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IM PEARLS Flashcards

1
Q

Underlying cause of Chest Pain in Stable Angina

A

Fixed atherosclerotic stenosis of coronary arteries - Increased myocardial oxygen demand - LACTIC ACIDOSIS

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2
Q

Precursor lesion of atherosclerosis

A

FATTY STREAK containing foam cells (macrophages)

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3
Q

Why does pain radiate to the left arm in Stable Angina

A

Synapses shared with C4 and C5 sensory fibers

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4
Q

What does pain radiating to the upper back (trapezius) indicate?

A

PERICARDIAL involvement

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5
Q

Major Risk Factors for Chronic Stable Angina

A

DM, SMOKING, family history of CAD or premature CAD (M<50(F)

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6
Q

Minor Risk Factor for Chronic Stable Angina

A

Age, Obesity (independent RF), Estrogen Deficiency (Males & Menopaused), Homocysteinemia

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7
Q

Best initial test for Stable Angina; What are the Expected Findings?

A

ECG showing ST DEPRESSION, FLATTENING OF T WAVES sec to ischemia

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8
Q

Expected Findings on Cardiac Enzymes in Stable Angina

A

Cardiac Enzymes NOT ELEVATED

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9
Q

Next best step in management of Stable Angina if ECG is nondiagnostic

A

EXCERCISE STRESS TESTING or Treadmill Stress Test (for MI Risk Stratification: (+) High Risk, (-) Low Risk)

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10
Q

If unable to walk, what stress test will you order in a Stable Angina patient?

A

DOBUTAMINE or DYPRIDAMOLE Stress Test (Increase Heart Rate and Contractility)

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11
Q

Stable Angina patient has BASELINE ECG ABNORMALITIES, what stress test is appropriate?

A

NUCLEAR STRESS TEST (Thallium, Sestamibi)

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12
Q

Most Appropriate Treatment in Stable Angina

A

LIFESTYLE MODIFICATION, OPD: Aspirin, Beta Blockers, Statins, Nitrates - Symptomatic Relief; NO Mortality Risk Reduction

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13
Q

Complications associated with Stable Angina

A

ACUTE MYOCARDIAL INFARCTION, ANEURYSMS

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14
Q

Patient’s chest pain unrelieved by rest or nitrates

A

UNSTABLE ANGINA (Crescendo Angina)

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15
Q

If Stress Test is Positive, what is the next Best Step in Management?

A

ANGIOGRAPHY (Preventive in MI), start ANTICOAGULATION, ASPIRIN, CLOPIDOGREL, NITRATES and BETA BLOCKERS

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16
Q

Underlying pathology in MI

A

RUPTURED ATHEROSCLEROTIC PLAQUE

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17
Q

Blood vessel involved in Acute MI

A

LEFT ANTERIOR DESCENDING ARTERY

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18
Q

Heart Wall involved in Acute MI

A

ANTEROSEPTAL WALL

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19
Q

Heart Wall involved in ECG Leads V1, V2

A

SEPTAL WALL (supplied by Left Anterior Descending)

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20
Q

Heart Wall involved in ECG Leads V3, V4

A

ANTERIOR WALL (supplied by Left Anterior Descending)

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21
Q

Heart Wall involved in ECG Leads II, III, aVF

A

INFERIOR WALL (supplied by Right Coronary Artery)

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22
Q

Heart Wall involved in ECG Leads I & aVL, V5 & V6

A

LATERAL WALL (supplied by Left Circumflex Artery)

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23
Q

2 Forms of Acute MI: Distinguish the two.

A

STEMI: Q Waves, new LBBB, ST elevations in 2 or more contiguous leads or chest leads (Noncontiguous Leads=PERICARDITIS); NSTEMI: T Wave inversion, ST Depression

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24
Q

Which patient population will MI present in atypical fashion?

A

ELDERLY (Autonomic Nervous System manifestations are subtle or irregular) and DIABETICS

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25
Q

Cardiac Enzymes requested in Acute MI

A

TROPONINS & CM-MB

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26
Q

Rise within 4 hours, detectable for 2 weeks, BEST marker for RECENT MI (artificially increased in CKD)

A

TROPONINS

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27
Q

Rise within 4 hours, peaks at 24 hours, normalizes in 2-3 days, BEST marker for REINFARCTION

A

CK-MB

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28
Q

Most Important initial intervention at the ER for Acute MI

A

MONA - Morphine, Oxygen, Nitrates (CI in Inferior Wall MI due to hypotension sec to decreased preload), Aspirin

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29
Q

GOLD STANDARD in treatment of Acute MI

A

PERCUTANEOUS CORONARY INTERVENTION (if brought to ER within 90 minutes)

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30
Q

Difference of Management in STEMI & NSTEMI

A

STEMI: PCI or Thrombolysis if PCI not available (most effective at 6 hours, effective up to 12 hours), anticoagulation with Heparin; NSTEMI: PCI, anticoagulation with Heparin (thrombolysis has NO benefit in NSTEMI)

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31
Q

Absolute Contraindication to Thrombolysis in Acute MI

A

Hemorrhagic CVD, Brain Tumor, Head Trauma, Ischemic CVD within last 1 year, Active Bleeding (exc Menses), Aortic Dissection, BP Cutoff >180/110mmHg

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32
Q

Medication shown to Improve Acute MI Survival

A

ASPIRIN, BETA BLOCKERS (Dec Demand), ACE(prevent CHF)/ARBs (if with LV dysfunction)

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33
Q

Acute Complications of Acute MI

A

PUMP FAILURE (Acute CHF; Inpatients) & ARRHYTHMIAS (Ventricular Fibrillation; Outpatients)

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34
Q

How is Extent of Pump Failure Stratified?

A

KILLIP CLASSIFICATION - I: No evidence of HF; II: Mild to moderate HF (S3 Gallop, Lung Rales, or JVD); III: Overt pulmonary edema; IV: Cardiogenic Shock

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35
Q

Why is there Pulmonary Edema in Acute MI

A

PUMP FAILURE (LV Dysfuntion) - Backflow of Blood into Pulmonary Vessels

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36
Q

Associated Complications for Acute MI

A

Myocardial Aneurysm, Papillary Muscle Rupture, Rupture of Interventricular Septum, Free Wall Rupture, Pericarditis (Dressler Syndrome)

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37
Q

2-7 Days post MI, MCC: Inferior Wall Ischemia, Sx: Pansystolic Murmur radiating to Axilla, Mitral Regurg Murmur, Dx: 2D Echo, Tx: Surgical Repair

A

PAPILLARY MUSCLE RUPTURE

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38
Q

3-5 days post MI, MCC: Anterior Wall MI, Sx: Acute R-Sided CHF, Harsh holosystolic murmur in LLSB, thrill, Tx: Balloon Catheterization, Surgical Repair

A

RUPTURE OF IV SEPTUM (Benign)

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39
Q

5 days-2 weeks post MI, MCC: Lateral Wall MI, Sx: Sudden chest pain, Acute HF, Hemopericardium, Tamponade, PEA, Death 90%, Tx: Pericardiocentesis, Emergency Thoracotomy

A

FREE WALL RUPTURE

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40
Q

1 month post MI, Sx: Persistent ST elevation, Tx: Warfarin, Surgical Repair

A

MYOCARDIAL ANEURYSM

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41
Q

Weeks to Months post MI, Sx: Pleuritic chest pain, Pericardial Friction Rub, Fever, Tx: High-Dose Aspirin, Ibuprofen (NSAIDS)

A

DRESSLER SYNDROME

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42
Q

Management for Severe Bleeding upon Heparinization of Acute MI patient

A

Stop Heparin. Give PROTAMINE SULFATE.

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43
Q

Management of Thrombocytopenia upon Heparinization of Acute MI patient

A

Stop Heparin. Give LEPIRUDIN/ ARGATROBAN

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44
Q

Underlying cause of Congestive Heart Failure

A

VENTRICULAR DYSFUNCTION sec to CORONARY ARTERY DISEASE/ HYPERTENSION

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45
Q

Congestive Heart Failure caused by a pulmonary etiology

A

COR PULMONALE

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46
Q

Histopathologic change of CHF

A

CONCENTRIC (Inc Cardiac Muscle Width) LV HYPERTROPHY due to Pressure Overload (contrast to Eccentric {Dilation of Chamber} LVH in Hyperthyroidism) & SIDEROPHAGES (Hemosiderin-laden macrophages or HEART FAILURE CELLS)

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47
Q

Forms of CHF

A

SYSTOLIC (Weak LV) vs DIASTOLIC (hear unable to accommodate, does not relax enough) HF; LOW OUTPUT vs HIGH OUTPUT HF; LEFT-SIDED vs RIGHT-SIDED HF

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48
Q

Differentiaten Systolic from Diastolic Heart Failure

A

Systolic HF has LOW EF (40-50%)

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49
Q

Differentiate Low from High Output Heart Failure

A

LOW OUTPUT HF has CO 3L/MIN PER M2 (Hyperthyroidism, Anemia, Beri-Beri, Pregnancy, AV Fistula)

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50
Q

Differentiate Left from Right-Sided HF

A

Left-Sided HF: PULMONARY CONGESTION, ORTHOPNEA, WEAKNESS; Right-Sided HF: PERIPHERAL EDEMA, CONGESTIVE HEPATOMEGALY, SYSTEMIC VENOUS DISTENTION

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51
Q

Assessment of Functional Status of CHF

A

NYHA FUNCTIONAL CLASSIFICATION: I- No Limitation of Physical Activity, II- Slight Limitation of Physical Activity, III- Marked Limitation of Physical Activity, IV- Complete Limitation of Physical Activity (Symptomatic even at rest)

