Exam Review 2015
PATHO PHYSIOLOGY
BHAGATH MS RAJEEV BISWAS
PATHO-PHYSIOLOGY EXAM REVIEW 2015
INDEX CHAPTER
TITLE
LECTURE PERIODS
1
INTRODUCTION OF PATHOPHYSIOLOGY
1
2
CONSPECTUS OF DISEASES
2
3
DISORDERS OF WATER AND ELECTROLYTE METABOLISM
6
4
ACID BASE BALANCE & DISTURBANCES
5
5
HYPOXIA
3
6
FEVER
3
7
SHOCK
4
8
HEART INSUFFICENCY
6
9
RESPIRATORY FAILURE
6
10
HEPATIC ENCEPALOPATHY
6
11
RENAL FAILURE
6
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Review questions from Professors 1 1. WHAT FACTORS ARE INVOLVED IN ETIOLOGY OF DISEASES? Factors involved in the etiology of disease are as follows :
[etiology :: the cause or set of causes ]
> EXTRINSIC FACTOR BIOLOGICAL AGENTS: microorganisms and parasites: Influenza A virus subtype H7N9 (bird flu virus)
CHEMICAL AGENTS: non-specific and specific
PHYSICAL AGENTS: mechanical injuries, extremes of temperature, electricity, and radiation
NUTRITIONAL IMBALANCE: excesses or deficiencies
> INTRINSIC FACTOR GENETIC FACTORS: gene mutation, sickle cell anemia, colorblindness CONGENITAL FACTORS: abnormal embryonic developmental error IMMUNOLOGICAL FACTORS: the immune response is deficient or inappropriately strong or misdirected. PSYCHOLOGICAL FACTORS: Anxiety, strong or persistent psychological stress, such as hypertension, peptic ulcer, coronary heart disease, and depression.
2、WHAT DO YOU KNOW ABOUT FUNDAMENTAL MECHANISMS FOR DISEASES? Fundamental mechanism for disease are : NEURAL mechanism HUMORAL mechanism ORGANIC mechanism CELLULAR mechanism MOLECULAR mechanism 1 3、WHAT DO YOU KNOW ABOUT GENERAL RULES FOR PATHOGENESIS OF DISEASES? General rules for pathogenesis of disease are : (1) Disruption of homeostasis (2) Process of damage and anti-damage (3) Alternation of cause and effect (4) Correlation between systemic and local regulations
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4、HOW DO YOU KNOW ABOUT DEATH ESPECIALLY BRAIN DEATH ACCORDING TO WHO CRITERIA? Criteria for death according to WHO Cessation of spontaneous respiration Irreversible coma Absence of cephalic reflexes Dilated and fixed pupils Absence of any electrical activity of the brain Absence of brain blood flow
5、WHAT DO YOU KNOW ABOUT DEHYDRATION INCLUDING ITS CLASSIFICATION? >DEHYDRATION is an excess loss of body fluid. >Dehydration is classified into ::
6、WHAT IS HYPOTONIC DEHYDRATION? PLEASE EXPLAIN ITS CHARACTERISTICS, ETIOLOGY, EFFECTS ON THE BODY AND CLINICAL MANIFESTATION. HYPOTONIC DEHYDRATION (Hypovolemic hyponatremia) >The dehydration in which the salt loss is in excess of water loss and the remaining ECF of the body is hypotonic is termed of hypotonic dehydration.
CHARACTERISTICS:: — Loss of salt more than water — Serum Na+ < 130mmol/L — Plasma osmotic pressure < 280mOsm/L ETIOLOGY Excessive amount of sodium can be lost in gastrointestinal secretions. (vomiting, diarrhea or gastric suction) Sodium deficit may result from excessive sweating. Sodium deficit may result from excessive water loss from kidney (prolonged diuretic therapy, adrenal deficiency or low aldosterone or renal tubular acidosis) Most of conditions occurs when the fluid loss is replaced with water only.
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EFFECTS ON THE BODY 1
2
CLINICAL MANIFESTATION
7、WHAT IS HYPERTONIC DEHYDRATION? PLEASE EXPLAIN ITS CHARACTERISTICS, ETIOLOGY, EFFECTS ON THE BODY AND CLINICAL MANIFESTATION. HYPERTONIC DEHYDRATION (Hypovolemic hypernatremia) >The dehydration in which the water loss is in excess of salt loss and the remaining ECF of the body is hypertonic is termed of hypertonic dehydration.
