with pleuritic pain, cough and dyspnea
○ Findings include decreased breath sounds with decreased or absent tactile fremiti and
dullness on percussion
○ Tracheal deviation and pleural rub may also be noted
4. How to interpret pleural fluid analysis using Lights Criteria?
5. How to diagnose pulmonary tuberculosis? How to manage

6. How is Community Acquired pneumonia classified? What are the different antibiotic options?

Risk Stratification Potential Pathogens Empiric Therapy

 Low-risk CAP Streptococcus pneumoniae
Haemophilus influenza
Chlamydphila pneumoniae
Mycoplasma pneumoniae
Moraxella catarrhalis
Enteric Gram-negative bacilli
(among those with co-morbids)
Previously healthy:
Amoxicillin or extended macrolides
(suspected atypical pathogen)
With stable comorbid illness:
β-lactam / β-lactamase inhibitor
combination (BLIC) or second- generation
oral cephalosporin + extended macrolides

Alternative:
Third-generation oral cephalosporin +
extended macrolide

Moderate-risk CAP Streptococcus pneumoniae IV non-antipseudomonal β-lactam

Haemophilus influenza
Chlamydphila pneumoniae
Mycoplasma pneumoniae
Moraxella catarrhalis
Enteric Gram-negative bacilli
Legionella pneumophila
Anaerobes (risk of aspiration)
(BLIC, cephalosporin or carbapenem)
+ extended macrolide
or
IV non-antipseudomonal β-lactam + IV
extended macrolide or IV respiratory FQ

High-risk CAP Streptococcus pneumoniae No risk for P. aeruginosa:

Haemophilus influenza
Chlamydphila pneumoniae
Mycoplasma pneumoniae
Moraxella catarrhalis
Enteric Gram-negative bacilli
Legionella pneumophila
Anaerobes (risk of aspiration)
Staphylococcus aureus
Pseudomonas aeruginosa
IV non-antipseudomonal β-lactam +IV
extended macrolide or IV respiratory
FQ
With risk for P. aeruginosa:
IV antipneumococcal antipseudomonal
β-lactam + IV extended macrolide +
aminoglycoside
or

IV antipneumococal antipseudomonal
β-lactam + IV ciprofloxacin/levofloxacin
(high-dose)

1. Extended macrolides: azithromycin dehydrate, clarithromycin

2. Oral β-lactam/β-lactamase inhibitor (BLIC): amoxicillin-clavulanic acid, amoxicillin-sulbactam, sultamicillin
3. Oral second-generation cephalosporin: cefaclor, cefuroxime axetil
4. Oral third-generation cephalosporin: cefdinir, cefixime, cefpodoxime proxetil
5. IV non-antipseudomonal β-lactam (BLIC, cephalosporin or carbapenem): amoxicillin-clavulanic acid, ampicillin-
sulbactam, cefotiam, cefoxitin, cefuroxime Na, cefotaxime, ceftizoxime, ceftriaxone, ertapenem
6. Respiratory fluoroquinolones: levofloxacin, moxifloxacin
7. IV antipneumococal, antipseudomonal β-lactam (BLIC, cephalosporin or carbapenem): cefoperazone-
sulbactam, piperacillin-tazobactam,
ticarcillin-clavulanic acid, cefipime, cefpirome, imipenem-cilastatin, meropenem
8. Aminoglycosides: gentamicin, tobramycin, netilmicin, amikacin

7. Most common cause of community acquired pneumonia?

Most common access: Aspiration from the oropharynx
Most common isolate in Blood CS: S. pneumoniae

8. What are the different atypical organisms that cause atypical pneumonia? Why are they called “Atypical”?
What is the drug of choice?
9. How to diagnose Hospital Acquired pneumonia? What empiric antibiotics can be given?

Hospital-Acquired Pneumonia (HAP)— >48 hours

● Episodes of pneumonia not associated with mechanical ventilation
● HAP in non-intubated patients, both inside and outside the ICU, is similar to VAP save for the
higher frequency of non-MDR pathogens and better underlying host immunity in non-intubated
patients → the lower frequency of MDR pathogens allows monotherapy in a majority of HAP cases
● The only pathogens that may be more common in the non-VAP population are the anaerobes (due
to a higher risk of macroaspiration)
● More difficult to obtain lower respiratory samples appropriate for culture in non-intubated patients

10. What is the definition of Ventilator Associated Pneumonia?

Ventilator-Associated Pneumonia (VAP)

● The greatest difference between VAP and HCAP/HAP is the return to dependence on
expectorated sputum for a microbiologic diagnosis of VAP, which is further complicated by
frequent colonization by pathogens in patients with HAP or HCAP
● Common pathogenic mechanisms include oropharyngeal colonization with pathogenic bacteria,
cross-infection from other colonized patients, large volume aspiration, microaspiration around ET
tub and altered lower respiratory host defenses
● Clinical manifestations: same in VAP as with any other forms of pneumonia: fever, leukocytosis,
increase in secretions, and pulmonary consolidation on PE, along with a new or changing
radiographic infiltrate

11. What are the lung protective strategies in intubated patients?

a. Tidal volume is set at 6ml/kg of predicted body weight
b. Volutrauma is avoided by setting plateau pressure at <30cm H2O
c. PEEP is maintained at >5cm H2O. For estimated BMI > 30, PEEP is set at 8cmH2O; BMI > 40
PEEP at 10cm H2O
d. FiO2 set at 30-40 after intubation
e. Respiratory rate is limited to 20-30 cycles per minute
f. Aspiration precautions are also observed

12. FEV1, FVC, and FEV1/FVc between Obstructive and Restrictive lung diseases
INFECTIOUS DISEASES:
1. What is the 1-hour bundle of care in patients with Septic Shock?
2. What comprises the qSOFA?
Three criteria:
1. Hypotension (SBP ≤100 mmHg)
2. Altered Mental Status (GCS <15)
3. Tachycardia (≥22 breaths per minute)
3. What is the latest definition of Sepsis and Septic Shock?
The new recommendations define sepsis as life-threatening organ dysfunction due to a dysregulated host
response to infection. Septic shock is defined as a subset of sepsis in which particularly profound circulatory,
cellular, and metabolic abnormalities substantially increase mortality.
4. What is the difference between Prophylactic, Empiric, and Definitive Antibiotics?

Empiric Definitive Prophylactic

● Infecting organism/s not yet ● Organism/s identified and ● Prevent an initial infection or
identified specific therapy chosen its recurrence after infection
● More “broad spectrum” ● More “narrow” spectrum

5. What antibiotics have ANTI PSEUDOMONAL COVERAGE? Drug of choice of ESBL? Drug of choice for
MRSA?
a. Drug of choice of ESBL: Carbapenems
b. Drug of choice for MRSA: Vancomycin
 6. Drug of choice for VRSA?
Quinupristin-dalfopristin and lineolid are the two newer antimicrobial agents currently available with activity
against drug-resistant staphylocci (including most VISA and VRSA strains in vitro).
7. What is the difference between Ertapenem vs Meropenem/Imipenem?
Imipenem, were often susceptible to degradation by the enzyme dehydropeptidase-1 (DHP-1) located in
renal tubules and required co-administration with a DHP-1 inhibitor such as cilastatin. Later additions to the
class such as meropenem, ertapenem and doripenem demonstrated increased stability to DHP-1 and are
administered without a DHP-1 inhibitor.
Carbapenems (imipenem, meropenem, doripenem) possess broad-spectrum in vitro activity, which includes
activity against many Gram-positive, Gram-negative and anaerobic bacteria; carbapenems lack activity
against Enterococcus faecium, methicillin-resistant Staphylococcus aureus and Stenotrophomonas
maltophilia
Compared with imipenem, meropenem and doripenem, the spectrum of activity of ertapenem is more limited
primarily because it lacks activity against Pseudomonas aeruginosa and Enterococcus spp.