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52
Q

Criteria for Diagnosis of CHF

A

FRINGHAM CRITERIA: MAJOR (PRINCES H) - Paroxysmal nocturnal dyspnea, Rales, Increased CVP, Neck vein distention, Cardiomegaly, acute pulmonary Edema, S3 Gallop, Hepatojugular Reflux; MINOR - bipedal edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, decreased vital capacity, tachycardia, weight loss

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53
Q

ORTHOPNEA in CHF

A

Redistribution of fluid from splanchic circulation and lower extremities into central during recumbency

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54
Q

PAROXYSMAL NOCTURNAL DYSPNEA in CHF

A

Inc Pressure in Bronchial Arteries -> Airway Compression with Interstitial Pulmonary Edema

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55
Q

Irregular Pattern of Respiration seen in CHF

A

CHEYNE-STOKE RESPIRATION due to Diminished Sensitivity of Respiratory Center to Arterial PCO2

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56
Q

CRACKLES in CHF

A

Transudation of fluid from intravascular space into he alveoli

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57
Q

ABDOMINAL PAIN In CHF

A

Chronic passive congestion of liver lead to distention of Glisson’s Capsule (pain-sensitive)

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58
Q

Most important Diagnostic Test in CHF

A

2D ECHOCARDIOGRAPHY (EJECTION FRACTION)

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59
Q

Use of Brain Natreuretic Peptide in CHF

A

Differentiates cardiogenic from noncardiogenic pulmonary edema during shortness of breath (Normal BNP excludes CHF as cause of shortness of breath)

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60
Q

Most likely seen on Chest Xray in CHF

A

CARDIOMEGALY, PULMONARY CONGESTION (pulmonary vessel markings at apex), KERLEY B LINES

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61
Q

Most important treatment for pulmonary edema in CHF

A

LOOP DIURETICS (FUROSEMIDE)

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62
Q

Treatment modalities shown to decrease mortality in CHF

A

ACE-Is/ARBs (EF<35 in FC IV)

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63
Q

Drug that decreases hospitallization but has no effect on overall mortality of CHF patients

A

DIGOXIN

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64
Q

Heart valve involved in Infective Endocarditis

A

TRICUSPID VALVE

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65
Q

Most common microbial etiology in Infective Endocarditis

A

STAPHYLOCOCCUS AUREUS

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66
Q

Complications of Infective Endocarditis

A

RUPTURE OF CHORDAE TENDINAE, SEPTIC EMBOLISM

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67
Q

Virulence Factor of Causative Organism in IE that conveys Penicillin Resistance

A

PENICILLINASE

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68
Q

Virulence Factor of the Causative Organism in IE that conveys Complement Inactivation

A

PROTEIN A

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69
Q

Virulence Factor of Causative Organism in IE that conveys Ability to Cause Chordae Rupture

A

HYALURONIDASE

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70
Q

Most Common Cause of Acute IE? In IV Drug Abusers?

A

BOTH STAPHYLOCOCCUS AUREUS

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71
Q

Most Common Cause of Subacute IE? In Native-Valve IE?

A

BOTH VIRIDANS STREP

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72
Q

Most Common Cause of Prosthetic Valve IE

A

STAPHYLOCOCCUS EPIDERMIDIS

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73
Q

Most Common Cause of Culture-Negative IE

A

HACEK

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74
Q

Most Common Cause of IE in Colon Cancer Setting

A

S. BOVIS (MARANTIC ENDOCARDITIS)

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75
Q

IE in GIT Surgery

A

ENTEROBIUS FAECALIS

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76
Q

IE in SLE patient setting

A

LIBMAN-SACKS ENDOCARDITIS or VERRUCOUS ENDOCARDITIS

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77
Q

Best initial test for Infective Endocarditis

A

TRANSTHORACIC ECHOCARDIOGRAPHY

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78
Q

Other Diagnostic Test may be needed for Diagnosis of IE

A

BLOOD CULTURES from 2 NON-CONTIGUOUS SITE

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79
Q

Clinical Criteria for Diagnosis of IE

A

DUKE’S CRITERIA: MAJOR - 2 Positive Blood Culture, Positive Echocardiography (Vegetations); MINOR - Predisposing valve abnormality, Fever, Vascular Phenomena, Immunologic Phenomena, One Positive Culture, Suggestive Echocardiography

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80
Q

Vascular Phenomena associated with IE

A

MAJOR ARTERIAL EMBOLI, SEPTIC PULMONARY INFARCTS, MYCOTIC ANEURYSM, INTRACRANIAL HEMORRHAGE, CONJUNCTIVAL HEMORRHAGE, SPLINTER HEMORRHAGE, JANEWAY LESIONS

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81
Q

Immunologic Phenomena associated with IE

A

GLOMERULONEPHRITIS, OSLER’S NODES, ROTH’S SPOTS, RHEUMATOID FACTOR

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82
Q

Most Appropriate Empiric Therapy for IE until Culture is available

A

VANCOMYCIN + GENTAMICIN

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83
Q

Considered High-Risk Patiets requiring Prophylaxis before a Dental Procedure

A

PROSTHETIC VALVES, PRIOR IE, UNREPAIRED CYANOTIC CHD, RECENTLY-REPAIRED CHD, INCOMPLETELY-REPAIRED CHD, VALVULOPATHY POST-TRANSPLANT

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84
Q

Drug given for Standard Prophylaxis before Dental Procedures? If patient has Penicillin Allergy?

A

AMOXICILLIN; if WITH ALLERGY - CLINDAMYCIN or CLARITHROMYCIN

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85
Q

Underlying Cardiac Defect in RHD (Mitral Stenosis)

A

MITRAL VALVULAR DAMAGE DUE TO PREVIOUS RHEUMATIC FEVER

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86
Q

Histopathologic Changes in the Myocardium in RHD

A

“2 Russians”: ASCHOFF BODIES (ANITSCHKOW MYOCYTES)

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87
Q

Hemodynamic Changes occuring in the heart in RHD

A

INCREASED LEFT ATRIAL DIASTOLIC PRESSURE

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88
Q

Acute Rheumatic Fever Diagnosis

A

JONES CRITERIA: 2 Major or 1 Major & 2 Minor: MAJOR (JONES) - migratory polyarthritis (Joints), pancarditis (Oh my heart!), subcutaneous Nodules, Erythema marginatum, Sydenham’s chorea; MINOR - Arthralgia, Fever, Elevated ESR/CRP, Prolonged PR interval

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89
Q

Infection usually preceding ARF

A

STREPTOCOCCUS PYOGENES (GABHS) INFECTIONS - SKIN (IMPETIGO) or PHARYNGITIS

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90
Q

Pathophysiologic Mechanism of ARF

A

TYPE II REACTION ( IMMUNOLOGIC CROSS-REACTION due to STREPTOCOCCAL M PROTEIN)

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91
Q

Long term sequelae of repeated bouts of ARF characterized by Permanent Valvular Damage

A

RHEUMATIC HEART DISEASE

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92
Q

Most common Valvular Defects in ARF

A

MITRAL REGURGITATION

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93
Q

Most Common Valvular Defects in RHD

A

MITRAL STENOSIS

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94
Q

Best initial Test for RHD

A

2D ECHOCARDIOGRAPHY

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95
Q

Most Appropriate Treatment for RHD

A

SURGICAL REPAIR (VALVOTOMY, COMMISUROTOMY), ANTICOAGULATION, DIURETICS

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96
Q

Most common Valvular Heart Disease

A

MITRAL VALVE PROLAPSE (Most Common), MITRAL STENOSIS, MITRAL REGURGITATION, AORTIC STENOSIS, ATRIAL REGURGITATION

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97
Q

Conditions associated with MVP

A

EHLERS-DANLOS SYNDROME, MARFA. SYNDROME, POLYCYSTIC KIDNEY DISEASE

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98
Q

Murmur of MVP

A

MIDSYSTOLIC CLICK followed by MIDSYSTOLIC to LATE SYSTOLIC MURMUR at APEX

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99
Q

Murmur of Mitral Stenosis

A

OPENING SNAP followed by MID-DIASTOLIC RUMBLE, LOUD S1 and P2

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100
Q

Clinical Presentation of Mitral Stenosis

A

Usually ASYMPTOMATIC until ATRIAL FIBRILLATION or PREGNANCY develops

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101
Q

Murmur of Mitral Regurgitation

A

HOLOSYSTOLIC MURMUR at APEX radiating to AXILLA

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102
Q

Other signs of Mitral Regurgitation

A

HYPERDYNAMIC PRECORDIUM, BRISK CAROTID UPSTROKE

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103
Q

Murmur of Aortic Stenosis

A

EARLY SYSTOLIC EJECTION MURMUR at 2ND RIGHT ICS, radiating to CAROTIDS

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104
Q

Signs of Severe Aortic Stenosis

A

GALLAVARDIN PHENOMENON (Murmur disappears over sternum, reappears in apex) & PULSUS PARVUS ET TARDUS (small or weak pulse that rises slowly and delayed in occurence)

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105
Q

Murmur of Aortic Regurgitation

A

CORRIGAN PULSE: rapid rise and fall of carotid pulse; QUINCKE PULSE: subungual cappilary pulsations; DUROZIEZ SIGN: diastolic murmur over partially-compressed femoral artery; DE MUSSET SIGN: headbobbing with heartbeat; HILL SIGN: systolic BP >30mmHg in legs than arms; TRAUBE SIGN: pistol shot femoral pulses

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106
Q

Effect of Valsalva On murmur

A

INCREASES INTRATHORACIC PRESSURE, DECREASING VENOUS RETURN, DECREASING THE INTENSITY OF MURMURS

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107
Q

Effect of Squatting on Murmur

A

INCREASES VENOUS RETURN, INCREASING INTENSITY OF MURMURS

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108
Q

Pathophysiologic Type of Pericarditis

A

SEROUS, FIBRINOUS & HEMORRHAGIC

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109
Q

Most common infectious etiology of Pericarditis

A

COXSACKIE VIRUS TYPE B

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110
Q

Best initial test for Pericarditis? What are Expected Findings?