CHARACTERISTICS::
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— Loss of water more than sodium — Serum Na+ >150mmol/L — Plasma osmotic pressure > 310mmol/L ETIOLOGY::
EFFECTS ON THE BODY::
CLINICAL MANIFESTATION::
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8、WHAT IS EDEMA? WHAT ARE MAIN MECHANISMS UNDERLINE EDEMA? >Edema is defined as soft tissue swelling mainly due to excess fluid in interstitial compartment. >Hydrops is defined as special edema. MECHANISM 1. Disturbance of Transcapillary Fluid Exchange Four interrelated mechanisms result in Disturbance of Transcapillary Fluid Exchange ★ Deceased colloid osmotic pressure in the capillary ★ Increased capillary hydrostatic pressure ★ Increased capillary permeability ★ Lymphatic obstruction or increased interstitial colloid osmotic pressure 2. Sodium and Water Retention:The mechanism of Sodium water retention can be described by following steps
9、PLEASE EXPLAIN THE POSSIBLE MECHANISMS INVOLVED IN DISTURBANCE OF TRANSCAPILLARY FLUID EXCHANGE. > Four interrelated mechanisms result in Disturbance of Transcapillary Fluid Exchange ★ Deceased colloid osmotic pressure in the capillary ★ Increased capillary hydrostatic pressure ★ Increased capillary permeability ★ Lymphatic obstruction or increased interstitial colloid osmotic pressure
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10、WHAT IS HYPOKALEMIA? HOW DO YOU KNOW ABOUT ITS ETIOLOGY AND PATHOGENESIS? Hypokalemia is Serum [K+] < 3.5mmol/L with or without K+ deficiency. ETIOLOGY AND PATHOGENESIS
Ⅰ. Inadequate Intake Fasting, anorexia, inability to eat prolonged I.V. alimentation without K+ Ⅱ. Excessive Loss 1. Gastrointestinal loss 2.Excessive renal losses (1) Diuretics (2) Some diseases of the kidney Renal tubular acidosis (3) Excess of adrenocortical hormones Aldosteronism, Cushing’s syndrome (4) Alkalosis 3. Excessive loss from the skin burns or scalds Ⅲ. Transfer of K+ from the ECF to ICF Alkalosis 11、WHAT IS HYPERKALEMIA? HOW DO YOU KNOW ABOUT ITS ETIOLOGY AND PATHOGENESIS? Hyperkalemia is Serum [K+]>5.5mmol/L, a medical emergency ETIOLOGY AND PATHOGENESIS Inadequate excretion of K+
Renal failure, hypoaldosteronism, K+ sparing diuretics Redistribution of K+ in the body tissue injury, acidosis, insulin deficiency, familial hyperkalemic periodic paralysis Increased intake of K+—rapid I.V. K+ administration
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12、PLEASE EXPLAIN SUPERPOLARIZATION BLOCK AND DEPOLARIZATION BLOCK?
Super-polarization:-
In hypokalemia K+ in ECF are low, as a result a lot of K+ will move from ICF-ECF, thus there will be
more –ive charge inside and more +ive outside thus resulting in Superpolarization.
Depolarization:-
In hyperkalemia high concentration K+ in ECF will decrease the Influx of K+ from ICF
less –ive charge inside the cell and less +ive
charge in ECF. Above factors lead to depolarization
13、WHAT ARE HYPOKALEMIA AND ALKALOSIS? PLEASE EXPLAIN THE RELATIONS BETWEEN THEM. HYPOKALEMIA Hypokalemia is defined as decrease in serum potassium level less than 3.5mmol/L with or without K+ deficiency.
ALKALOSIS o If pH is higher than 7.45 o There are mainly two types :: a) METABOLIC ALKALOSIS Primary increase of [HCO3- ]
b) RESPIRATORY ALKALOSIS Primary decrease of [HCO3- ] or Primary decrease of [HCO3 ](PaCO2 ) due to hyperventilation.
RELATION BETWEEN HYPOKALEMIA AND ALKALOSIS Because of H+-K+ exchange and Cl` -HCO`3 exchange , hypokalemia can result in metabolic alkalosis. i) Ion exchange between intracellular & extra cellular fluid H+ moves out of the cell while Na+ and K+ moves into the cell to maintain electrochemical balance during alkalosis which may cause hypokalemia ii) Regulation of renal K+excretion
K+ - Na+ exchange in Distal convoluted tubule
In Alkalosis H+ -Na+ exchange decreases and K+ -Na+ exchange increases. Because K+-Na+ exchange in distal convoluted tubules can excrete K+ & reabsorb Na+ , while H+ - Na+ exchange can excrete H+ and reabsorb Na+ . There is a competitive inhibition between K+ Na+ exchange and H+ - Na+ exchange. Therefore alkalosis is often accompanied by Hypokalemia. 14、WHAT ARE HYPERKALEMIA AND ACIDOSIS? PLEASE EXPLAIN THE RELATIONS BETWEEN THEM. HYPERKALEMIA Hyperkalemia is Serum [K+]>5.5mmol/L, a medical emergency
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ACIDOSIS o If pH less than 7.35 o There are mainly two types :: a) METABOLIC ACIDOSIS Primary decrease in plasma [HCO3- ]
b) RESPIRATORY ACIDOSIS Increase of [HCO3 ](PaCO2 )
RELATION BETWEEN HYPERKALEMIA AND ACIDOSIS An increased K+ concentration in ECF promotes H+-K+ exchange, results in translocation of intracellular H+ into extracellular fluid and metabolic acidosis. i) Ion exchange between ICF and ECF When Extra-cellular H+ increase, H+ diffuse into cell an Intra-cellular K+ moves out of the cell so as to keep electro-neutrality. So acidosis is always accompanied with hyperkalemia ii) Regulation of renal K+ excretion K+ - Na+ exchange and H+- Na+ exchange in DCT (Distal Convoluted Tubule) In acidosis, H+- Na+ exchange increases & K+- Na+ exchange decreases. Therefore in acidosis is often accompanied by hyperkalemia.
15、WHAT IS METABOLIC ACIDOSIS? WHAT DO YOU KNOW ABOUT ITS ETIOLOGY, CLASSIFICATION AND METABOLIC AND FUNCTIONAL ALTERATIONS?