8. How to interpret culture results?

Identify the details of the patient, sample (sputum, bood, etc)
Identify the bacteria (gram negative, positive)
Identify specific bacteria by specific culture media
Identify antibiotic susceptibility
9. What are the different phases of dengue? What complications may arise in each phase?
Febrile phase - The febrile phase of DENV infection is characterized by sudden high-grade fever (≥38.5°C)
accompanied by headache, vomiting, myalgia, arthralgia, and a transient macular rash in some cases
Critical phase - The vast majority of infections that progress to a critical phase result from second DENV
infections that occur more than 18 months after a resolved first infection. However, a subset of critical
infections occur in children less than one year of age, at the time maternal antibody is below protective
levels and the child experiences a primary wild type infection. Hemorrhagic manifestations may be observed
in the febrile phase and/or critical phase.
Recovery phase - During the recovery phase, plasma leakage and hemorrhage resolve, vital signs stabilize,
and accumulated fluids are resorbed. An additional rash (a confluent, erythematous eruption with small
islands of unaffected skin that is often pruritic) may appear during the recovery phase (within one to two
days of defervescence and lasting one to five days).
10. What is the modified dukes criteria in the diagnosis of infective endocarditis?

11. What is febrile neutropenia? How is neutropenia classified? How to compute for Absolute Neutrophil Count?
Neutropenic fever is defined as a single oral temperature greater than or equal to 101 F, or a temperature
greater than or equal to 100.4 F for at least an hour, with an absolute neutrophilic count (ANC) of less than
1500 cells/microliter.

In adults, the lower limit of normal neutrophils is 1500 neutrophils per microliter of blood; any number below
that is considered neutropenia. Neutropenia grows more severe as the absolute neutrophil count declines
from 1500 to 1000 or even below 500.
 12. What is the criteria to diagnose fever of unknown origin? What are the common causes?
1. Fever ≥38.3°C (≥101°F) on at least two occasions

2. Illness duration of ≥3 weeks

3. No known immunocompromised state

4. Diagnosis that remains uncertain after a thorough history-taking, physical examination, and the following
obligatory investigations: determination of erythrocyte sedimentation rate (ESR) and Creactive protein (CRP)
level; platelet count; leukocyte count and differential; measurement of levels of hemoglobin, electrolytes,
creatinine, total protein, alkaline phosphatase, alan ine aminotransferase, aspartate aminotransferase,
lactate dehydrogenase, creatine kinase, ferritin, antinuclear antibodies, and rheumatoid factor; protein
electrophoresis; urinalysis; blood cultures (n = 3); urine culture; chest x-ray; abdominal ultrasonography; and
tuberculin skin test (TST) or interferon γ release assay (IGRA).
13. What is the screening test for HIV? What is the confirmatory test?
Screening test: ELISA Test
Confirmatory: Western Blot
14. How is HIV categorized? What is AIDS? What is the CD4 Count in AIDS?

The final phase of HIV is progression to AIDS, characterized by a breakdown of host defense, a dramatic increase in
viral load, and severe, life threatening clinical disease.
Typical presentation:
● Long lasting fever (>1 month)
● Fatigue
● Weight loss
● Diarrhea
● Generalized lymph node enlargement
15. What is the prophylaxis for Pneumocystis jirovecii? What CD4 level should we start prophylaxis? What is the
difference between the prophylactic and treatment doses of Pneumocystis infection? How long should we
give prophylaxis?
Trimethoprim-sulfamethoxazole (TMP-SMX) is the recommended first-line agent for PCP prophylaxis based upon its
proven efficacy

Treatment
TMP-SMX (15 to 20 mg/kg/day of the trimethoprim component) orally or IV given in three or four divided doses
Prophylaxis
1 DS tablet daily (DS: double-strength oral tablet, 160 mg trimethoprim with 800 mg sulfamethoxazole)
1 SS tablet daily (SS: single-strength oral tablet, 80 mg trimethoprim with 400 mg sulfamethoxazole)
 16. What is the indication of giving steroids in patients with pneumocystis infection?
Corticosteroids are used as adjunctive initial therapy only in patients with HIV infection who have severe
PJP.
17. What is the prophlaxis for Mycobacterium avium complex (MAC)? What CD4 level warrants prophylaxis?
What is the dose and frequency?
Mycobacterium avium complex (MAC) causes disseminated disease in up to 40% of patients with advanced
human immunodeficiency virus (HIV) disease in the United States. A U.S. Public Health Service Task Force
convened to address the prophylaxis and therapy of MAC recommends that patients with HIV infection and
less than 100 CD4+ T-lymphocytes/uL be administered prophylaxis against MAC. The recommended
regimen is rifabutin, 300 mg by mouth daily, for the patient's lifetime. If disseminated MAC develops, a
treatment regimen containing clarithromycin or azithromycin and at least one other agent is recommended.
Diagnosis, therapy, and prophylaxis for HIV-infected children follow similar guidelines.

NEPHROLOGY
1. How do you classify Acute Kidney Injury? Examples of each.
● PRE-RENAL
○ Caused by reduction of blood flow to the kidney.
○ May be part of systemic hypoperfusion resulting from hypovolemia or hypotension.
○ Tubular and glomerular function tend to stay normal
○ Examples:
■ Hypovolemia caused by hemorrhage, severe burns, diarrhea, etc.
■ Hypotension from decreased cardiac output: cardiogenic shock, acute
coronary syndrome
■ Hypotension from systemic vasodilation: septic shock, anaphylaxis
■ Renal vasoconstriction: NSAIDs, iodinated contrast, amphotericin B,
calcineurin inhibitors, hepatorenal syndrome
■ Glomerular efferent arteriolar vasodilation: ACE i’s, ARBs
● INTRINSIC
○ Include conditions that affect the glomerulus or tubule that is associated with the release
of vasoconstrictors from the renal afferent pathways.
○ Examples:
■ Acute tubular necrosis
■ Acute interstitial nephritis
■ Glomerulonephritis
■ Intratubular obstruction
● POST-RENAL
○ Mainly include obstructive causes which lead to congestion of the filtration system leading
to a shift in the filtration driving forces.
○ Examples:
■ Renal/ureteral calculi
■ Tumors
■ Blood clots
2. What is the difference between pre renal and renal AKI based on the BUN-Creatinine Ratio? How to
compute for the BCR?
a. For prerenal causes, BUN-Creatinine ratio is often increased due to decreased renal perfusion
secondary to hypovolemia or hypotension. BCR > 15:1
b. For post renal causes, BCR is often decreased due to obstruction. BCR <15:1

3. What is the definition of AKI?

- Acute Kidney Injury (AKI) is defined by the impairment of kidney filtration and excretory function
over days to weeks, resulting in the retention of nitrogenous and other waste products normally
cleared by the kidneys. AKI can result in accumulation of water, sodium, and other metabolic
products which may result in several electrolyte imbalance.