A

ECG showing DIFFUSE ST ELEVATIONS and PR DEPRESSION

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111
Q

Most appropriate treatment for Pericarditis

A

NSAIDS

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112
Q

Triad of Cardiac Tamponade

A

BECKS TRIAD: HYPOTENSION, JVD, DISTANT/MUFFLED HEART SOUNDS

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113
Q

Other Classic Signs of Cardiac Tamponade

A

PULSUS PARADOXUS (>10 mmHg fall in BP with inspiration), KUSSMAUL SIGN (sharp increase in JVP with inspiration), EWART SIGN (dullness, increased fremeti, egophony at left scapula), WATER BOTTLE HEART

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114
Q

ECG findings in Cardiac Tamponade

A

DECREASED QRS VOLTAGE AND ELECTRICAL ALTERNANS

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115
Q

Most appropriate treatment for Cardiac Tamponade

A

PERICARDIOCENTESIS

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116
Q

Differentiate Constrictive from Acute Pericarditis

A

CONSTRICTIVE PERICARDITIS PRESENTS WITH JVD, SIGNS OF RIGHT-SIDED HF and PERICARDIAL KNOCK (CALCIFIED OR CASTED PERICARDIUM)

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117
Q

Best initial step for Constrictive Pericarditis? Expected finding?

A

TRANSTHORACIC ECHOCARDIOGRAPHY showing INCREASED PERICARDIAL THICKNESS with CALCIFICATION

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118
Q

Most appropriate treatment for Constrictive Pericarditis

A

MILD CASES: Diuretics, ACE-Inhibitors SEVERE CASES: Pericardiectomy

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119
Q

Underlying cause for Acromegaly

A

Pituitary tumor secreting excess amount of GH

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120
Q

Important thing to compare in Acromegaly

A

COMPARE CURRENT APPEARANCE WITH OLD PHOTOS TO SEE DIFFERENCE IN FACI FEATURES

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121
Q

Loss of Peripheral Vision in Acromegaly

A

PITUITARY TUMOR compressing the OPTIC CHIASM, causing BITEMPORAL HEMIANOPSIA

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122
Q

Prone to Develop Carpal Tunnel Syndrome in Acromegaly

A

BONE OVERGROWTH COMPRESSES MEDIAN NERVE

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123
Q

Best initial test for Acromegaly

A

SERUM IGF-1 LEVELS

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124
Q

Best confirmatory Test for Acromegaly

A

SERUM GH after an OGTT (Glucose normally suppresses GH)

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125
Q

Most appropriate management for Acromegaly

A

TRANSSPHENOIDAL RESECTION OF TUMOR

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126
Q

Drug may be Given preoperatively to Shrink tumor size in Acromegaly

A

OCTREOTIDE (SOMATOSTATIN ANALOGUE)

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127
Q

Underlying cause for Prolactinoma

A

Pituitary tumor secreting excess amounts of PROLACTIN (antagonistic of GnRH)

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128
Q

Amenorrhea in Prolactinoma

A

DECREASED GnRH -> DEC FSH & LH -> INTERRUPTION OF MENSTRUAL CYCLE

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129
Q

Physiologic downregulators of Prolactin Secretion

A

DOPAMINE (antagonistic of Prolactin), ESTROGEN, PROGESTERONE, SOMATOSTATIN

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130
Q

Best initial management for Prolactinoma

A

Drug therapy with BROMOCRIPTINE or CABERGOLINE (DOPAMINE AGONISTS)

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131
Q

Drugs known to cause Secondary HyperProlactinemia

A

METOCLOPRAMIDE, AMITRYPTILINE, PHENOTHIAZINES, ANTIPSYCHOTICS

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132
Q

Underlying cause of SIADH

A

LUNG CANCER COMPOSED OF NEUROENDOCRINE CELLS -> AUTONOMOUS PRODUCTION OF EXCESS ADH

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133
Q

Decreased Sodium in SIADH

A

INCREASED WATER RETENTION -> DILUTIONAL HYPONATREMIA

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134
Q

Seizures in SIADH

A

Decreased Sodium creates osmotic gradient causing water movement into the brain -> CEREBRAL EDEMA

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135
Q

Underlying cause of DI

A

HEAD TRAUMA caused DESTRUCTION of the POSTERIOR PITUITARY GLAND

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136
Q

2 Types of DI

A

CENTRAL DI due to ADH Deficiency and NEPHROGENIC DI due to UNRESPONSIVENESS TO ADH

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137
Q

Distinguish between Central DI & Nephrogenic DI

A

WATER DEPRIVATION TEST: CENTRAL DI - Increased Urine Osmolality after ADH administration at the 6th hour of test; NEPHROGENIC DI - No increase in Urine Osmolality after ADH Administration at the 6th hour of test; PSYCHOGENIC POLYDIPSIA - increasing Urine Osmolality even if before ADH admin and further increase after ADH admin

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138
Q

Treatment for DI

A

CENTRAL DI: Give VASOPRESSIN; NEPHROGENIC DI: administer THIAZIDES (dec urine flow to DCT -> induce formation of functional ADH)

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139
Q

Drugs notorious for causing Nephrogenic DI

A

LITHIUM, DEMECLOCYCLINE

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140
Q

Underling cause for Grave’s Disease

A

AUTOANTIBODIES STIMULATE HYPERSECRETION OF THYROID HORMONES

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141
Q

Autoantibodies present in Grave’s

A

ANTI-TSH RECEPTOR ANTIBODIES

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142
Q

Drugs that cause similar condition as Grave’s

A

AMIODARONE, CLOFIBRATE, METHADONE

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143
Q

Drug of Choice for Grave’s? Feared Side Effect?

A

THIONAMIDES (PTU, MM); SE - AGRANULOCYTOSIS

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144
Q

Most Appropriate Diagnostic Test for Grave’s? Expected results?

A

Free T4, TSH (Increased FT4, Decreased TSH)

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145
Q

Most Appropriate Treatment for Grave’s

A

RADIOACTIVR IODINE ABLATION THERAPY

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146
Q

Expected treatment Complication of RAI used in Grave’s

A

SECONDARY HYPOTHYROIDISM

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147
Q

Drugs given preoperatively if Surgical Intervention contemplated in Grave’s

A

IODIDES to decrease Gland Vascularity

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148
Q

TRH Decrease, TSH Decrease, T4 Increase (Target Organs)

A

PRIMARY HYPERTHYROIDISM

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149
Q

TRH Decreased, TSH Increased, T4 Increased (Pituitary Problem)

A

SECONDARY HYPERTHYROIDISM

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150
Q

TRH Increased, TSH Increased, T4 Increased (Hypothalamic Problem)

A

TERTIARY HYPERTHYROIDISM

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151
Q

Weight Loss in Grave’s

A

EXCESS T3/T4 -> Increased CATABOLISM

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152
Q

Increased Sweating, Increased Bowel Movement & Tachycardia in Grave’s

A

EXCESS T3/T4 -> SYMPATHETIC OVERACTIVITY

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153
Q

Irregular Menses in Grave’s

A

EXCESS T3/T4 -> Inc Sex Hormone Binding Globulin levels, Inc Total Serum Estrogen -> Inc LH and Decreasing mid-cycle LH surge

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154
Q

Exophthalmos in Grave’s

A

Increased Volume of Retrobulbar Tissue due to Deposition of GAGs as a result of Lymphoytic Infiltration

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155
Q

Fine Finger Tremors in Grave’s

A

EXCESS T3/T4 -> Inc Synaptic Transmission and Inc Cerebration -> Reflex Oscillation of Muscle Spindles

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156
Q

Underlying Cause of Hypothyroiditis

A

Antibodies against Thyroglobulin and Thyroid Peroxidase lead to Autoimmune Destruction of Thyroid Gland

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157
Q

TRH Increased, TSH Increased, T4 Decreased (Target Organ Problem)

A

PRIMARY HYPOTHYROIDISM

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158
Q

TRH Increased, TSH Decreased, T4 Decreased (Pituitary Problem)

A

SECONDARY HYPOTHYROIDISM

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159
Q

TRH Decreased, TSH Decreased, T4 Decreased (Hypothalamic Problem)

A

TERTIARY HYPOTHYROIDISM

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160
Q

Fatigue and Weight Gain in Hypothyroidism

A

LOW T3/T4 -> DECREASED METABOLISM

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161
Q

Bradycardia in Hypothyroidism

A

LOW T3/T4 -> DECREASED SYMPATHETIC DRIVE

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162
Q

Coarse, Dry Skin in Hypothyroidism

A

LOW T3/T4 -> DECREASED HEAT PRODUCTION and DECREASED SWEATING

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163
Q

Depression in Hypothyroidism

A

LOW T3/T4 -> DECREASED SYNAPTIC TRANSMISSION IN BRAIN and DECREASED PRODUCTION OF NEUROTRANSMITTERS (SEROTONIN)

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164
Q

Amenorrhea in Hypothyroidism

A

LOW T3/T4 -> INCREASED TRH -> INC PROLACTIN, DEC GnRH, DEC FSH/LH

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165
Q

Bilateral Eyelid Edema

A

DEPOSITION OF GAGS as a result of LYMPHOCYTIC INFILTRATION of the CONNCECTIVE TISSUE of the SKIN

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166
Q

Underlying Cause of Hyperparathyroidism

A

PARATHYROID TUMOR SECRETING LARGE AMOUNTS OF PTH into BLOODSTREAM

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167
Q

Increased PTH, Increased s. Calcium, Decreased s. Phosphate (Target Organs Problem)