METABOLIC ACIDOSIS is defined as a decrease of pH induced by primary decrease in plasma HCO3- concentration. ETIOLOGY > High AG(Anion Gap) type ---- Fixed acid [HCO3- ] Fixed acids are acid produced from an 1. Production of fixed acids incomplete metabolism of 2. Retention of fixed acids --- GFR carbohydrates, fats, and proteins. 3. Acid intake – aspirin etc. > Normal AG type ---- hyperchloremic 1. HCO3- reabsorption or regeneration in renal tubules: Renal tubular acidosis ( RTA ) Renal failure Carbonic anhydrase inhibitor 2. HCO3- losses in alimentary tract: Diarrhea 3. HCl, NH4Cl intake 4. Hyperkalemia
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CLASSIFICATION > Acute: no compensation occurs > Chronic: compensation occurs METABOLIC & FUNCTIONAL ALTERATION
16、WHAT IS HYPOXIA? WHAT DO YOU KNOW ABOUT THE CLASSIFICATION OF HYPOXIA? HYPOXIA Tissue cells can not be supplied with O2 or can not utilize O2 properly metabolic, functional and structural alterations > CLASSIFICATION OF HYPOXIA 1. Hypotonic hypoxia ( hypoxic hypoxia )- PaO2↓ Etiology : 1) Decrease on PO2 inspired 2) Pulmonary dysfunction 3) V→A shunts 4) Respiratory Dysfucntion 2. Hemic hypoxia ( isotonic hypoxia )
Etiology : 1) Anemia
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2) Carbon Monoxide Poisoning 3) Methemoglobinemia: HbFe3+OH 3. Circulatory hypoxia ( hypokinetic hypoxia )
Etiology : 1)general circulatory failure 2)local circulatory disorders
4. Histogenous hypoxia ( histotoxic hypoxia )
Etiology : 1) inhibition of mitochondrial oxydative phosphorylation 2) mitochondria injury 3) Vitamin deficiency --- B1
17、COULD YOU EXPLAIN THE CHARACTERISTIC ALTERATIONS OF BLOOD O2 (INCLUDING PAO2, O2 CAPACITY, O2 CONTENT, CAO2-CVO2) IN ANY TWO TYPES OF HYPOXIA? The main Characteristics alternation of blood O2 vary with type of Hypoxia and are as follow. 1-Hypotonic Hypoxia:PaO2, oxgen stimulation and CaO2 decline, while CO2 max is normal. 2-Hemic Hypoxia:Reduced CO2 max &CaO2, but PaO2 abd SaO2 are normal 3-Ciculatory Hypoxia:PaO2,CO2max and SaO2 are normal.The difference between oxygen content in arery and vein is large because slow blood flow resulted from ischemia/congestion makes the time that blood flows by the tissue capillary longer,so the quantity of oxygen cell taken from unit blood volume is increased 4-Histogenic Hypoxia:PaO2, SaO2,CO2max and CaO2 are normal. Oxygen content in vein is increased because cells utilize less oxygen.
18、WHAT IS CYANOSIS? DOES CYANOSIS REPRESENT HYPOXIA? AND DOES CYANOSIS APPEAR IN ANY TYPE OF HYPOXIA? WHY? >CYANOSIS a dark bluish or purplish coloration of the skin, nail beds, lips, or mucous membranes due to deficient oxygenation of the blood.
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>Yes, it represents Hypoxia >It can be found in three types of hypoxia 1-Hypotonic hypoxia Effects:: PaO2↓→ SaO2↓→ CaO2↓ hypotonic hypoxemia, （CaO2－CvO2）↓ cyanosis
2-Hemic hypoxia Effects:: CO2max↓↓ CaO2 ↓↓ （CaO2－CvO2） ↓ Enterogenous cyanosis
3-Circulatory hypoxia Effects:: perfusion↓↓→ CvO2↓ →（CaO2－CvO2）↑ cyanosis
*** note :: you can add etiology too on the basis of the marks. 19、PLEASE EXPLAIN TEMPERATURE ELEVATION ACCORDING TO ITS CLASSIFICATION. > TEMPERATURE ELEVATION ACCORDING TO ITS CLASSIFICATION
HYPERTHERMIA:: disorder in temperature regulation It is a passive process There is no change of the set point
FEVER:: is defined as a regulatory body temperature elevation response to the pyrogen, it is related to an upward shift of the set-point in thermoregulatory center
20、WHAT IS FEVER? COULD YOU EXPLAIN ITS MAIN MECHANISM? FEVER is defined as a regulatory body temperature elevation response to the pyrogen, it is related to an upward shift of the set-point in thermoregulatory center.
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MECHANISM
21、WHAT IS SHOCK? HOW ABOUT ITS CLASSIFICATION ACCORDING TO ETIOLOGY? > Shock is defined as a kind of acute, systemic pathological process characterized by decreased
effective circulatory blood volume, inadequate tissue perfusion, resulting in abnormal cellular metabolism and altered function of multiple organs. > Shock is a syndrome mainly due to microcirculation disturbance. >CLASSIFICATION ACCORDING TO ETIOLOGY
(1) LOSS OF BLOOD OR FLUID blood loss → hemorrhagic shock fluid loss → dehydration shock (collapse) burn → burn shock (2) TRAUMA → traumatic shock (3) INFECTION → infectious shock, endotoxic shock, septic shock (4) ANAPHYLAXIS → anaphylactic shock (5) NEUROSTIMULATION → neurogenic shock (6) HEART FAILURE → cardiogenic shock
22、WHAT ARE THREE PHASES OF HYPOVOLEMIC SHOCK ACCORDING TO MICROCIRCULATION THEORY? WHAT DO YOU KNOW ABOUT FIRST PHASE INCLUDING ITS MECHANISM, COMPENSATION CHANGES AND CLINICAL MANIFESTATION? > Three phases of hypovolemic shock ::
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MICROCIRCULATORY ISCHEMIC PHASE MICROCIRCULATORY STAGNANT PHASE MICROCIRCULATORY FAILURE PHASE (Refractory phase) >THE FIRST PHASE IS MICROCIRCULATORY ISCHEMIC PHASE
Sympathetic-adrenal system activation Angiotensin Ⅱ, TXA2, endothelin, etc.
Compensation 1:
AUTOTRANSFUSION
It is the first-line defensive response which results from constriction of the capacitance vessel by disgorging stored blood. effective circulation blood volume ↓ → epinephrine and norepinephrine, renninangiotensin-aldosterone system ↑↑
Compensation 2:
AUTOPERFUSION
It is the second-line defensive response which results from decreased capillary hydrostatic pressure by promoting tissue fluid circumfluence. precapillary resistance > postcapillary resistance Hydrostatic pressure in capillary↓
Compensation 3:
RE-DISTRIBUTION OF BLOOD VOLUME
It is the third-line defensive response which serve to raise blood pressure back toward normal and ensure adequate blood flow supplying to the brain and heart.