4. What are the different indications of EMERGENCY Hemodialysis?

- Severe hyperkalemia which is resistant to medical therapy
- Pulmonary edema refractory to medical therapy
- Worsening severe metabolic acidosis (pH < 7.2 or > 10)
5. What should be the urine output inorder to say that it is inadequate?
- Inadequate urine output or oliguria, is defined as a 24-hour urine output <400 mL or less than 20
mL/hr.

6. What are the different medications that can be given in patients with hyperkalemia? How can these
medications help with hyperkalemia?
- As per Harrison’s, the treatment of hyperkalemia is divided into three stages:
1. Immediate antagonism of the cardiac effects of hyperkalemia
IV 10% Calcium gluconate IV serves to protect the heart as it raises the cardiac
action potential threshold and reduces excitability, without changing the resting membrane
potential.
2. Rapid reduction in plasma K+ concentration by redistribution into cells.
Insulin lowers plasma K+ concentration by shifting K+ into cells. The
recommended dose for Regular Insulin is 10 units via IV followed immediately by 50 mL of
50% dextrose. Addition of beta-2 agonists such as Nebulized Albuterol 10-20 mg in 4 mL
of normal saline has an additive effect on plasma K+ concentration
3. Removal of potassium
This is typically accomplished using cation exchange resins, diuretics, and/or
dialysis. Sodium Polystyrene Sulfonate (SPS) 15-30 g of powder with 33% sorbitol
exchanges Na+ for K+ in the GI tract and increases the fecal excretion of K+.

7. What is the expected ECG changes in hyperkalemia? Hypokalemia?

- - Typical ECG findings in hyperkalemia progress from tall, “peaked” T waves and a
shortened QT interval to lengthening PR interval and loss of P waves, and
then to widening of the QRS complex culminating in a “sine wave” morphology
and death if not treated.
- - Expected ECG changes seen in hypokalemia include dynamic changes in T-wave
morphology, ST segment depression, and U waves, which are often best seen in the
mid-precordial leads (V2–V4). The PR interval can also be prolonged along
with an increase in the amplitude of the P wave.
8. How to compute for the potassium deficit in hypokalemia?
- K deficit (meqs)=(ideal K−current K ) x 0.27 x 100
9. What are the different types of hyponatremia? What are the common examples for each type?

- Hypovolemic Hyponatremia
 Hypovolemia causes a marked neurohormonal activation, increasing circulating levels of
AVP which helps preserve blood pressure via vascular and baroreceptor V 1A receptors and
increases water reabsorption via renal V2 receptors; increased V2 receptors can lead to
hyponatremia in the setting of increased water intake. Common causes of hypovolemic
hyponatremia include GI loss (diarrhea, vomiting, etc) and insensible loss (sweating, burns).
- Euvolemic Hyponatremia
This can occur in moderate to severe hypothyroidism, with correction after achieving a
euthyroid state. Moreover, the predominant glucocorticoid deficiency in secondary adrenal failure is
associated with euvolemic hyponatremia. Glucocorticoids exert a negative feedback on AVP
release by the posterior pituitary such that hydrocortisone replacement in these patients can rapidly
normalize the AVP response to osmolality, reducing circulating AVP. The most common cause of
euvolemic hyponatremia is Syndrome of Inappropriate Antidiuresis (SIAD)
- Hypervolemic Hyponatremia
Patients with hypervolemic hyponatremia develop an increase in total-body Na-Cl that is
accompanied by a greater increase in total-body water, leading to the reduction of plasma
Na+ concentration. Common causes include congestive heart failure, cirrhosis, and
nephrotic syndrome.

10. How do NSAIDS cause AKI? How do ACE/ARBs cause AKI?

Diuretics can also contribute to AKI by causing hypovolaemia. NSAIDs are associated with an increased risk
of AKI, due to blockade of the COX-2 enzyme preventing prostacyclin synthesis, which causes afferent
arteriolar vasoconstriction. The effect of ACEI and ARB on glomerular perfusion (by reducing
hyperfiltration) is the primary mechanism by which ACEIs and ARBs slow the progression of these types of
kidney disease.
11. How is CKD staged?
- To stage CKD, it is necessary to estimate the GFR rather than relying on serum creatinine
concentration.

12. What are the different renal replacement strategies?

a. Hemodialysis - Hemodialysis requires the use of a semipermeable membrane that will allow the
passage of water and small molecular weight solute such as UREA, but not large molecules
such as CREATININE.
 1. INTERMITTENT HEMODIALYSIS Outpatient setting Most commonly used Done 2-4 times a
week with a duration of 4 hours Shorter period of time (3-5 hours), less anticoagulation,
better correction of hyperkalemia
2. SLOW LOW EFFICIENCY DIALYSIS (SLED) Hospital and ICU setting (for critically-ill patients)
May last for 6 hours to 24 hours or more
3. CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT) Hospital and ICU setting (for
critically-ill patients) May last for 6 hours to 24 hours or more
b. Peritoneal Dialysis - 1.5 to 3L of a dextrose-containing solution is infused into the peritoneal
cavity and allowed to dwell in a set period of time, usually 2-4 hours.
c. Kidney Transplantation - Treatment of choice for advanced chronic kidney disease

13. What are the common clinical findings of Nephrotic syndrome?

- Nephrotic syndrome is defined as the onset of heavy proteinuria (>3.0 g/24 hr), hypertension,
hypercholesterolemia, hypoalbuminemia, edema/anasarca, and microscopic hematuria. Patients
with nephrotic syndrome may have normal GFR initially, but with persistent hyperfiltration and
continued nephron loss.

14. What is the nephrotic range proteinuria?

- Nephrotic-range proteinuria is typically defined as greater than 3 to 3.5 g of protein in a 24-hour
urine collection.

15. What are the different classes of diuretics? What are the mechanisms of action? Examples of each
16. What are the different pathophysiologic mechanisms of edema based on Starling Forces?
NEUROLOGY
1. What is the golden hour for Stroke? - 60 minutes from the onset of the symptoms
2. What is the difference between an infarct and a bleed in CT scan? - Infarct appears hypodense on CT while
bleed appears hyperdense especially during acute period
3. What are the indications of surgical intervention in patients with CVD bleed?
4. What is the recommended dose of Alteplase in the general population? In Asians?
5. What are the relative and absolute contraindications of Alteplase infusion
6. What is dense MCA sign?
7. How to compute for the GCS?
 a.
8. What are the red flags of headache?
9. What are the different causes of primary headache
10. What is the difference between an Epidural and subdural hemorrhage based on the CT scan findings and
the vessel involved?
11. What is the CT scan finding of subaranchoid hemorrhage? How is it graded? Why is nimodipine given?
12. What is the common cause of subarachnoid hemorrhage? What is the most common non-traumatic cause of
subarachnoid hemorrhage?
13. What is the most common site of hypertensive bleed?
14. What is the most common location of intracranial aneurysm?
15. What is the diagnostic test of choice for CNS infection?
16. How to do Brudzinsky and Kernig?
17. What is the CSF findings in patients with CNS infection?
18. What is the Cushing’s Triad? Explain the monro kellie doctrine.
19. What medications can be given to decrease the intracranial pressure? What is their mechanism of action?
20. What are the different levels of sensorium?
21. How to test for the corneal reflex? Dolls Eyes?
22. What are the afferent and efferent neurons involved in Pupillary Light Reflex? Corneal Reflex?