A

PRIMARY HYPERPARATHYROIDISM

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168
Q

Increased PTH, Decreased s. Calcium, Decreased s. Phosphate

A

SECONDARY HYPERPARATHYROIDISM (Pituitary Problem)

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169
Q

Depression and Fatigue in Hyperparathyroidism

A

UNKNOWN

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170
Q

Kidney Stones in Hyperparathyroidism

A

INCREASED URINARY CALCIUM CONCENTRATION

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171
Q

Muscle Weakness in Hyperparathyroidism

A

EXCESS PTH -> INCREASED PROTEIN BREAKDOWN and MUSCULAR ATROPHY

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172
Q

Other Expected Symptoms in Hyperparathyroidism

A

PAINFUL BONES, RENAL STONES, ABDOMINAL GROANS, PSYCHIATRIC OVERTONES

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173
Q

Most Appropriate Treatment in Hyperparathyroidism

A

SURGICAL PARATHYROIDECTOMY

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174
Q

Structure Injured during Surgical Treatment of Hyperparathyroidism

A

RECURRENT LARYNGEAL NERVE

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175
Q

Malignancy may Present Similarly with Hyperparathyroidism

A

HYPERCALCEMIA OF MALIGNANCY (usually SCCA OF LUNGS) due to PRODUCTION OF PTHrp (related protein)

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176
Q

Other Diseases that can Result in Secondary Forms of Hyperparathyroidism

A

CHRONIC KIDNEY DISEASE, CHRONIC PANCREATITIS. MALABSORPTION

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177
Q

Underlying Cause of Hypoparathyroidisn

A

INADVERTENT REMOVAL OF THE PARATHYROID GLAND DURING THYROID SURGERY

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178
Q

Decreased PTH, Decreased s. Calcium, Increased s. Phosphate

A

PRIMARY HYPOPARATHYROIDISIM

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179
Q

Decreased PTH, Increased s. Calcium, Increased s. Phosphate

A

SECONDARY HYPERPARATHYROIDISM

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180
Q

Muscle Twitching in Hypoparathyroidism

A

LOW SERUM CALCIUM -> INCREASED EXCITABILITY OF MOTOR NEURONS by DECREASING THRESHOLD POTENTIAL (HYPOCALCEMIC TETANY)

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181
Q

Underlying Cause of DM I

A

AUTOIMMUNE DESTRUCTION OF BETA CELLS IN PANCREAS, LEADING TO INSULIN DEFICIENCY

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182
Q

Increased Glucose, Decreased Insulin, Decreased C Peptide

A

TYPE 1 DM

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183
Q

Increased Glucose, Increased/Normal Insulin, Increased/Normal C Peptide

184
Q

Bedwetting in DM

A

DUE TO OSMOTIC DIURETIC EFFECT OF GLUCOSE

185
Q

Increased Urine Glucose in DM

A

TRANSPORT MAXIMA FOR GLUCOSE HAS BEEN REACHED

186
Q

Weight Loss in DM

A

DECREASED INSULIN -> INCREASED PROTEIN DEGRADATION and MUSCLE WASTING

187
Q

Polydipsia in DM

A

INCREASED THIRST AS A RESPONSE TO FREQUENT URINATION

188
Q

Polyphagia in DM

A

DECREASED UPTAKE OF GLUCOSE INTO TARGET CELLS IN THE BODY TRIGGERS EXCESSIVE HUNGER

189
Q

Delayed Age of Presentation in DM

A

RESIDUAL BETA-CELL FUNCTION (HONEYMOON PERIOD)

190
Q

Diagnostic Test for DM

A

RBS with SSx, FBS >126, HbA1C >6.5, 2 HOUR 75g OGTT (most validated)

191
Q

Most appropriate treatment

A

INSULIN REGIMEN, GLUCOSE MONITORING

192
Q

Complications Expected if left Untreated

A

ACUTE SETTING: Diabetic Ketoacidosis CHRONIC COMPLICATIONS: Macro/Microvascular, Neuropathy, Cataracts, Nephropathy

193
Q

Considerations in Early Morning Hyperglycemia

A

SOMOGYI EFFECT, DAWN PHENOMENON and WANING OF INSULIN

194
Q

Irregular intake of meal at night with Insulin Admin cause 3 AM Hypoglycemia but Negative Feedback Mechanism cause Early Morning Hyperglycemia

A

SOMOGYI EFFECT

195
Q

Controlled Sugar Level throughout the night but with Early Morning Hyperglycemia

A

DAWN PHENOMENON

196
Q

Hyperglycemia at 3AM with Early Morning Hyperglycemia despite Insulin Admin

A

WANING OF INSULIN

197
Q

3 AM Hyperglycemia with Very High Early Morning Hyperglycemia

A

WANING & DAWN PHENOMENON

198
Q

Pathognomonic Triad of DKA

A

HYPERGLYCEMIA, KETONEMIA, HAGMA

199
Q

Pathogenesis of DKA

A

UNCONTROLLED HYPERGLYCEMIA causes KETOACIDOSIS

200
Q

Labs requested in DKA

A

URINE KETONES, ABG, SERUM GLUCOSE

201
Q

Fruity Breath in DKA

A

KETONE BODIES (ACETOACETATE and BETA-HYDROXY- BUTYRATE)

202
Q

FActors that can Incite DKA

A

INFECTION, ISCHEMIA, INFARCTION, IGNORANCE, INTOXICATION

203
Q

Most Appropriate Treatment in DKA

A

FLUID REPLACEMENT and INSULIN DRIP

204
Q

Underlying Cause of Pheochromocytoma

A

Excess Catecholamine Production from Neoplastic Chromaffin Cells in Adrenal Medulla

205
Q

Headaches in Pheochromocytoma

A

DUE TO INCREASED BLOOD PRESSURE

206
Q

Diaphoresis, Tremors, Tachycardia, and Hypertension in Pheochromocytoma

A

DUE TO EXCESSIVE ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM as a result of EXCESS CATECHOLAMINES IN CIRCULATION

207
Q

Classic Triad of Pheochromocytoma

A

TACHYCARDIA. SWEATING, HEADACHES

208
Q

Most Appropriate Diagnostic Test for Pheochromocytoma

A

URINE VANILLYLMANDELIC ACID (URINE METANEPHRINES)

209
Q

Most Appropriate Imaging Study for Pheochromocytoma

A

ABDOMINAL CT SCAN

210
Q

Most Appropriate Treatment for Pheochromocytoma

A

SURGICAL RESECTION

211
Q

Drugs Given Prior to Surgical Intervention in Pheochromocytoma

A

PHENOXYBENZAMINE (Irreversible Alpha Blocker), PHENTOLAMINE (Reversible Alpha Blocker) or LABETALOL (Beta Blocker)

212
Q

Cancer Syndromes associated with Pheochromocytoma? Multiple Endocrine Neoplasia (MEN)?

A

MEN IIa: PCC, Medullary Thyroid Cancer, PTH; MEN IIb: PCC, Medullary Thyroid Cancer, Neuromas

213
Q

Rule of 10s for Pheochromocytoma

A

10% bilateral, 10% extra-adrenal, 10% malignant, 10% familial, 10% pediatric, 10% without BP elevation

214
Q

Underlying Cause for Conn Syndrome (Primary HyperAldosteronism)

A

EXCESS ALDOSTERONE PRODUCTION from ADRENAL CORTEX TUMOR

215
Q

Increased Aldosterone, Decreased Renin, Increased ECF Volume, No Change in Sodium Excretion, Absent Edema, Etiology - Adrenal Tumor (Conn Syndrome)

A

PRIMARY HYPERALDOSTERONISM

216
Q

Increased Aldosterone, Increased Renin, Increased ECF Volume, Decreased Sodium Excretion, Presence of Edema, Etiology - RENIN-SECRETING TUMOR, RENAL ARTERY STENOSIS

A

SECONDARY HYPERALDOSTERONISM

217
Q

Persistent Hypertension in Conn Syndrome

A

DUE TO EXCESSIVE ALDOSTERONE PRODUCTION

218
Q

Normal Sodium Excretion and No Edema despite of Increased ECF Volume

A

due to SODIUM ESCAPE PHENOMENON (Increased BP -> Inc ANP production -> Normalization of Sodium Excretion and Prevents Edema)

219
Q

Fatigue and Muscle Weakness in Conn Syndrome

A

due to DECREASED POTASSIUM LEVELS

220
Q

Polyuria in Conn Syndrome

A

DECREASED POTASSIUM IMPAIRS URINE CONCENTRATING ABILITY (Counter Current Multiplier Uses Na-K-Cl Co-Transport)

221
Q

Metabolic Alkalosis in Conn Syndrome

A
  1. Hydrogen ion loss into urine and migration into potassium-depleted cells 2. Potassium deficiency increases capacity of Proximal Convoluted Tubule to Reabsorb Filtered Bicarbonate
222
Q

Most appropriate Treatment in Conn Syndrome

A

SURGICAL REMOVAL OF ADRENAL MASS

223
Q

Management for Unresectable Tumor in Conn Syndrome

A

ALDOSTERONE ANTAGONISTS (SPINOROLACTONE and EPLERENONE)

224
Q

Underlying Cause of Cushing’s Syndrome

A

EXCESS CORTISOL PRODUCTION FROM ADRENAL CORTEX TUMOR

225
Q

Most common Cause of Cushing Syndrome

A

IATROGENIC (EXCESS STEROID INTAKE)

226
Q

Increased Cortisol, Decreased ACTH, No effect on High-Dose Dexa Suppression, Eti: CORTISOL PRODUCING ADRENAL TUMOR