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> CLINICAL MANIFESTATION
23、HOW ABOUT THE CLASSIFICATION AND TYPICAL PHASES OF SHOCK ACCORDING TO ITS PATHOGENESIS BASED ON "MICROCIRCULATION THEORY"?
CLASSIFICATION OF SHOCK ACCORDING TO THE PATHOGENSIS
(1) Decreased blood volume → HYPOVOLEMIC SHOCK (2) Increased vascular bed volume → VASOGENIC SHOCK (3) Impaired heart pump function → CARDIOGENIC SHOCK
*** NOTE:: refer question number 22 also. 24、WHY THE EARLY PHASE (ISCHEMIC HYPOXIC PHASE) OF SHOCK IS ALSO CALLED COMPENSATORY PHASE? ISCHEMIC HYPOXIC PHASE is initial non-progressive satge during which compensatory mechanisms are activated and perfusion of vital organ is maintained.
25、WHAT MECHANISMS ARE INCLUDED IN THE FORMATION OF EDEMA RESULTING FROM RIGHT HEART FAILURE? <new question added by prof this year>
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Review questions from Professors 2 26. WHAT IS HEART FAILURE? WHAT IS CONGESTIVE HEART FAILURE? Heart failure or cardiac failure is a complex clinical syndrome characterized by the inability of the heart to pump enough blood to meet the metabolic requirements of the body due to impaired systolic and/or diastolic function of the heart. Congestive heart failure (CHF) represents a complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention, and reduced longevity. 27. WHAT ARE THE BASIC CAUSES OF HEART FAILURE? TYPE COMMON DISEASE >Myocardial Injury Primary Injury Myocardial infraction, myocarditis, cardiomyopathy and myocardial Secondary Injury
toxicosis Coronary artery disease, severe anemia, severe lung disease, vitamin B defect and diabetes
>Cardiac Overload Pressure Overload Systemic hypertension, pulmonary hypertension, semilunar valve stenosis Volume Overload
and ventricular outflow obstruction Semilunar valve regurgitation, left to right shunt, hyperthyroidism, and arteriovenous fistula
>Restriction of Cardiac Filling
Mitral or/and tricuspid stenosis, restrictive cardiomyopathy, constrictive pericarditis and pericardial tamponade
>Arrhythmia
Tachycardia, bradycardia, frequent premature beat, atrioventricular block, ventricular or atrial fibrillation
28. WHAT ARE THE PREDISPOSING FACTORS OF HEART FAILURE? 60-90%
Infection Arrhythmias Pregnancy & Parturition Acid-base imbalance Water and electrolytes imbalance
29. WHAT IS LOW OUTPUT HEART FAILURE? WHAT IS HIGH OUTPUT HEART FAILURE? WHAT IS THE DIFFERENCE BETWEEN THEM? Low-output heart failure is a common type of heart failure in which cardiac output decreases, as in most forms of heart disease, leading to clinical manifestation of impaired peripheral circulation and peripheral vasoconstriction (cold, pale extremities, cyanosis, narrowed pulse pressure). High output heart failure is an uncommon type of heart failure in which the cardiac output remains high enough to maintain a brisk circulation with warm extremities but is inadequate to meet demand for the metabolism of the body; it is most often associated with hyperthyroidism. anemia, arteriovenous fistulas, beriberi, osteitis deformans, or sensis.
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30. WHAT ARE THE MECHANISM FOR DYSFUNCTION OF MYOCARDIAL ENERGY METABOLISM? THE MECHANISM FOR DYSFUNCTION OF MYOCARDIAL ENERGY METABOLISM ARE :: ď&#x192;&#x2DC; Disorder of Myocadial Energy PRODUCTION ď&#x192;&#x2DC; Disorder of Myocardial Energy STORAGE ď&#x192;&#x2DC; Disorder of Myocardial Energy UTILIZATION OR
Dysfunction of myocardial energy metabolism contains disorder of myocardial energy production, storage and utilization. >Mechanism for disorder of myocardial energy production: Ischemic heart disease (such as coronary artery disease), shock (with low blood pressure), severe anemia (with reduced red blood cells and hemoglobins) and hypoxia (found in severe lung disease) decrease oxygen supply to myocardial cells. These will lead to disorder of myocardial energy production such as ATP deficiency in myocardial cells. >Mechanism for disorder of myocardial energy storage: When oxygen supply is normal, CPK can catalyze the reactions of creatine and ATP in mitochondria, and formation of creatine phosphate (CP). On the contrary, when oxygen supply is less, CPK can catalyze the reaction of creatine phosphate to generate ATP by transferring high-energy phosphate to ADP in cytoplasm. So, creatine phosphate is the storage form of ATP. >Mechanism for disorder of myocardial energy utilization: In the normal condition, myosin head functions as a more efficient ATPase to hydrolyze ATP and initiate the contraction. In human, disorder of myocardial energy utilization is related to myosin regulatory light chain (MRLC). There are two kinds of MRLC isoenzymes, including ventricular-type MRLC and atrial-type MRLC. Ventricular-type MRLC has high activity and atrial-type MRLC has low activity. Some patients with excessive myocardial hypertrophy have low level of ventricular-type MRLC and high level of atrial-type MRLC. This change also decreases myosin-ATPase activity and induce disorder of myocardial energy utilization and then heart failure. 31. *** WHAT ARE THE MECHANISM FOR DYSFUNCTION OF MYOCARDIAL EXITATIONCONTRACTION COUPLING? THE MECHANISM FOR DYSFUNCTION OF MYOCARDIAL EXITATION-CONTRACTION COUPLING ARE :: ď&#x192;&#x2DC; Dysfunction of Extracellular đ??śđ?&#x2018;&#x17D;2+ Influx ď&#x192;&#x2DC; Dysfunction of Sarcoplasmic Reticulum Handling đ??śđ?&#x2018;&#x17D;2+ ď&#x192;&#x2DC; Dysfunction of đ??śđ?&#x2018;&#x17D;2+ Binding to Troponin