GASTROENTEROLOGY
1. What are the 4 most common complications of Peptic Ulcer Disease?
● Bleeding
● Penetration
● Perforation
● Gastric outlet obstruction
2. What are the most common causes of PUD?
● Helicobacter pylori (H. pylori) and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs)
3. What is the triple and quadruple therapy of H. pylori infection?

4. How is H.pylori diagnosed?

● Urea breath test
● H. pylori stool antigen test
5. How is Achalasia diagnosed? What are the different types of Achalasia? How to compute for Eckardt Score?
● Achalasia is diagnosed through upper endoscopy and esophageal barium swallow
● Types of achalasia

○
● Eckardt Score
 6. What are the causes of upper and lower GI Bleeding?
○ Upper GI bleed
■ esophageal varices
■ gastritis, peptic ulcers
■ Inflammation
■ Cancer
○ Lower GI bleed
■ Diverticulitis
■ Infections
■ Polyps
■ Inflammatory bowel disease
■ Hemorrhoids
■ Anal fissures
■ Cancer.
7. How to differentiate partial and complete gut obstruction based on the symptoms?
Symptom Small Bowel Obstruction Large Bowel Obstruction

Pain Intermittent, colicky Continuous

Improves with vomiting

Vomiting Frequent Intermittent

Large volume Feculent

Tenderness on palpation More focal More diffuse

Distention Less marked Marked with obstipation

8. What are the values of requesting for an upright Chest X-ray, Supine Abdominal X-ray, and Upright
Abdominal X-ray in the evaluation of gut obstruction? What are the expected results? What is the
measurement to consider that the bowel loops are dilated?
Assessment for pneumoperitoneum on supine films can be difficult. Therefore, when perforation is
suspected, an erect chest X-ray, which can detect as little as 1 mL of intraperitoneal gas, should be
obtained. When interpreting supine abdominal radiographs, subtle findings that may suggest the presence of
pneumoperitoneum include lucency on both sides of the bowel (Rigler's sign), lucency outlining the falciform
ligament or the liver, or geometrically shaped lucencies, such as triangles of gas trapped between bowel
loops. Large-volume pneumoperitoneum on supine radiographs can be observed as a large ovoid central
lucency (football sign). A gas-filled colon interposed between the liver and right hemi-diaphragm can mimic
pneumoperitoneum (Chilaiditi sign).
Radiographic diagnostic signs for small bowel obstruction and large bowel obstruction
● Small bowel obstruction
- Supine or prone:
 1. Dilated small bowel > 2.5–3 cm
 2. Paucity of colorectal gas
 3. Stretch sign
 4. Gasless abdomen
 5. Dilated stomach
 ● Upright or decubitus:
 1. Multiple air–fluid levels
 2. Air–fluid level wider than 2.5 cm
 3. Air–fluid levels in the same small bowel loop of unequal heights
 4. String-of-beads sign
● Large bowel obstruction
 1. Dilated colon > 6 cm or cecum > 9 cm
 2. Paucity of rectal gas
 3. +/− small bowel dilation depending on duration and presence of closed loop

9. How to manage gut obstruction?

○ Exploratory laparotomy
○ Bowel rest (place the patient in NPO)
○ Supportive care
■ IV fluid therapy
■ Electrolyte repletion
■ Parenteral non-opioid analgesics
■ Nasogastric tube insertion
10. What are the different causes of small bowel obstruction?
○ Bowel adhesions from history of abdominal surgery and abdominal tuberculosis
○ Incarcerated hernias
○ Merckel diverticulum
○ Gallstone ileus
○ Malignant tumor
11. What are the differentials for an upper gastrointestinal bleeding? For a lower gastrointestinal bleeding? How
will you differentiate UGIB vs LGIB clinically?
○ Upper GI bleeding
■ Peptic ulcer disease
■ Esophagitis
■ Erosive gastritis
■ Esophageal tumor
■ Gastric cancer
○ Lower GI bleeding
■ Ulcerative colitis
■ Crohn's disease
■ Diverticular disease
■ Rectal ulcer
■ Hemorrhoids
■ Colorectal cancer
■ Colonic polyps
■ Anal fissures
○ In differentiating UGIB and LGIB clinically:
■ UGIB
1. Hemetamesis
2. Melena
■ LGIB
1. Hematochezia
2. Previous episode of LGIB
12. What are the 2 inflammatory bowel diseases? How do you differentiate the 2
Characteristics Ulcerative Colitis Crohn's Disease

Site of disease Colon (proctosigmoiditis, left-sided Colon (⅔), Ileum (⅔), infrequent in
colitis, pancolitis, backwash colitis duodenum and jejunum

Clinical features Fever, abdominal pain, bloody Fever, abdominal pain, diarrhea,
diarrhea, weight loss weight loss, fatigue

Intestinal complications Strictures absent, fistulas absent, Strictures present (fibrotic and
punctate ulcers, pseudopolyps, stenotic), fissures and fistulas
shortened colon, rectum involved, common, deep ulcerations,
perianal disease absent cobblestone appearance, perianal
 disease

Inflammation Primarily mucosal cryptitis, crypt Transmural, crypt abscess,

abscess, granulomas absent, granulomas, associated with IL-12,23,
associated with IL-13 IFN-Gamma, IL-17 production

Surgical requirement Patient usually do not require surgery Surgery is used as treatment