A

ADRENAL CUSHING SYNDROME

227
Q

Increased Cortisol, Increased ACTH, Suppressed High-Dose Dexa Suppression, Eti: ACTH-Producing Pituitary Tumor

A

PITUITARY CUSHING SYNDROME

228
Q

Increased Cortisol, Increased ACTH, No effect on High-Dose Dexa Suppression, Etio: ACTH-Producing Lung Tumor

A

ECTOPIC CUSHING SYNDROME

229
Q

Hypertension in Cushing Syndrome

A
  1. Excess cortisol -> Inc Vascular Responsiveness to Catecholamines -> Inc Total Peripheral Resistance 2. At High Doses, Glucocorticoids display mineralocorticoid effects -> SALT and WATER RETENTION
230
Q

Central Obesity in Cushing Syndrome

A

Catabolism of Skin Proteins lead to Weakening and Rupture of Collagen Fibers in the Dermis

231
Q

Easy Bruising and Violaceous Abdominal Striae in Cushing Syndrome

A

EXCESS CORTISOL LEADS TO INSULIN RESISTANCE and ADIPOSE TISSUE DEPOSITION at CHARACTERISTIC SITES (MOON FACIES, BUFFALO HUMP)

232
Q

Acne and Hirsutism in Cushing’s Syndrome

A
  1. Excess adrenal androgens 2. Excess insulin stimulates ovarian theca cells to produce androgens
233
Q

Proximal Weakness and Edema in Cushing’s

A

Due to EXCESS PROTEIN CATABOLISM and PROTEIN DEPLETION

234
Q

Most appropriate treatment in Cushing’s

A

SURGICAL RESECTION of the ADRENAL MASS

235
Q

Management for Surgically Unresectable Tumors

A

KETOCONAZOLE, METYRAPONE

236
Q

Underlying Cause of Addison’s Disease

A

AUTOIMMUNE DESTRUCTION OF ADRENAL GLANDS

237
Q

Increased CRH, Increased ACTH, Decreased Cortisol, Decreased Aldosterone, Decreased Androgens, (+) Hypotension, Dark Skin Color, Etio: AUTOIMMUNE ADRENALITIS

A

PRIMARY ADRENAL INSUFFICIENCY

238
Q

Increased CRH, Decreased ACTH, Decreased Cortisol, Normal Aldosterone, Decreased Androgens, (-) Hypotension, Pale Skin Color, Etio: PITUITARY NOT SECRETING ACTH

A

SECONDARY ADRENAL INSUFFICIENCY

239
Q

Decreased CRH, Decreased ACTH, Decreased Cortisol, Normal Aldosterone, Decreased Androgen, (-) Hypotension, Pale Skin Color, Etio: STEROID WITHDRAWAL

A

TERTIARY ADRENAL INSUFFICIENCY

240
Q

Muscle Weakness, Weight Loss and Anorexia in Adrenal Insufficiency

A

DECREASED ENERGY MOBILIZATION DUE TO DECREASED CORTISOL

241
Q

Skin Darkening in Adrenal Insufficiency

A

INCREASED ACTH SECRETION LEADS TO EXCESS POMC-DERIVED HORMONES (a-MSH, b-MSH)

242
Q

Orthostatic Hypotension in Adrenal Insufficiency

A

Decreased Aldosterone -> DECREASED RESPONSIVENESS OF RAA

243
Q

Decreased Sodium and Increased Potassium Levels in Adrenal Insufficiency

A

DECREASED ALDOSTERONE ACTIVITY

244
Q

Decreased Glucose Level in Adrenal Insufficiency

A

DECREASED CORTISOL causes INCREASED INSULIN SENSITIVITY

245
Q

Decreased Pubic Hair in Adrenal Insufficiency

A

DUE TO ADRENAL ANDROGEN DEFICIENCY

246
Q

Signs of Androgen Deficiency more seen in Females with Adrenal Insufficiency

A

ADRENALS are MAIN SOURCE OF ANDROGENS IN FEMALES (TESTIS in MALES)

247
Q

Occurence of severe hypotension (shock) as a result of extreme adrenal hormone deficiency (in patients with Depressed HPA axis)

A

ADRENAL CRISIS

248
Q

Adrenal Crisis in setting of Fulminant Meningococcemia

A

WATERHOUSE-FRIDERICHSEN SYNDROME (due to BILATERAL ADRENAL HEMORRHAGE)

249
Q

Most Appropriate Diagnostic Test Adrenal Insufficiency

A

ACTH STIMULATION TEST (COSYNTROPIN TEST)

250
Q

Interpretation of ACTH STIMULATION TEST (COSYNTROPIN TEST)

A

PRIMARY AI: Low Cortisol + Low ACTH; SECONDARY/TERTIARY AI: Low Cortisol + High ACTH

251
Q

Most Appropriate Treatment in Adrenal Insufficiency

A

GLUCOCORTICOID and MINERALOCORTICOID REPLACEMENT, AGGRESSIVE HYDRATION

252
Q

Most common Cause of Acute Pancreatitis

A

GALLSTONES > ALCOHOLIC BINGE DRINKING

253
Q

Other important Cause of Acute Pancreatitis

A

Trauma, Steroids, Mumps, Autoimmune, Scorpion Bites, Hyperlipidemia, Drugs (Antivirals)

254
Q

Characteristic Signs on PE of Acute Pancreatitis

A

GRAY TURNER (FLANK) & CULLEN (PERIUMBILICAL)

255
Q

Most Common Appropriate Diagnostic Test

A

SERUM AMYLASE (MORE SENSITIVE) & SERUM LIPASE (MORE SPECIFIC)

256
Q

Important Imaging Study in Acute Pancreatitis

A

ABDOMINAL CT SCAN (SENTINEL LOOPS)

257
Q

Most Appropriate Treatment for Acute Pancreatitis

A

BOWEL REST (NPO), HYDRATION, ANALGESICS

258
Q

Most Appropriate Analgesic for Treatment of Acute Pancreatitis

A

MEPERIDINE (DOES NOT CAUSE SO DYSFUNCTION)

259
Q

Complications of Acute Pancreatitis

A

Hemorrhage, Pseudocyst, Chronic Pancreatitis

260
Q

Criteria used for Prognostication in Acute Pancreatitis

A

RANSON’S CRITERIA: AT PRESENTATION (GALAW) - Glucose >200mg/dL, Age >55, LDH >250u/L, AST >250u/L, WBC >16,000/mm3; AT 48 HOURS (CHOBBS) - Calcium 10%, pO2 5mg/dL, Base deficit >5mg/dL, Sequestration of Fluid ls >6L

261
Q

Prognostication of Acute Pancreatitis using Ranson’s Criteria

A

0-2: 2% mortality, 3-4: 15% mortality, 5-6: 40% mortality, 7-8: 100% mortality

262
Q

Antibiotics indicated for Acute Pancreatitis

A

ONLY INDICATED IN SEVERE PANCREATITIS WHEN >30% NECROSIS ON CT SCAN

263
Q

Indication for Surgery in Acute Pancreatitis

A

PSEUDOCYST, ABSCESS, BILIARY PANCREATITIS

264
Q

Clinical Presentation of Chronic Pancreatitis

A

ABDOMINAL PAIN WITH SIGNS OF MALABSORPTION DUE TO PANCREATIC INSUFFICIENCY

265
Q

Most Common Cause of Chronic Pancreatitis

A

LONG TERM ALCOHOL ABUSE

266
Q

Treatment for Chronic Pancreatitis

A

DIETARY MODIFICATION (SMALL, LOW-FAT MEALS), ENZYME REPLACEMENT (PANCRELIPASE)

267
Q

Risk Factors for Esophageal Adenocarcinoma

A

ACHALASIA, BARRETT ESOPHAGUS, CIGARETTE SMOKING, DIVERTICULA, ETHANOL, FAMILIAL

268
Q

Most Appropriate Diagnostic Test for Esophageal Adenocarcinoma

A

BARIUM SWALLOW, followed by EGD with BIOPSY

269
Q

Seen on Biopsy in Esophageal Adenocarcinoma

A

SQUAMOCOLUMNAR METAPLASIA (BARRETT ESOPHAGUS) and NEOPLASTIC CHANGES (INVASION)

270
Q

Most Appropriate Treatment for Esophageal Adenocarcinoma

A

ESOPHAGECTOMY with GASTRIC PULL-UP with or without CHEMORADIATION (Controversial)

271
Q

2 Types of Esophageal Cancer? Associated conditions?

A

BARRETT’S ESOPHAGUS = ESOPHAGEAL ADENOCARCINOMA; PLUMMER-VINSON SYNDROME = SCCA

272
Q

Localization and Incidence for Esophageal AdenoCarcinoma and SCCA

A

NOW EQUAL IN INCIDENCE; ESOPHAGEAL ADENOCARCINOMA in Distal 3rd, ESOPHAGEAL SCCA in Middle 3rd

273
Q

Differentiate Esophageal Cancer from Achalasia clinically

A

ACHALASIA: dysphagia to solids and liquids simultaneously; ESOPHAGEAL CA: dysphagia first to solids progressing to liquids

274
Q

Alcoholic who had Frequent Retching and Vomiting leading to Severe Hematemesis

A

ESOPHAGEAL RUPTURE

275
Q

Differentiate 2 Most Likely Cause of Esophageal Rupture

A

MALLORY-WEISS SYNDROME: Partial Thickness tearing at GEJ; BOERHAAVE’S SYNDROME: ANTIBIOTICS, SURGERY, IV HYDRATION (almost 100% mortality)