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OR There are three mechanisms for dysfunction of myocardial excitation contraction coupling. >Dysfunction of extracellular Ca2+ influx: When hyperkalemia occurs, potassium competitively inhibits calcium ions moving inward. So, in the case, free calcium ions inside cardiomyocytes is low and myocardial contractility decreases. >Dysfunction of sarcoplasmic reticulum handling calcium ions: There are three causes below. The first one is reduced uptake of calcium ions by sarcoplasmic reticulum (SR). The second cause of dysfunction of sarcoplasmic reticulum handling calcium ions is reduced storage of calcium ions by sarcoplasmic reticulum. The last cause of dysfunction of sarcoplasmic reticulum handling calcium ions is reduced release of calcium ions by sarcoplasmic reticulum. >Dysfunction of calcium ion binding to troponin: It is important that calcium ions bind to troponin to trigger excitation-contraction coupling. This action can be impaired by the inadequate calcium ion concentration or/and decreased affinity between calcium ions and troponin C. hydrogen ions also increases the affinity between sarcoplasmic reticulum and calcium ions resulting in less calcium ions released from sarcoplasmic reticulum after myocardial depolarization. Impaired delivery of calcium ions by sarcoplasmic reticulum secondary to deficiency of ATP is also responsible for dysfunction to troponin. 32. WHAT ARE THE MECHANISM OF DECREASED MYOCARDIAL CONTRACTILITY? THE MECHANISM OF DECREASED MYOCARDIAL CONTRACTILITY ARE :: ď&#x192;&#x2DC; Injury of Myocardium ď&#x192;&#x2DC; Dysfunction of Myocardial Energy Meabolism ď&#x192;&#x2DC; Dysfunction of Myocardial Excitation- Contraction Coupling 33. WHAT ARE THE PATHOGENISIS OF HEART FAILURE? Initiation of muscle contraction in normal heart by đ??śđ?&#x2018;&#x17D;2+ ď&#x192;&#x2DC; Decreased Myocardial Contractility ď&#x192;&#x2DC; Ventricular Diastolic Dysfunction ď&#x192;&#x2DC; Asymmetry and Asynchronism in Ventricular Contraction and Relaxation 34. WHAT IS TONOGENIC CARDIC DIALATION? WHAT IS POSITIVE INOTROPIC EFFECT? TONOGENIC CARDIAC DILATATION o Mechanism: Increase in Ventricular End- Systolic Volume o Significance: Increase the force of contraction during systole o Decompostion: ď&#x192;&#x2DC; Myogenic Cardiac Dilation ď&#x192;&#x2DC; Increase in Myocardial Oxygen Consumption ď&#x192;&#x2DC; Myocardial Ischemia OR TONOGENIC CARDIAC DILATATION is a cardiac compensation reaction, in which the heart can increase muscle fibres tension and the force of contraction during systole via the Frank-Starling mechanism when the ventricular end-systolic volume and venous return increase.
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HETEROMETRIC AUTOREGULATION POSITIVE INOTROPIC EFFECT Mechanism: Sympathetic Nervous Excitation Significance: Increase in Myocardial Contractility Increase in Myocardial Diastolic Function Decomposition Increase in Myocardial Oxygen Consumption Desensitization of Myocardium to Noradrenalin OR POSITIVE INTROPIC EFFECT is the condition, in which strength of cardiac contraction is regulated to increase in response to influences that do not depend on change in fiber length , the FrankStarling curve. HOMEOMETRIC AUTOREGULATION 35. WHAT IS CONCENTRIC MYOCARDIAL HYPERTROPY? WHAT IS ECCENTRIC MYOCARDIAL HYPERTROPY? WHAT IS THE DIFFERENCE BETWEEN CONCENTRIC AND ECCENTRIC MYOCARDIAL HYPERTROPY? >Concentric myocardial hypertrophy: Concentric hypertrophy is the cardiac response to pressure overload, through which the heart adds new sarcomeres in-parallel to existing sarcomeres to cause the increase in ventricular wall thickness and the decrease in both wall tension and cardiac compliance without the dilation of the cardiac chamber. >Eccentric myocardial hypertrophy: Eccentric hypertrophy is the cardiac response to volume overload, through which the heart adds new sarcomeres in-series to existing sarcomeres to cause the dilation of the cardiac chamber and the decrease in both wall tension and cardiac compliance without increasing the ventricular wall thickness. Mechanisms of excessive myocardial hypertrophy-induced heart failure: The first mechanism is dysfunction of myocardial energy metabolism, including disorder of myocardial energy production, decrease of myocardial energy storage, and disorder of myocardial energy utilization. The second mechanism is dysfunction of myocardial excitation-contraction coupling, including dysfunction of extracellular calcium ions influx and dysfunction of sarcoplasmic reticulum handling calcium ions. The third mechanism is decrease in ventricular compliance. 36. WHAT ARE CARDIAC COMPENSATIONS OF HEART FAILURE? The Cardiac Compensations of Heart Failure are :: Increased Heart Rate Positive Inotropic Effect Tonogenic Cardiac Dilatation Myocardial Hypertrophy
OR The very important compensatory reactions of heart failure are cardiac compensation. Cardiac compensation reactions contain increased heart rate, positive inotropic effect, tonogenic cardiac dilatation and myocardial hypertrophy. Positive inotropic effect is the second reaction of cardiac compensation. Tonogenic cardiac dilatation is the third reaction of cardiac compensation. At last, myocardial hypertrophy is also the cardiac compensation reaction.