13. How is irritable bowel disease diagnosed?

Irritable bowel syndrome (IBS) should be suspected in patients with chronic abdominal pain and altered
bowel habits (constipation and/or diarrhea). A clinical diagnosis of IBS requires the fulfillment of symptom-
based diagnostic criteria and a limited evaluation to exclude underlying organic disease.
Rome IV criteria for IBS – According to the Rome IV criteria, IBS is defined as recurrent abdominal pain, on
average, at least one day per week in the last three months, associated with two or more of the following
criteria:
● Related to defecation
● Associated with a change in stool frequency
● Associated with a change in stool form (appearance)
IBS subtypes – Subtypes of IBS are recognized based on the patient's reported predominant bowel habit on
days with abnormal bowel movements. The Bristol stool form scale (BSFS) should be used to record stool
consistency. Subtypes can only confidently be established when the patient is evaluated off medications used
to treat bowel habit abnormalities. IBS subtypes are defined for clinical practice as follows:
● IBS with predominant constipation – Patient reports that abnormal bowel movements are usually
constipation (type 1 and 2 in the BSFS)
● IBS with predominant diarrhea – Patient reports that abnormal bowel movements are usually diarrhea
(type 6 and 7 in the BSFS)
● IBS with mixed bowel habits – Patient reports that abnormal bowel movements are usually both
constipation and diarrhea (more than one-fourth of all the abnormal bowel movements were constipation
and more than one-fourth were diarrhea)
● IBS unclassified – Patients who meet diagnostic criteria for IBS but cannot be accurately categorized into
one of the other three subtypes.
Manning Criteria:
● Onset of pain linked to more frequent bowel movements
● Looser stools associated with onset of pain
● Pain relieved by a passage of stool
● Noticeable abdominal bloating
● Sensation of incomplete evacuation >25% of the time
● Diarrhea with mucus >25% of the time
Initial evaluation – Initial evaluation in all patients with suspected IBS includes a history and physical examination
and limited testing to evaluate for the presence of alarm features concerning organic disease.
● In all patients with suspected IBS, we perform a complete blood count and age-appropriate colorectal cancer
screening.
● In patients with diarrhea, we perform the following:
- Fecal calprotectin or fecal lactoferrin
- Stool testing for giardia
- Serologic testing for celiac disease
- C-reactive protein levels only if fecal calprotectin and fecal lactoferrin cannot be performed.
14.What diagnostic tests will you request to evaluate a liver problem?
14. What are the modes of transmission of the different viral hepatitis?
15. How to interpret hepatitis profile?

16. What is the amount of alcohol intake inorder for it to be considered as significant (in males vs females)?
17. What are the different stigmata of a chronic liver disease?
○ spider telangiectasias
○ palmar erythema
○ Dupuytren's contractures
○ Gynecomastia
○ testicular atrophy
18. What are the complications of liver cirrhosis?
○ Complications accompanying hepatic cirrhosis can include:
○ Portal hypertension
○ Edema in the abdomen and lower extremities
○ Jaundice
○ Splenomegaly
○ Infections
○ Hemorrhage
○ Hepatic encephalopathy
19. How to test for asterixis?
○ Asterixis can be elicited on physical examination by having the patient extend their arms, dorsiflex
the wrists, and spreading the fingers (similar to pushing against a wall) with their eyes closed. This
is used to test for the “flap” at the wrist and is the most common method of assessment.
20. How to compute for the Child Pugh score?
 21. What are the most common etiologies of pancreatitis? What are the criteria that should be fulfilled in order to
diagnose pancreatitis? How is pancreatitis managed? What is the indication of starting antibiotics?
● Stones (biliary pancreatitis)
● Alcohol
● Idiopathic
● Hypertriglyceridemia
Criteria:

Management:
● Bowel rest
 ● Hydration
22. What is the difference between cholecystitis vs cholelithiasis vs choledocholithiasis vs cholangitis?
CHOLECYSTITIS CHOLELITHIASIS CHOLEDOCHOLITHIASIS CHOLANGITIS

Inflammation of the Presence of stones in the Presence of stones in the Presence of Charcot’s triad
gallbladder gallbladder common bile duct

23. What is the Charcots triad and Reynolds Pentad?

Charcot’s triad: Jaundice, Fever, Abdominal pain
Reynold’s Pentad: Jaundice, Fever, Abdominal Pain, Altered Mental Status, and Hypotension

ENDOCRINOLOGY
1. How is diabetes diagnosed? Who and when to screen?

2. What are the different insulins based on the onset of action? Which are considered basal insulins? Which
are bolus insulins?

3. What is Dawn vs Somogyi effect? What is pathophysiology behind these phenomenon?

 A phenomenon known as the dawn phenomenon was introduced by Dr. Schimdt in the 1980s, stating
that morning hyperglycemia is due to the decreased levels of endogenous insulin
secreted at night. The dawn phenomenon also contributes to morning hyperglycemia to increased
concentrations of insulin antagonist hormones. The dawn phenomenon is comparable to the Somogyi
phenomenon, which attributes morning hyperglycemia to counterregulatory hormones from low glucose. The
dawn phenomenon has been noted to occur more commonly than the Somogyi phenomenon. While the two
theories are not seen in all cases of insulin-dependent diabetics, it is important to note that the best way to
prevent either is optimal diabetes control with the proper insulin therapy.
The Somogyi phenomenon states that early morning hyperglycemia occurs due to a rebound effect from
late-night hypoglycemia. However, the dawn phenomenon does not include hypoglycemic
episodes to be a factor.
The dawn phenomenon is a recurring abnormally of high plasma glucose levels in the morning before
breakfast., the dawn phenomenon can be divided into two types: physiological and
pathological. Both types occur at the same time of the day between 3 a.m. and 5 a.m. but differ
in the value of plasma glucose levels. The physiological dawn phenomenon is associated
with a natural decrease of insulin secretion between 3 a.m. and 5 a.m. combined with an
elevation of blood glucose level remaining up to standard. This decrease in insulin secretion
unblocks the secretion of insulin-antagonistic hormones with hypoglycemic properties, particularly GH. The
morning plasma glucose level growth in nondiabetic people with undisturbed insulin secretion is
compensated by an additional burst of insulin. In turn, diabetic patients may experience the
pathological dawn phenomenon, where the morning plasma glucose level is abnormally high due to
insulin secretion disturbances plus the effects of nocturnal GH secretion. The dawn phenomenon is a
combination of an initial decrease in insulin requirements between midnight and 3 a.m., followed
by an increase in insulin needs between approximately 5 a.m. and 8 a.m. Therefore, the dawn
phenomenon can occur among people with type 1 and type 2 diabetes mellitus with
deterioration of beta cell function and without insulin therapy. The decrease of endogenous insulin causes
insufficient repression of insulin-antagonistic hormone secretion, mainly GH, cortisol, and
catecholamines, leading to hyperglycemia. Because of the impaired function of pancreas beta cells, there
is also an insufficient insulin secretion in response to hyperglycemia which causes long-acting
hyperglycemia, detected by patientsafter awakening as the dawn phenomenon. Likewise, the dawn
phenomenon occurs when the action of exogenous insulin administered to the patient the previous day
is running out, and at the same time overlapping physiological growth of insulin-antagonistic hormones is
observed. There is also the phenomenon called ‘the extended dawn phenomenon. This
is seen when the high morning glucose level remains high until mid-morning. The cause
of the extended dawn phenomenon can be too many carbohydrates in the breakfast
meal, or the pathologically extended stage of growth hormone secretion, which is not repressed
by hyperglycemia, seen more often among diabetic patients.
The Somogyi effect, also known as the "chronic Somogyi rebound" or "posthypoglycemic hyperglycemia,"
is described as the paradoxical tendency of the body to react to hypoglycemia by producing
hyperglycemia. Somogyi proposed that when blood glucose levels drop too low during the
late evening, activation of counterregulatory hormones such as adrenaline, corticosteroids,
growth hormone, and glucagon may be observed, leading to activation of gluconeogenesis and resultant
hyperglycemia in the early morning.
4. What are the different classes of oral hypoglycemic agents? What are their common
contraindications/adverse effects?