276
Q

Underlying Pathology in PUD

A

GASTRIC and HYPERSECRETION LEADING TO ULCERS

277
Q

Most Appropriate Diagnostic Test for PUD

A

ENDOSCOPY with BIOPSY

278
Q

Conditions encompassed by PUD

A

GASTRIC ULCERS and DUODENAL ULCERS

279
Q

Most common location of PUD

A

DUODENAL BULB

280
Q

Differentiate Gastric Ulcer and Peptic Ulcer

A

GASTRIC ULCER: Pain worse on food intake, no nocturnal pains; PEPTIC ULCER: Pain relieved with food intake, awakens patient at night

281
Q

Most appropriate treatment for PUD

A

PROTON PUMP INHIBITORS; if (+) H Pylori: OMEPRAZOLE + CLARITHROMYCIN + AMOXICILLIN

282
Q

Possible Complications for PUD

A

HEMORRHAGE > PERFORATION > GASTRIC OUTLET OBSTRUCTION

283
Q

Treatment of PUD when Refractory to Medical Management

A

DUODENAL ULCER: Truncal Vagotomy with Pyloroplasty; GASTRIC ULCER: Bilroth I or II Reconstruction

284
Q

PUD patient continues to be Refractory to Management. Pancreatic mass on CT scan

A

GASTRINOMA (ZOLLINGER-ELLISON SYNDROME)

285
Q

Most common anatomic location of Gastrinomas

A

PASSARO’S TRIANGLE: junctions of cystic duct/ CBD, 2nd/3rd portion of duodenum, head/ neck of pancreas)

286
Q

Most Appropriate Diagnostic Test for Gastrinomas

A

PENTAGASTRIN STIMULATION TEST, SECRETIN STIMULATION TEST

287
Q

Usual Location of Ulcers in Zollinger-Ellison Syndrome

A

Simultaneous, recurrent gastric and duodenal ulcers (postbulbar)

288
Q

Underlying pathology in Chronic Liver Disease

A

ADVANCED LIVER CIRRHOSIS COMPLICATED by PORTOSYSTEMIC SHUNTING

289
Q

Most common cause of Chronic Liver Disease

A

ALCOHOLISM and VIRAL HEPATITIS

290
Q

Differentiate among Common Causes of Chronic Liver Disease

A

AST/ALT RATIO > 2 in ALCOHOLIC LIVER DISEASE = 1 in VIRAL HEPATITIS

291
Q

Histopathologic Hallmark seen in Alcoholic Liver Disease compared to Viral Hepatitis

A

MALLORY BODIES (Malloy Lasingero) = ALD, COUNCILMAN BODIES (Councillor Manyakis) = VIRAL HEPATITIS

292
Q

3 Stages of Alcoholic Liver Disease

A

STEATOSIS, HEPATITIS, CIRRHOSIS

293
Q

Other Signs and Symptoms of Liver Disease

A

CLD: palmar erythema, testicular atrophy, spider angioma, Duputyren contracture; PH: hemorrhoids, caput medusae, varices ruptured esophageal varices

294
Q

Gynecomastia, Spider Angiomata and Palmar Erythema in Chronic Liver Disease

A

Due to High Circulating Estrogen Levels

295
Q

Muehrcke Nails, Peripheral Edema and Prolonged Bleeding Time in Chronic Liver Disease

A

Due to HYPOALBUMINEMIA, HYPOPROTEINEMIA

296
Q

Thrombocytopenia, Anemia and Leukopenia in Chronic Liver Disease

A

Due to HYPERSPLENISM

297
Q

Ruling Out Other Causes of Ascites other than Portal Hypertension

A

SERUM ASCITES ALBUMIN GRADIENT (SAAG): >1.1 - Portal Hypertension, <1.1 - Malignancy or Infection

298
Q

Most Appropriate Treatment for Chronic Liver Disease

A

TIPS PROCEDURE

299
Q

Definitive Treatment for Chronic Liver Disease

A

LIVER TRANSPLANT

300
Q

Complications if Chronic Liver Disease is Left Untreated

A

Massive UGIB, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, bacterial peritonitis

301
Q

Signs if Hepatic Failure

A

HYPERAMMONEMIA, FETOR HEPATICUS

302
Q

Hepatic Encephalopathy and Asterixis in Chronic Liver Disease

A

ACCUMULATION OF AMMONIA IN CNS

303
Q

Responsible for Fetor Hepaticus

A

MUSTY, FECAL SMELL due to ACCUMULATION OF MERCAPTANS

304
Q

Treatment of Hepatic Encephalopathy

A

LACTULOSE (promotes bowel movement and excretion of Ammonia, acidification of colon, deactivation of colonic bacteria), Protein restriction (branched-chain amino acid), Neomycin

305
Q

Underlying pathology in Ulcerative Colitis

A

INFLAMMATORY BOWEL DISEASE

306
Q

Types of Ulcerative Colitis

A

ULCERATIVE COLITIS & CROHN DISEASE

307
Q

Can be ANYWHERE in GIT, with SKIP LESIONS and RECTAL SPARING, TRANSMURAL inflammation, COBBLESTONE MUCOSA, NONCASEATING GRANULOMAS

A

CROHN’s DISEASE

308
Q

Found in COLON only, MUCOSAL inflammation, LEAD PIPE colon, PSEUDOPOLYPS, CRYPT ABSCESSES

A

ULCERATIVE COLITIS

309
Q

Extracolonic Manifestation associated with Ulcerative Colitis

A

Arthritis, Episcleritis, Uveitis, Pyoderma Gangrenosum

310
Q

Increased Risk of Malignancy in Ulcerative Colitis

A

COLON CANCER

311
Q

Bacterial Infection causing Flare-Ups in Ulcerative Colitis

A

CLOSTRIDIUM DIFFICILE

312
Q

Complications of Ulcerative Colitis? Definitive treatment?

A

EXSANGUINATION, TOXIC MEGACOLON; Definitive Tx - TOTAL COLECTOMY

313
Q

Most Likely Cause of Acute Tubular Necrosis

A

RENAL HYPOPERFUSION due to HYPOVOLEMIA (hemorrhage), RHABDOMYOLYSIS

314
Q

Other Laboratory Tests requested in ATN

A

SERUM ELECTROLYTES, BUN, CREA

315
Q

Differentiate Azotemia from Uremia

A

AZOTEMIA: Biochemical (Inc Urea); UREMIA: Clinical Signs and Symptoms

316
Q

3 Important Causes of Azotemia

A

PRERENAL DISEASE, INTRINSIC RENAL DISEASE and POSTRENAL DISEASE (OBSTRUCTIVE UROPATHY)

317
Q

BUN/Crea ratio >20, Fe Sodium <1%, due to Hypovolemia, Hemorrhage

A

PRERENAL AZOTEMIA

318
Q

BUN/Crea Ratio 2%, due to PSGN, Drugs, HTN

A

INTRINSIC RENAL

319
Q

BUN/Crea ratio 10-20, Fe Sodium Intermediate, due to Prostate, Cervical Cancer

A

OBSTRUCTIVE UROPATHY

320
Q

Continuing significant irreversible reduction in nephron number

A

CHRONIC KIDNEY DISEASE

321
Q

Most common cause of Chronic Kidney Disease

A

DIABETES MELLITUS

322
Q

Staging for Chronic Kidney Disease

A

Stage 0: with Risk Factor, Stage 1: GFR >90, Stage 2: GFR 60-89, Stage 3: GFR 30-59, Stage 4: GFR 15-29, Stage 5: GFR <15 (ESRD)

323
Q

Indications for Dialysis in CKD

A

ACIDOSIS, ELECTROLYTES (Hyperkalemia), Ingestion of Toxins, Overload, Uremia

324
Q

2 Modes of Dialysis

A

HEMODIALYSIS (Tesio Catheter and AV graft) & PERITONEAL DIALYSIS (Tenchkoff Catheter)

325
Q

Anemia in CKD? Type of Anemia?

A

Inability to produce EPO causes NORMOCYTIC, NORMOCHROMIC ANEMIA

326
Q

Secondary Hyperparathyroidism in CKD

A

Failing kidneys FAIL TO REABSORB CALCIUM -> HYPOCALCEMIA

327
Q

Vitamin D supplementation in CKD

A

Inability to form active Vitamin D (1,25-DHCC) due to kidney damage

328
Q

Clinical Effect of Hypocalcemia, Hyperphosphatemia and Low Vitamin D in CKD

A

RENAL OSTEODYSTROPHY (CHONDROCALCINOSIS, OSTEOPENIA)

329
Q

Most common Cause of Death in CKD

A

CAD/MI (ESRD is a CAD equivalent)

330
Q

Medications Given to Prevent Cardiac Complications in CKD

A

BETA-BLOCKERS, ACE-Inhibitors, STATINS

331
Q

Most common cause of Acute Pyrlonephritis

A

ESCHERICHIA COLI

332
Q

Most Appropriate Treatment for Acute Pyelonephritis

A

EMPIRIC ANTIBIOTIC THERAPY (QUINOLONES)

333
Q

Complication of Acute Pyelonephritis in Diabetics

A

RENAL PAPILLARY NECROSIS

334
Q

Facultative Gram-Negative Rods with Swarming Motility in Urine Culture in Acute Pylonephritis

A

PROTEUS MIRABILIS

335
Q

Infections more common on Females in Acute Pyelonephritis

A

Females have SHORTER URETHRA

336
Q

Underlying pathology in Nephrotic Syndrome

A

IN SITU IMMUNE COMPLEX FORMATION/ DEPOSITION

337
Q

Most Common Cause of Nephrotic Syndrome in Adults

A

MEMBRANOUS NEPHROPATHY

338
Q

Most Common Cause of Nephrotic Syndrome in Children

A

MINIMAL CHANGE DISEASE

339
Q

Renal Biopsy in Nephrotic Syndrome

A

LM: Diffuse capillary wall thickening, EM: Subepithelial deposits, IF: Granular deposits