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Besides the cardiac compensation, the patients with heart failure also have systemic compensation, including activation of sympathetic nervous system, activation of renin-angiotensin system, increase in blood volume, redistribution of blood flow, increase in red blood cells and increase in ability to utilize oxygen. 37. WHAT ARE THE IMPACTS OF HEART FAILURE ON BODY? The impacts of Heart Failure on Body are :: Alteration in Cardiac Function Change of Blood Pressure Respiratory Distress Systemic Congrestion Other Clinical Manifestion 38. WHAT IS DYSPNEA ON EXERTION? DYSPNEA ON EXERTION (DOE or exertional dyspnea) indicates dyspnea that occurs or worsens during physical activity. Doing exercise will increase blood return to the heart, increase of heart rate and increase in oxygen consumption of body. These changes lead to or aggravate the accumulation of fluid in the lungs, or pulmonary edema, and then dyspnea on exertion. 39. WHAT IS ORTHOPNEA? ORTHOPNEA is dyspnea which occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair, seen in congestive heart failure. OR Orthopnea is a condition in which there is difficulty in breathing that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair, as in congestive heart failure. 40. WHAT IS PAROXYSMAL NOCTURNAL DYSPNEA? PAROXYSMAL NOCTURNAL DYSPNEA (PND) is defined as sudden, severe shortness of breath at night that awakens a person from sleep, often with coughing and wheezing. PND is most closely associated with congestive heart failure. PND is often relieved by sitting upright. OR Paroxysmal nocturnal dyspnea (PND) is defined as sudden, severe shortness of breath at night that awakens a person from sleep, often with coughing and wheezing. PND is most closely associated with congestive heart failure. PND is often relieved by sitting upright. 41. WHAT IS RESPIRATORY FAILURE? Repiratory failure is a syndrome in which the external respiratory system fails to adequately oxygenate the venous blood (HYPOXAEMIA) with or without retention of carbon dioxide (HYPERCAPNIA) PaO2 < 8 kPa (60 mmHg) PaCO2 > 6.67 kPa (50 mmHg) OR Respiratory failure is a syndrome by which external respiration fails to adequately oxygenate venous blood which leads to hypoxenimea, with or without carbon dioxide retention, hypercapnia. PO2- 60mmHg and below PC02-50mmHg and above
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Respiratory failure is classified according to four main factors. According to blood gas alteration ᴥ Type I ->hypoxemic RF is characterized by decrease in PO2 and normal PCO2 ᴥ Type II-> Hypercapnia RF is characterized by decrease in PO2 and increase in PC02 According to pathogenesis ᴥ Ventilator RF -> Caused by airway obstruction and respiratory pump lesion. Decrease of PO2 and increase of PC02 ᴥ Gas-exchange RF -> caused by solid lung lesion. Decrease of PO2 but PCO2 can be normal, increased or decreased According to primary site ᴥ Central RF-> Damage/disorder to central nervous system ᴥ Peripheral RF-> damage/disorder of the respiratory organs or thoracic cage According to duration ᴥ Acute RF-> Occurs rapidly over hours and days ᴥ Chronic RF-> occurs slowly over months and years, allows for compensation. 42. WHAT ARE TYPE I AND TYPE II RESPIRATORY FAILURE?
According to Alterations of Blood Gas Type I Respiratory Failure PaO2 PaCO2 Hypoxaemic Respiratory Failure
Type II Respiratory Failure PaO2 PaCO2 Hypercapnic Respiratory Failure OR According to alterations of blood gas, respiratory failure is divided into two types; including Type I respiratory failure & Type II respiratory failure. In type I respiratory failure, PaO2 decreases while PaCO2 is normal. So, this kind of respiratory failure is also called as HYPOXAEMIC RESPIRATORY FAILURE. Unlike type I respiratory failure, in type II respiratory failure, PaO2 decreases whereas PaCO2 increases. So, type II respiratory failure is also called as HYPERCAPNIC RESPIRATORY FAILURE. OR Type I failure is also known as HYPOXEMIA RF o Blood gas: Decrease PO2 and normal, increased or decreased PCO2 o Cause: Lung solid lesion e.g. pulmonary fibrosis, atelectasis, pulmonary edema and pneumonia o Pathogenesis: Gas-Exchange RF characterized by three main pathogenic mechanisms Diffusion impairment -> decrease of respiratory membrane, abnormally think respiratory membrane, decrease in diffusion time Ventilation-perfusion mismatch ᴥ Partial alveolar perfusion (dead space –like ventilation) ᴥ Partial alveolar ventilation (functional shunt ventilation) Increase in anatomic shunt Type II is also known as HYPERCAPNIA RF. o Blood gas: Decrease in PO2 and increase of PC02
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PATHO-PHYSIOLOGY EXAM REVIEW 2015 o
o
Cause: respiratory pump damage Restrictive hypoventilation caused by respiratory pump damage ᴥ Decrease in contractile function of inspiratory muscles -> brain trauma, myasthenia gravis ᴥ Decrease in chest wall distension ->thorax deformation, pleural fibrosis ᴥ Decrease in lung distension -> pneomothorax, hydrothorax ᴥ Decrease in lung compliance -> pulmonary fibrosis and decrease in surfactant airway obstruction-> ᴥ Acute airway obstruction -> foreign objects, laryngeal edema ᴥ Chronic airway obstruction-> chronic bronchitis, asthma Pathogenesis: ventilator RF characterized by two main pathogenic mechanisms Restrictive hypoventilation caused by respiratory pump damage ᴥ Decrease in contractile function of inspiratory muscles -> brain trauma, myasthenia gravis ᴥ Decrease in chest wall distension ->thorax deformation, pleural fibrosis ᴥ Decrease in lung distension -> pneomothorax, hydrothorax ᴥ Decrease in lung compliance -> pulmonary fibrosis and decrease in surfactant obstruction hypoventilation caused by airway obstruction ᴥ central airway obstruction outside of chest -> inspiratory dyspnoea inside of chest->expiratory dyspnoea ᴥ peripheral airway obstruction ->expiratory dyspnoea