Oral Agent MOA Common

contraindications/adverse effects
hypoglycemic
agents

Biguanides Metformin Metformin is a biguanide Contraindications Acute or chronic

antihyperglycemic agent which
improves glucose tolerance by
lowering both basal and
postprandial plasma glucose. It
exerts its effect by decreasing
hepatic glucose production
through inhibition of
gluconeogenesis and
glycogenolysis, delaying intestinal
metabolic acidosis, including
diabetic ketoacidosis (with or without
coma); diabetic pre-coma; acute conditions
which may alter renal function (e.g.
dehydration, severe infection, shock),
acute or chronic conditions which may
cause tissue hypoxia (e.g. acute unstable
heart failure; respiratory failure, recent MI;
pulmonary embolism, acute significant
 absorption of glucose, and
improving insulin sensitivity by
increasing peripheral glucose
uptake and utilization.
Sulfonylureas Glibenclamid Glimepiride, an antidiabetic
e/Gliburide sulfonylurea, reduces blood
Glipizide glucose by stimulating the insulin
Glimepiride release from pancreatic β-cells
Gliclazide and decreases glucose output
from the liver. Additionally, it
increases insulin sensitivity at
peripheral target sites.
meglitinides Repaglinide Repaglinide is a short-acting
Nateglinide meglitinide analogue which lowers
blood glucose by blocking
ATP-dependent K channels in the
β-cell membrane resulting in
depolarisation. This leads to the
blood loss, sepsis, gangrene, pancreatitis),
acute alcohol intoxication or
alcoholism. Hepatic or severe
renal impairment (eGFR <30 mL/min).
Concomitant intravascular administration of
iodinated contrast agents.
Adverse Reactions
> Significant: Vitamin B12 deficiency
(prolonged use).
> Gastrointestinal disorders: Nausea,
vomiting, abdominal pain or distress,
flatulence, diarrhoea, dyspepsia,
taste disturbance.
> Metabolism and nutrition disorders:
Loss of appetite.
> Musculoskeletal and connective tissue
disorders: Asthenia.
> Potentially Fatal: Lactic acidosis.
Glimepiride Contraindications
Hypersensitivity to glimepiride, other
sulfonylureas, or sulfonamides. Type 1
diabetes mellitus, diabetic coma,
ketoacidosis. Severe renal or hepatic
impairment
Adverse Reactions
> Significant: Hypoglycaemia (may be
severe), haemolytic anemia (particularly in
patients with G6PD
deficiency), hypersensitivity reaction (e.g.
anaphylaxis, angioedema,
Stevens-Johnson syndrome), weight gain.
> Blood and lymphatic system disorders:
Leucopenia, agranulocytosis, aplastic
anemia, pancytopenia, thrombocytopenia.
> Endocrine disorders: Syndrome of
inappropriate antidiuretic hormone
secretion (SIADH).
> Eye disorders: Visual disturbances.
> Gastrointestinal disorders: Abdominal
pain, diarrhea, nausea, vomiting,
dysgeusia.
> Hepatobiliary disorders: Cholestasis,
jaundice, hepatitis, liver failure,
hepatic porphyria.
> Metabolism and nutrition
disorders: Disulfiram-like
reactions, hyponatraemia.
> Nervous system disorders: Headache,
dizziness.
> Skin and subcutaneous tissue
disorders: Photosensitivity, alopecia
Contraindications Diabetic
ketoacidosis with or without
coma, type 1 diabetes mellitus.
Concomitant use with gemfibrozil.
Adverse Reactions
 opening of Ca channels. The
resulting Ca influx stimulates the
release of insulin from the
pancreatic βcells
thiazolidinediones Rosiglitazone Pioglitazone, a thiazolidinedione,
Pioglitazone is a potent and highly
selective agonist for the
peroxisome proliferator-
activated receptor-γ (PPAR-γ).
Activation of these receptors
promotes the production of gene
products involved in lipid and
glucose metabolism. It also
improves insulin response to
target cells without increasing the
pancreatic secretion of
insulin.
α-glucosidase Acarbose Miglitol Acarbose competitively and
inhibitors reversibly inhibits
membrane bound intestinal
αglucosidases and pancreatic
α-amylase resulting in the
delayed absorption of glucose and
degradation of ingested
complex carbohydrates and
> Significant: Severe hypoglycaemia, acute
coronary syndrome (e.g. MI).
> Gastrointestinal disorders:
Abdominal pain, diarrhea.
> Musculoskeletal and connective
tissue disorders: Arthralgia, back pain.
> Nervous system disorders:
Headache.
> Respiratory, thoracic and mediastinal
disorders: Upper respiratory tract
infection, sinusitis, bronchitis
Contraindications
History or current heart failure (New
York Heart Association [NYHA] stages IIV);
diabetic ketoacidosis, active or
history of bladder cancer; uninvestigated
macroscopic haematuria, hepatic
impairment
Adverse Reactions
> Significant: Decreased Hb or
haematocrit, hypoglycaemia (if
combined with other antidiabetic agents
or insulin), macular
oedema with decreased visual
acuity, weight gain; increased risk of
bladder carcinoma, bone fracture
(higher risk in women), and cardiac
failure; fluid retention,
resumption of ovulation.
> Blood and lymphatic system disorders:
Anaemia.
> Eye disorders: Visual disturbance.
> Gastrointestinal disorders:
Flatulence.
> General disorders and administration
site conditions: edema.
> Musculoskeletal and connective
tissue disorders: Arthralgia.
> Nervous system disorders:
Hypoaesthesia, headache,
dizziness.
> Renal and urinary disorders: Haematuria.
> Reproductive system and breast
disorders: Erectile dysfunction.
> Respiratory, thoracic and
mediastinal disorders: Upper
respiratory tract infection,
dyspnoea, bronchitis.
> Potentially Fatal: Very rarely, hepatic
failure.
Contraindications
Inflammatory bowel disease, colonic
ulceration, partial intestinal
obstruction or predisposition to
intestinalobstruction; chronic intestinal
disease associated with
marked disorders of digestion or
absorption; conditions that may
 disaccharides in the small
intestine. This action leads to a
reduced post-prandial rise in
blood glucose, therefore
decreasing blood glucose
fluctuations.
DPP-4 inhibitors. Sitagliptin Sitagliptin, a dipeptidyl peptidase-
Vildagliptin 4 (DPP-4) inhibitor, improves
Saxagliptin glycaemic control by enhancing
the levels and prolonging the
effects of active incretin
hormones such as glucagon-like
peptide-1 (GLP-1) and
glucosedependent insulinotropic
polypeptide (GIP). These
hormones regulate glucose
homeostasis and are
rapidly inactivated by the DPP-4
enzymes. Both GLP-1
and GIP increase insulin
synthesis and release from
pancreatic β cells by intracellular
signaling pathways involving
cyclic AMP, while GLP-1 lowers
glucagon secretion from
pancreatic α cells
resulting in lower hepatic
glucose production.
Sitagliptin prevents the hydrolysis
of incretin hormones caused by
DPP-4 enzyme, thereby
increasing and prolonging
active incretin levels that
elevate insulin release and
decrease glucagon concentrations
in the circulation (glucose
dependent manner).
5. What is the pathophysiology of DKA?
Insulin deficiency and an increase in counterregulatory hormones (glucagon, catecholamines, cortisol) cause
the body to metabolize triglycerides and amino acids instead of glucose for
deteriorate due to elevated gas formation
in the intestine (e.g. hernia), diabetic
ketoacidosis, cirrhosis. Hepatic
impairment.
Adverse Reactions
> Significant: Increased serum
transaminase levels. Rarely,
hyperbilirubinemia.
> Blood and lymphatic system disorders:
Thrombocytopenia.
> General disorders and administration
site conditions: Rarely,
edema.
> Gastrointestinal disorders:
Flatulence, diarrhea, abdominal
pain, nausea, vomiting, dyspepsia. Rarely,
pneumatosis cystoides
intestinalis, ileus or subileus.
> Hepatobiliary disorders: Rarely,
jaundice, hepatitis.
> Immune system disorders:
Hypersensitivity skin reactions (e.g. rash,
erythema, exanthema, urticaria).
> Potentially Fatal: Fulminant hepatitis.
Contraindications
Hypersensitivity.
Adverse Reactions
> Significant: Hypoglycaemia (particularly
in combination with sulfonylureas or
insulins); worsening renal function,
including acute renal failure (may require
dialysis); severe and disabling arthralgia,
bullous pemphigoid.
> Gastrointestinal disorders: Constipation,
vomiting, mouth ulceration, stomatitis.
> Musculoskeletal and connective tissue
disorders: Myalgia, back pain.
> Nervous system disorders:
Headache, dizziness.
> Respiratory, thoracic and
mediastinal disorders:
Nasopharyngitis, upper respiratory
tract infection, interstitial lung
disease.
> Skin and subcutaneous tissue
disorders: Rash, urticaria, pruritus.
> Potentially Fatal: Acute pancreatitis
including haemorrhagic or necrotising
pancreatitis, serious hypersensitivity
reactions (e.g. anaphylaxis, angioedema,
cutaneous vasculitis, exfoliative skin
conditions including Stevens-Johnson
syndrome).
energy. Serum levels of
glycerol and free fatty acids rise because of unrestrained lipolysis. Alanine levels rise because of muscle
catabolism. Glycerol and alanine provide a substrate for hepatic gluconeogenesis, which is
stimulated by the excess of glucagon that accompanies insulin deficiency.
Glucagon also stimulates the mitochondrial conversion of free fatty acids into ketones. Insulin
normally blocks ketogenesis by inhibiting the transport of free fatty acid derivatives into the mitochondrial matrix,
but ketogenesis proceeds in the absence of insulin. The major ketoacids produced, acetoacetic acid and beta-
hydroxybutyric acid, are strong organic acids that create metabolic acidosis. Acetone derived from the
metabolism of acetoacetic acid accumulates in serum and is slowly disposed of by respiration.
Hyperglycemia due to insulin deficiency causes osmotic diuresis that leads to marked urinary losses of water
and electrolytes. Urinary excretion of ketones obligates additional losses of sodium and
potassium. Serum sodium may fall due to natriuresis or rise due to excretion of large volumes of free
water. Potassium is also lost in large quantities. Despite a significant total body deficit of
potassium, initial serum potassium is typically normal or elevated because of the extracellular migration of
potassium in response to acidosis. Potassium levels generally fall further during treatment as insulin therapy
drives potassium into cells. If serum Potassium is not monitored and replaced as needed, life-threatening
hypokalemia may develop.