340
Q

Nephrotic Range Proteinuria

A

> 3.5g protein in 24H urine collection

341
Q

Most Appropriate Treatment for Nephrotic Syndrome

A

STEROIDS (PREDNISONE): Better response in Minimal Change Disease

342
Q

Complications arising from Nephrotic Syndrome

A

SPONTANEOUS BACTERIAL PERITONITIS, THROMBOMBOLIC EVENTS, HYPERLIPIDEMIA

343
Q

If Nephrotic Syndrome patient Unresponsive to Steroids after 2 Months

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

344
Q

Most Common Cause of Nephrotic Syndrome in Children

A

MINIMAL CHANGE DISEASE (LIPOID NEPHROSIS)

345
Q

Types of Renal Tubular Acidosis

A

TYPE I RTA, TYPE II RTA, TYPE IV RTA

346
Q

Most Common Cause of RTA

A

TYPE I RTA: Sporadic, Hep B or Hep C; TYPE II RTA: Multiple Myeloma, Amyloidosis; TYPE IV RTA: DM, Hypoaldosteronism

347
Q

Pathophysiologic Mechanism for RTA

A

TYPE I RTA: Inability to secrete H+ in DCT; TYPE II RTA: Inability to reabsorb HCO3 in PCT; TYPE IV RTA: Decreased Aldosterone

348
Q

High Urine pH (Basic), (+) STONES, Low Potassium, Diagnosis by Acid Load (give NH4Cl), Tx via HCO3 + K tabs

A

TYPE I RTA (Distal)

349
Q

Low Urine pH (Acidic), (-) Stones, Low Potassium, Diagnosis by HCO3 LOAD (Give HCO3), Tx via HCO3 + K tabs + diuretics (HCTZ)

A

TYPE II RTA (PROXIMAL)

350
Q

Low Urine pH (Acidic), (-) Stones, HIGH POTASSIUM, Diagnosis by Na Restriction (High Urine Na), Tx via Fludrocortisone

A

TYPE IV RTA (DM)

351
Q

Defect at Thick Ascending Loop, Na-K-2Cl Symport Channel, more on Children, Normal/ Increased Urine Ca2+ (Stones), Impaired Concentrating Ability, Dec GFR (AS IF LOOP DIURETIC ABUSER, MORE SEVERE)

A

BARTERR’S SYNDROME

352
Q

Defect at Distal Convoluted Tubule, Na-Cl Symport Channel, more on Adults, Dec Urine Ca2+ (No Stones), Normal Concentrating Ability, Normal GFR (AS IF THIAZIDE DIURETIC ABUSER)

A

GITELMAN’S SYNDROME

353
Q

Underlying Pathology in SLE

A

CHRONIC MULTISYSTEM AUTOIMMUNE DISEASE

354
Q

Type of Hypersensitivity in SLE

A

TYPE III HYPERSENSITIVITY

355
Q

Most Sensitive and Specific Serologic Tests for SLE

A

MOST SENSITIVE: ANA; MOST SPECIFIC: anti-dsDNA or anti-Smith

356
Q

Diagnostic Criteria for SLE

A

AT LEAST 4/11: Serositis, Oral Ulcers, ANA, Photosensitivity, Blood, Renal, Arthritis, Immunologic, Neuropsychiatric, Malar Rash, Discoid Rash

357
Q

Most Common Criterion for SLE

A

HEMATOLOGIC CHANGES (LEUKOPENIA)

358
Q

Drugs causing Similar Presentation as SLE? Auto- antibodies associated?

A

HYDRALAZINE, ISONIAZID, PROCAINAMIDE, PENICILLAMINE; ANTI-HISTONE ANTIBODIES

359
Q

False Positive Syphilis Test in SLE

A

Anti- Cardiolipin Antibodies; RPR is embedded in Cardiolipin

360
Q

Complications in Pregnant SLE patient? Pathogenesis?

A

RECURRENT ABORTIONS due to APAS (due to Lupus Anticoagulant and AntiCardiolipin Antibodies)

361
Q

Most Appropriate Treatment for Acute Flare-Ups in SLE

A

CORTICOSTEROIDS

362
Q

Most Appropriate Treatment for Cutaneous Lesions

A

ANTIMALARIALS with or without CORTICOSTEROIDS (Low Dose)

363
Q

Most Appropriate Treatment to Induce Disease Remission in SLE

A

IMMUNOSUPPRESSIVES (CYCLOPHOSPHAMIDE) + CORTICOSTEROIDS

364
Q

Management for Development of Unexplained Proteinuria and Hematuria

A

RENAL BIOPSY

365
Q

Most Catastrophic Organ Involvement in SLE

A

SLE NEPHRITIS

366
Q

Various Forms of Renal Involvement

A

I: Minimal Mesangial 10-25%, II: Mesangial Proliferative, III: Focal Proliferative 20-35%, IV: Diffuse Proliferative 35-60% (Most Common/ Most Severe; HP- Wire-Loop Lesions), V: Membranous 10-15% (Nephrotic Change Proteinuria)

367
Q

Underlying Pathology in Osteoarthritis

A

CHRONIC, SLOWLY PROGRESSIVE, EROSIVE DAMAGE TO JOINT SURFACES -> LOSS OF ARTICULAR CARTILAGE

368
Q

Etiology of Osteoarthritis

A

DIRECTLY PROPORTIONAL to INCREASING AGE and TRAUMA to the JOINT (Most Common Cause of Joint Disease)

369
Q

Most Appropriate Diagnostic Test in Osteoarthritis

A

XRAY OF AFFECTED JOINTS (Joint Space Narrowing, Osteophytes, Bone Cysts)

370
Q

Most Appropriate Treatment in Osteoarthritis

A

WEIGHT LOSS, MODERATE EXERCISE, ACETAMINOPHEN (Best Initial Analgesic), INTRAARTICULAR STEROIDS IF THERE IS NO PAIN CONTROL, JOINT REPLACEMENT for SEVERE DISEASE

371
Q

Differentiate Rheumatoid Arthritis from Osteoarthritis

A

RHEUMATOID ARTHRITIS: Bilateral, Symmetrical Joint Involvement (usually MCP joints), Morning Stiffness >30min, Autoimmune Phenomena (Rheumatoid Nodules, Episcleritis, Vasculitis)

372
Q

Underlying Pathology in Gout

A

Defect in Urate Metabolism due to Overproduction (Idiopathic, Increased turnover of cells, enzyme deficiency) or underexcretion (Renal Insufficiency, Acidosis, Thiazides, Aspirin)

373
Q

Most Acurate Diagnostic Test in Gout

A

Joint Aspiration (Needle-Shaped Crystals with Negative Bifringence on Polarized Light Microscopy)

374
Q

Most appropriate treatment of Gout in ER

A

NSAIDS and COLCHICINE

375
Q

Safe Drug for Chronic Gout with Renal Insufficiency

A

ALLOPURINOL

376
Q

Calcium pyrophosphate deposition disease

A

PSEUDOGOUT

377
Q

Finding on Joint Aspiration in Gout

A

POSITIVELY BIFRINGENT RHOMBOID-SHAPED CRYSTALS

378
Q

Most Common Cause of Atypical Pneumonia

A

Mycoplasma (Most Common), Legionella, Chlamydia

379
Q

Diagnostic Test to Confirm Clinical Impression

A

MYCOPLASMA: IgM Titer or Cold Agglutinin Test; LEGIONELLA: Urinary Antigen Test; CHLAMYDIA: Serology or Antigen Detection

380
Q

Most Likely Cause of Disease in Atypical Pneumonia

A

MYCOPLASMA (Skin Rash, Hemolysis, Arthralgia)

381
Q

Other Clinical Clinical Cues to Rule Out Other Causes of Atypical Pneumonia

A

LEGIONELLA: Hyponatremia, Diarrhea; CHLAMYDIA: Atherosclerosis

382
Q

Most Appropriate Treatment in Atypical Pneumonia

A

Empiric Therapy with AZITHROMYCIN

383
Q

Most Common Cause of High Grade Fever, Rusty Sputum, and Lobar Pneumonia

A

STREPTOCOCCUS PNEUMONIAE

384
Q

Most Common Cause of Pneumonia with Currant Jelly Sputum

A

KLEBSIELLA PNEUMONIAE

385
Q

Pathologic Stages of Typical Bacterial Pneumonia

A

CONGESTION, RED HEPATIZATION, GREY HEPATIZATION, RESOLUTION

386
Q

Indication for Pseudomonas Coverage in CAP

A

PROLONGED BROAD-SPECTRUM ANTIBIOTIC THERAPY, BRONCHIECTASIS, MALNUTRITION, STEROID THERAPY

387
Q

Admission Criteria for patient with CAP

A

Confusion, Uremia, RR>30, low BP, Age >65 (CURB-65 CRITERIA, If 2 or more present, ADMIT)

388
Q

Light’s Criteria: LDH >200, LDH/Serum Ratio >0.6, Protein/Serum Ratio >0.5, Ex: Pneumonia, Cancer, Infections, RHD

389
Q

Light’s Criteria: LDH <0.5, Ex: CHF, Cirrhosis, Renal Failure

A

TRANSUDATE

390
Q

Underlying pathology in COPD

A

Destruction of Normal Alveoli-Capillary structures and enlargement of Airspace

391
Q

2 Disease Components in Spectrum of COPD

A

EMPHYSEMA and CHRONIC BRONCHITIS

392
Q

Most Important Risk Factor of COPD

393
Q

Other Important Diagnostic Test for COPD? Expected Findings?