43. WHAT ARE THE MECHANISM OF RESTRICTIVE HYPOVENTILATION? Mechanisms of Restrictive Hypoventilation Dysfunction of Respiratory Muscular Activity
Cerebral trauma, Brain tumor, Cephalitis, Central myelitis, Polyneuritis, Myasthenia gravis, Hypokalemia, Hypoxia, Acidosis
Degraded Compliance of the Chest Wall Severe thoracic deformity, Pleural fibrosis
Degraded Compliance of the Lungs Severe pulmonary fibrosis, Reduced alveolar surfactant
Hydrothorax and Pneumothorax Hydrothorax, Tensional pneumothorax
OR
Restrictive hypoventilation is mainly caused by the diseases that affect the contraction of inspiratory muscles and the distensibility of the alveoli. Following are the mechanisms of restrictive hypoventilation: First, it is dysfunction of respiratory muscular activity. Cerebral trauma, brain tumor, cephalitis, central myelitis, polyneuritis, myasthenia gravis, hypokalemia, hypoxia, acidosis and so on can reduce the contraction of inspiratory muscles and thus lead to restrictive hypoventilation. Second, it is the degraded compliance of the chest wall. Severe thoracic deformity and pleural fibrosis can restrict the distension of chest wall and induce restrictive hypoventilation. Third, it is the degraded compliance of the lung. Severe pulmonary fibrosis or reduced alveolar surfactant can lead to the degraded compliance of the lung, increase the elastic resistance of alveolar distension, and result in restrictive hypoventilation. Last, it is the hydrothorax and pneumothorax. Hydrothorax or tensional pneumothorax will press the lung, limit the distension of the lung, and then induce restrictive hypoventilation. OR
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PATHO-PHYSIOLOGY EXAM REVIEW 2015
Restrictive hypoventilation caused by respiratory pump damage characterized by; ᴥ Decrease in contractile function of inspiratory muscles -> brain trauma, myasthenia gravis ᴥ Decrease in chest wall distension ->thorax deformation, pleural fibrosis ᴥ Decrease in lung distension -> pneomothorax, hydrothorax ᴥ Decrease in lung compliance -> pulmonary fibrosis and decrease in surfactant
44. WHAT ARE THE MECHANISMS OF OBSTRUCTIVE HYPOVENTILATION? Mechanism of Obstructive Hypoventilation are :: Central Airway Operation o Outside of the Chest : Inspiratory Dyspnea o Inside of the Chest : Expiratory Dyspnea Peripheral Airway Obstruction o Expiratory Dyspnea OR >Obstructive hypoventilation is mainly found in airway constriction or obstruction. >Under the normal condition, more than 80% of the airway resistance comes from trachea and bronchus whose diameter is more than 2 mm (micrometer) while less than 20% of the airway resistance comes from peripheral small airway whose diameter is less than 2 mm. >So, airway obstruction can be divided into two groups, including; CENTRAL AIRWAY OBSTRUCTION and PERIPHERAL AIRWAY OBSTRUCTION. >Central airway obstruction locates outside of the chest: Central airway obstruction locates outside of the chest. In expiration phase, the pressure in the airway here is higher than the atmosphere, including this place. The airway here distends. So, in the phase of expiration, the airway resistance decreases and dyspnea lessens. In the phase of inspiration, the pressure in the airway here is lower than the atmosphere, including this place. The airway here constricts. >Central airway obstruction locates inside of the chest: In inspiration phase, the pressure in the airway here is higher than the intra-thoracic pressure, including this place. The airway here distends. So, in the phase of inspiration, the airway resistance decreases and dyspnea lessens. In the phase of expiration, the pressure in the airway here is lower than the intrathoracic pressure, including this place. The airway here constricts. It leads to the increase in the airway resistance and aggravation of dyspnea. So, when the central airway obstruction locates inside of the chest, the patient will have expiratory dyspnea. >Peripheral airway obstruction: When peripheral airway obstruction occurs the feature of dyspnea is expiratory dyspnea. OR Obstruction hypoventilation caused by airway obstruction characterized by; ᴥ central airway obstruction outside of chest -> inspiratory dyspnoea inside of chest->expiratory dyspnoea ᴥ peripheral airway obstruction ->expiratory dyspnoea
CASE STUDY
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PATHO-PHYSIOLOGY EXAM REVIEW 2015
A 25 year old man who fractured his pelvis, shin bone and other places in an airplane landing accident, was burned and breathed smoke that caused airway injury. Before this accident he was healthy. Physical examination: Bp 80/50 mmHg, respiratory rate 12 times/min. Treat with transfusion and lifesaver. A few of rales can be hear in lung. No aeropleura symptom was seen. Chest radiographs showed non apparent abnormality. Blood gas analysis: pH 7.47, PaO2 65mmHg, PaCO2 33mmHg. Do lienectomy because of rupture of spleen, empyrosis etc was treated. Inhale 40% oxygen. After 24 hours of hospitalization, the patient was short of breath, 30 times/min, appeared cyanosis. A lot of rales can be heard in lung. Chest radiographs showed diffuse fog-like infiltration. PaO2 35mmHg. Histological exam found effusion full of alveoli containing asphyxia membrane, macrophage and other inflammatory cell; alveolar membrane thickened, edema, widely injured.