6. What are the criteria in diagnosing DKA?

7. What are the pillars of management of DKA? When to give sodium bicarbonate?
● Intravenous Fluid Therapy
● Potassium
● Bicarbonate
○ If pH <6.9: start 100 mmol HC03- + 400 mL sterile water+ 20 mEq KCl to infuse for 2 hrs
(repeat every 2 hours until venous pH >7.0 and monitor serum K+ every 2 hours)
○ If pH >/= 6.9: no need to give HC03-
● Insulin Therapy

8. What is the difference between DKA and HHS

DKA typically affects people living with type 1 diabetes, whereas HHS usually occurs in people living with
type 2 diabetes. HHS tends to be more dangerous than DKA, but both conditions can be deadly if a person
does not receive treatment. Prompt medical attention is necessary in both cases
 9. How is Thyroid storm managed? What medications can be given? What is the definitive management?

Typically, propranolol 40 mg to 80 mg is given every 4 to 6 hours. Then, either a loading dose of propylthiouracil
(PTU) 500 mg to 1000 mg followed by 250 mg every 4 hours or Methimazole (MMI) 20 mg every 4 to 6 hours should
be given.
10. What is the most common ECG finding in patients with thyroid storm?
 Atrial Fibrillation
11. What is the Wolff chaikoff effect? Jod Basedow phenomenon?
Wolff-Chaikoff effect is an autoregulatory phenomenon, whereby a large amount of ingested iodine acutely
inhibits thyroid hormone synthesis within the follicular cells, irrespective of the serum level of thyroid-
stimulating hormone (TSH).
Jod-Basedow phenomenon occurs due to either overactivation of the entire thyroid gland or, more
commonly, autonomous nodules within the gland after iodine repletion without adequate feedback control
from the pituitary gland. This escape from the protective Wolff-Chaikoff effect is called the Jod-Basedow
phenomenon. Patients at risk are elderly and those from low iodine intake regions.

12. How to interpret thyroid function test?

ALLERGOLOGY
1. Criteria to diagnose anaphylaxis?
First Criteria: Sudden onset of an illness (within minutes to several hours), with involvement of the skin,
mucosal tissue, or both and at least one of the following:
a. Sudden respiratory symptoms and signs (shortness of breath, wheeze, cough, stridor, hypoxemia)
b. Sudden reduction of BP or symptoms of end-organ dysfunction (hypotonia, collapse, incontinence)
Second Criteria: involves two or more of the following that occur suddenly after exposure to a likely allergen
or other triggers for that patient within minutes to several hours.
a. Sudden skin or mucosal symptoms and signs
b. Sudden respiratory symptoms and signs
c. Sudden reduction in BP or symptoms of end-organ dysfunction
d. Sudden GIT symptoms (crampy abdominal pain, diarrhea, or vomiting)
Third Criteria: A reduced blood pressure after exposure to a known allergen for that patient within minutes to
several hours.
- Infants and children: low systolic BP (age-specific) or >30% decrease in systolic BP
- Adults: systolic BP of <90mmHg or >30% decrease from that person’s baseline

2. Drug of choice for anaphylactic shock? How is it administered?

Epinephrine is the first line treatment. It is administered intramuscularly into the antero-lateral thigh.
3. What are the 4 types of hypersensitivity reaction? Examples for each type?
ONCOLOGY
1. What are the different screening tests for common malignancies?
a. Breast Cancer: mammography, MRI
b. Cervical Cancer: PAP Smear, HPV test
c. Ovarian and Prostate: CA-125, PSA
d. Skin cancer: Skin exam
e. Colorectal cancer: Colonoscopy
f. Lung Cancer: Low-dose CT scan
2. What are the different tumor markers?