A

PULMONARY FUNCTION TEST showing DECREASED FEV1 and FEV1/FVC ratio

394
Q

Most Common Pattern of Involvement in COPD

A

CENTRIACINAR EMPHYSEMA OF UPPER LOBES

395
Q

Congenital Enzyme Deficiency associated with COPD? Morphologic pattern?

A

ALPHA-1 ANTITRYPSIN DEFICIENCY, with BIBASILAR PANACINAR EMPHYSEMA and LIVER CIRRHOSIS

396
Q

Drug of Choice for COPD

A

INHALED BRONCHODILATOR + ANTICHOLINERGIC; INHALED CORTICOSTEROIDS

397
Q

Only Treatments shown to Improve Survival in COPD

A

SMOKING CESSATION and HOME OXYGEN THERAPY

398
Q

Right-Sided CHF in COPD

A

COR PULMONALE (COPD STAGE V)

399
Q

Most Common Cause of Exacerbation in COPD

A

INFECTIONS (H. Influenzae, Influenza virus)

400
Q

Preventive Measures for COPD patients? Level of Prevention?

A

PNEUMOCOCCAL, Hib and INFLUENZA VACCINATIONS (PRIMARY PREVENTION)

401
Q

Drug of Choice for COPD with Comorbid Cardiac Conditions

A

IPRATROPIUM (BETA-AGONISTS cause TACHYCARDIA and ARRHYTHMIAS)

402
Q

Underlying Pathology in PE

A

DVT travels to LUNGS and OBSTRUCTS PULMONARY VASCULATURE

403
Q

Risk Factors for PE

A

HYPERCOAGULABILITY: Estrogens, Malignancy, Genetic Diseases; STASIS: Prolonged Immobilization; ENDOTHELIAL INJURY: Trauma, previous DVT (VIRCHOW’s TRIAD)

404
Q

Most Appropriate Diagnostic Test for PE? Expected Finding?

A

VENTILATION-PERFUSION SCAN (V/Q scan); Multiple Perfusion Defects with Normal Ventilation (V/Q ratio)

405
Q

Gold Standard for Diagnosis of PE

A

PULMONARY ANGIOGRAPHY (SPIRAL CT?)

406
Q

Most Common Acid-Base Disorder associated with PE

A

RESPIRATORY ALKALOSIS

407
Q

Most Common ECG finding in PE

A

SINUS TACHYCARDIA (also NSSTTWC or S1Q3T3 strain pattern)

408
Q

Most Appropriate Treatment for PE

A

ANTICOAGULATION

409
Q

Most Appropriate Treatment for PE patients with Contraindications

A

IVC FILTER

410
Q

Most Common Cause of Death in PE

A

PROGRESSIVE RIGHT-SIDED HEART FAILURE

411
Q

Causative Agent of TB

A

MYCOBACTERIUM TUBERCULOSIS

412
Q

Most Appropriate Diagnostic Test for TB

A

SPUTUM AFB x 3

413
Q

Phases of Infection of TB?

A

PRIMARY COMPLEX and REACTIVATION TB

414
Q

Mode of Transmission for TB

A

AIRBORNE DROPLETS

415
Q

Asymptomatic Case Detection for TB

A

PPD or MANTOUX test

416
Q

Chest XRay Findings in TB

A

SIMON’S FOCUS, CICATRICIAL CHANGES, CAVITATION at LUNG APEX

417
Q

Most Appropriate Treatment for TB

A

2 HRZE/ 4HR in 6 months

418
Q

Most Effective Treatment Strategy

419
Q

Adverse Effects associated with TB Treatment

A

INH: Neuro/Hepatotoxicity, RMP: RO urine, PZA: Arthralgia, Hepatotoxicity, EMB: Retrobulbar Neuritis

420
Q

Underlying Pathology in BAIAE

A

REVERSIBLE AIRWAY INFLAMMATION and OBSTRUCTION

421
Q

Type of Immune Reaction causing BAIAE

A

TYPE I REACTION (IgE Mediated)

422
Q

Bronchospasm in BAIAE

A

IgE-mediated degranulation of Mast Cells causing HISTAMINE RELEASE

423
Q

HP Hallmarks in BAIAE

A

CURSCHMANN’s SPIRALS, CHARCOT-LEYDEN CRYSTALS

424
Q

Best Initial Test for Diagnosis of BAIAE

A

PULMONARY FUNCTION TEST: 12% improvement with FEV1 after Beta-Agonist)

425
Q

Next best Diagnostic Test if Asthma patient is Not in Exacerbation

A

METHACOLINE CHALLENGE: >20% decrease in FEV1

426
Q

Poor Prognostic Factors for Asthma

A

PULSUS PARADOXUS, RESPIRATORY FATIGUE, CYANOSIS

427
Q

ABG in BAIAE

A

EARLY STAGE: Repiratory Alkalosis, Normal pO2, LATE STAGE: Respiratory Acidosis, IMPENDING RESPIRATORY FAILURE: Normal ABG

428
Q

Acute Exacerbation of Asthma Not Responding to Standard Treatments

A

STATUS ASTHMATICUS

429
Q

Treatment of Status Asthmaticus

A

IV HYDROCORTISONE, NEBULIZED EPINEPHRINE or ALBUTEROL, THEOPHYLLINE, MgSO4

430
Q

Types of Medication in Asthma Management

A

RELIEVERS (Reduce Bronchospasm): SABA, Ipratropium, Theophylline, IV Hydrocortisone; CONTROLLERS (Reduce Inflammation): Steroids, LABA, Leukotriene Antagonists, Mast Cell Stabilizers, anti-IgE antibodies

431
Q

2 Main Morphologic Forms of Lung Cancer

A

SMALL CELL LUNG CANCER, NON-SMALL CELL LUNG CANCER

432
Q

Most Significant Risk Factor for Lung Cancer

A

CIGARETTE SMOKING

433
Q

Next Step in Management of Lung Cancer

A

CHEST XRAY

434
Q

Gynecomastia, Clubbing and Acanthosis Nigricans in Lung Cancer

A

PARANEOPLASTIC SYNDROMES

435
Q

Most Appropriate Diagnostic Test after Imaging Studies

A

LUNG BIOPSY

436
Q

Centrally-Located Lung Mass upon CXray in Lung Cancer

A

SMALL CELL LUNG CANCER, SQUAMOUS CELL LUNG CANCER

437
Q

Differentiate Lung Cancer on Basis of Paraneoplastic Syndromes

A

SMALL CELL LUNG CANCER: Ectopic Cushing Syndrome, SIADH, Lambert-Eaton Myasthenia; SQUAMOUS CELL LUNG CANCER: Hypercalcemia, Clubbing, Gynecomastia

438
Q

Most Appropriate Treatment for Lung Cancer

A

CHEMOTHERAPY with or without RADIOTHERAPY

439
Q

Complications of Lung Cancer

A

SUPERIOR VENA CAVA SYNDROME, PANCOAST TUMOR leading to HORNER SYNDROME, AIRWAY OBSTRUCTION, HOARSENESS

440
Q

Prognosis for Lung Cancer

A

POOR (5-Year Survival Rate 10%)

441
Q

Underlying Pathology for Colorectal Cancer

A

BLEEDING COLORECTAL MASS causing OBSTRUCTION

442
Q

Most Appropriate Diagnostic Test for Colorectal Cancer

A

COLONOSCOPY with BIOPSY

443
Q

Appropriate Screening Test for those at Risk for Colorectal Cancer

A

FOBT (Yearly), SIGMOIDOSCOPY (Every 5 years), COLONOSCOPY (Every 10 years)

444
Q

Familial Colon Cancer Syndrome associated with Mutation of APC gene

A

FAMILIAL ADENOMATOUS POLYPOSIS

445
Q

Diagnosis for Colorectal Cancer

A

VISUALIZING: 100 Polyps during Colonoscopy

446
Q

FAP plus Brain Tumors (Medulloblastoma), Café-au-lait spots and Basal Cell Carcinoma

A

TURCOT SYNDROME

447
Q

FAP plus extraintestinal tumors: Osteomas, Nasopharyngeal Fibroma, Lipoma

A

GARDNER SYNDROME

448
Q

Hyperpigmented spots on Lips/ Bucc Mucosa and Hamartomatous Polyps (Not Premalignant)

A

PEUTZ-JEGHERS SYNDROME

449
Q

Hereditary Non-Polyposis Cancer due to Defective Mismatch Repair (Colon Cancer + Endometrial Cancer)

A

LYNCH SYNDROME

450
Q

Differentiate Right-Sided and Left-Sided Colon Cancer

A

RIGHT-SIDED: Fatigue and weakness due to Iron Deficiency Anemia; LEFT-SIDED: Occult Bleeding, Changes in Bowel Habits or Cramping Left Lower Quadrant discomfort

451
Q

Most Important Risk Factor for Colorectal Cancer

A

DIETARY HABITS (Low Fiber, High Refined Carbohydrates/ Fat)

452
Q

Most Important Prognostic Factor of Colorectal Cancer

A

Depth of Invasion, Presence or Absence of Lymph Node Metastases

453
Q

Describe Treatment for Colorectal Cancer

A

LOCALIZED DISEASE: Surgery; METASTATIC DISEASE: Chemotherapy

454
Q

Most Common Site of Metastasis

455
Q

Surgical Treatment Modalities based on Anatomic Location of Colorectal Cancer Tumor

A

CECUM, RIGHT COLON & PROXIMAL/ MID-TRANSVERSE: Right Hemicolectomy, SPLENIC FLEXURE and LEFT COLON: Left Hemicolectomy, SIGMOID/ RECTOSIGMOID: Sigmoid Colectomy, PROXIMAL RECTUM: Low Anterior Resection, DISTAL RECTUM: Abdomino Perineal Resection

Internal Medicine (1 decks)

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