3. What are the different classes of chemotherapeutic agents? Examples for each? Most common side effect?
● Alkylating agents: Chlorambucil, Cyclophosphamide, Cisplatin, and Carboplatin.
 ○ Side effects: hair loss, anemia, pancytopenia, reduced sperm count, nausea, vomiting, GI
upset
● Nitrosoureas: Carmustine and Lomustine.
○ Side effects: nausea, vomiting, facial flushing, myelosuppression, pulmonary toxicity
● Anti-metabolites: Fluorauracil, Methotrexate and Fludarabine.
○ Side effects: Nausea, vomiting, or loss of appetite, tiredness, weakness, or sore muscles,
headache and dizziness, inflammation of the mouth and lips, hair loss
● Plant alkaloids and natural products: Vincristine, Paclitaxel, and Topotecan.
○ Side effects: diarrhea, nausea, anemia, neutropenia (low count of low blood cells called
neutropenia), thrombocytopenia
● Anti-tumor antibiotics: Bleomycin, Doxorubicin and Mitoxantrone.
○ Side effects: tingling, nausea, vomiting, nerve pain, abdominal pain, diarrhea, fever, hair
loss, and skin rashes
● Hormonal agents:
○ Corticosteroids: Prednisone and Dexamethasone
■ Side effects: fluid retention, high blood pressure, problems with mood swings,
upset stomach, weight gain
○ Sex hormones: Tamoxifen and Leuprolide.
■ Side effects: irregular periods, excess body and facial hair, acne, vaginal
dryness, low sex drive, erectile dysfunction
● Biological response modifiers: Herceptin and Avastin, Erbitux and Rituxan
○ Side effects: fever, chills, muscle aches, weakness, loss of appetite, nausea, vomiting,
diarrhea and skin rash
4. What are the different paraneoplastic syndromes?
- Lambert-Eaton myasthenic syndrome, stiff-person syndrome, encephalomyelitis, myasthenia
gravis, cerebellar degeneration, limbic or brainstem encephalitis, neuromyotonia, opsoclonus, and
sensory neuropathy.
5. What are the common electrolyte abnormalities in tumor lysis syndrome?
- The metabolic derangements associated with tumor lysis syndrome are hyperkalemia,
hypocalcemia, hyperphosphatemia, and hyperuricemia.
HEMATOLOGY
1. What are the different diagnostic tests that you will request to evaluate anemia?
● Complete Blood Count
○ Includes hemoglobin, hematocrit, mean corpuscular volume (MCV), mean corpuscular
hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC).
● Reticulocyte count:
○ Serves as an estimate of bone marrow red blood cell output.
● Iron profile:
○ Includes serum iron, ferritin and total iron-binding content (TIBC).
● Peripheral blood smear:
○ Microscopic evaluation of red blood cell morphology.
● Bone marrow analysis
2. What are the common causes of anemia?
● Lack of iron-rich foods in the diet
● Lack of vitamin C in the diet
● Chronic blood loss due to parasitism or menstruation
● Increased demand of the body during pregnancy and lactation
● Low absorption of iron from food
● High requirement of infants, adolescent girls, pregnant and lactating women.
3. How to compute absolute reticulocyte count and reticulocyte index? How is it interpreted?

RI <2.5: hypoproliferative anemia or maturation disorder

RI >2.5: hemolytic anemia or hemorrhage
4. What are the common causes of bone marrow failure?
● Aplastic anemia
● Radiation and chemotherapy treatments. While these cancer-fighting therapies kill cancer cells,
they can also damage healthy cells, including stem cells in bone marrow. Aplastic anemia can be a
temporary side effect of these treatments.
 ● Exposure to toxic chemicals. Toxic chemicals, such as some used in pesticides and insecticides,
and benzene, an ingredient in gasoline, have been linked to aplastic anemia. This type of anemia
might improve if you avoid repeated exposure to the chemicals that caused your illness.
● Use of certain drugs. Some medications, such as those used to treat rheumatoid arthritis and some
antibiotics, can cause bone marrow failure.
● Autoimmune disorders. An autoimmune disorder, in which your immune system attacks healthy
cells, might involve stem cells in your bone marrow.
● A viral infection. Viral infections that affect bone marrow can play a role in the development of
aplastic anemia. Viruses that have been linked to aplastic anemia include hepatitis, Epstein-Barr,
cytomegalovirus, parvovirus B19 and HIV.
● Pregnancy. Your immune system might attack your bone marrow during pregnancy.

5. What is the different genetic translocations in different types of leukemia?

6. Drug of choice for CML?

Imatinib
7. Drug of choice for acute promyelocytic leukemia?
All-Trans Retinoic Acid (ATRA) - Tretinoin
8. How to differentiate Hodgkin’s vs non Hodgkin’s lymphoma on histology?
Giant B cells with bilobed nuclei with prominent inclusions termed Reed-Sternberg (RS) cells, are
present in Hodgkin’s Lymphoma but not in non-Hodgkin’s lymphoma.
9. Characteristic histologic feature of Burkitt lymphoma
● Starry sky appearance
● Sheets of lymphocytes with interspersed “tingible body” macrophages

10. What is the expected rise in the level of hemoglobin for every bag of prbc transfused?
1 bag of prbc= 10 g/L rise in hemoglobin level

RHEUMATOLOGY
1. What medications can be given in acute gouty arthritis? Prophylaxis for flare?
a. Acute Gouty Arthritis
i. Colchicine
ii. NSAID
iii. Hydrocortisone
iv. Allopurinol
b. Prophylaxis for flare
i. Colchicine
2. Supportive management for gout?
a. Hydration
b. Ice compress on affected joints
 c. Low purine diet
d. Avoid alcohol intake
3. Expected microscopy findings in gout? Pseudogout?
a. Gout
i. Negative birefringence
ii. Presence of monosodium urate crystals
b. Pseudogout
i. Calcium pyrophosphate
4. Criteria to diagnose SLE? Different immunologic tests for SLE?
a. Criteria
i. SLICC and EULAR
b. Immunologic test for SLE
i. ANA test
ii. Anti-dsdna
iii. Anti-sm
5. Most common joints involved in osteoarthritis?
a. Knee, hips, hands
6. Heberden's vs bouchard's nodes? swan neck vs boutonniere deformity?
a. Heberden- distal interphalangeal joints
b. Bouchard’s - proximal interphalangeal joints
c. Swan neck- the joint at the base of the finger bends in (flexes), the middle joint straightens out
(extends), and the outermost joint bends in (flexes)
d. Boutonniere deformity- the middle finger joint is bent inward (toward the palm), and the outermost
finger joint is bent outward (away from the palm)
7. Maneuvers to evaluate for carpal tunnel syndrome
a. Phalen’s
b. Tinel’s test
8. What are the different causes of spondyloarthropaties?
a.
9. Pathophysiology and causes of reactive arthritis? Triad of Reactive arthritis?
10. What comprises Jones Criteria in diagnosing rheumatic fever?