QUESTIONS
1. What disease did the patient get after 24 hours of hospitalization according to his symptoms? What feature is the disease? 2. Why did the patientâ&#x20AC;&#x2122;s PaO2 descend after 24 hours of hospitalization? Tell the pathophysiological mechanism. 3. How to correct hypoxia?
45. WHAT IS FUNCTIONAL SHUNT? FUNCTIONAL SHUNT is a pathogenic mechanism that causes ventilation-perfusion mismatch, decreases the ventilation-perfusion ratio below 0.8. Also knows as PARTIAL ALVEOLAR HYPOVENTILATION. o Itâ&#x20AC;&#x2122;s is caused when the airway/alveoli is obstructed or constricted e.g. bronchial asthma, chronic bronchitis. The alveolar is not ventilated but is well perfused. This Means the venous blood is not adequately oxygenated, it mixes with oxygenated blood causing decrease in the gas exchange and hypoxemia. Similar to alveola-venous shunt. o Normally functional shunt account for 3% of pulmonary flow, serious COPD it can raise to 30%50% of total pulmonary blood flow. This leads to Respiratory Failure Pulmonary Artery Hypoventilation Hypoxemia
Pulmonary Vein
Functional Shunt NORMAL
Venous Admixture
OR In the normal condition, both the ventilation and the perfusion in the alveolus are normal. Sometimes, its ventilation increases a little bit. So, after gas exchanging, the blood from the alveolar capillary contains normal level of oxygen. Unlike the normal condition, the ventilation decreases a lot, while the perfusion increases because of the local diseases. The alveolar ventilation/perfusion mismatch occurs. In other words, the ratio of ventilation to perfusion decreases. This would lead to dysfunction of gas
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exchanging. So, the blood from this alveolar capillary contains low concentration of oxygen. This will cause hypoxemia. This condition is in effect like arterio-venous shunt, and is therefore termed functional shunt or venous admixture. 46. WHAT IS DEAD SPACE LIKE VENTILATION? DEAD SPACE LIKE VENTILATION is a mechanism that causes ventilation-perfusion mismatch decreases the ventilation-perfusion ratio to below 0.8. Also known as PARTIAL ALVEOLAR HYPOPERFUSION
It’s caused when blood supply to the alveolar is limited like in pulmonary embolism or intravascular coagulation. Perfusion of alveolar decreases but ventilation does not. The alveolar is similar to other dead space areas because no gas exchange occurs here. This means that there is restricted gas exchange between alveolar and blood and their isn’t adequate oxidation, this leads to hypoxemia. Normally dead space volume is 30% of tidal volume, in pathologic state its 60%-70%. This leads to Respiratory Failure.
Pulmonary Artery
DEAD SPACE LIKE VENTILATION
NORMAL OR
The partial alveolar hyporperfusion can cause dead space like ventilation.In case of dead space like ventilation,the perfusion decreases a lot while the ventilation doesn’t decrease. On the contrary, the ventilation increases sometimes. The condition is similar to dead space ventilation, so it is termed dead space like ventilation. At this situation, the alveolar ventilation/perfusion mismatch occurs. In other words, the ratio of ventilation to perfusion increases. 47. WHY DOES DIFFUSION IMPAIRMENT OCCUR DURING RESPIRATORY FAILURE? DIFFUSION IMPAIRMENT causes gas-exchange RF due to impaired gas exchange across the alveolarcapillary membrane. It belongs to Type I RF. It’s characterized by 3 main mechanism o DECREASE OF RESPIRATORY MEMBRANE -> pulmonary lobotomy o ABNORMALLY THICKENS RESPIRATORY MEMBRANE Respiratory membrane has 6 layers at 1micrometer O2 takes 0.25-0.30 seconds to diffuse across, CO2 takes 0.13. ->pulmonary fibrosis increases interstitial space, hyaline membrane disease increases alveolus layer. o DECREASE IN DIFFUSION TIME, normal pulmonary circulation time is 0.75 seconds; O2 takes 0.25-0.3 seconds to diffuse across. This adequate time for blood oxygenation. Increase in physical activity increases cardiac output
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PATHO-PHYSIOLOGY EXAM REVIEW 2015
and pulmonary flow; the diffusion time may be so short that the blood is not adequately oxygenated. OR During respiratory failure, the perfusion in the diseased alveolus decreases a lot, the perfusion in the healthy alveolus must increase a lot. At the same time, the ventilation in the healthy alveolus is almost normal, not increases. The alveolar ventilation/perfusion mismatch occurs. This would cause dysfunction of gas exchanging. The blood from this healthy alveolus contains low concentration of oxygen. After mixture, the blood from both healthy and diseased alveoli does contain low concentration of oxygen. At last diffusion impairment occurs. 48. WHAT IS THE PATHOGENESIS OF RESPIRATORY FAILURE? Pathogenesis of Respiratory Failure are:: Dysfunction of Lung Ventilation o Restrictive Hypoventilation o Obstructive Hypoventilation Dysfunction of Lung Gas-Exchanging o Diffuse Impairment o Ventilation/ Perfusion Mismatch o Increase of Anatomic Shunt OR External respiration consists of lung ventilation and gas exchange, pathogenesis of respiratory failure is due to dysfunction of both processes. Divided into two main categories:: i) Restrictive hypoventilation
ii)
Obstructive hypoventilation
o
Restrictive hypoventilation caused by disease/disorder of the inspiratory muscles and dispensability of the alveoli -> respiratory pump damage Dysfunction of respiratory muscles action -> brain trauma, myasthenia gravis Decrease in chest wall distension ->thorax deformation, pleural fibrosis Decrease in lung distension -> pneomothorax, hydrothorax Decrease in lung compliance -> pulmonary fibrosis and decrease in surfactant o Obstructive hypoventilation is mainly caused by airway obstruction. Divided into two groups Central airway obstruction ᴥ Out of chest obstruction -> inspiratory dyspnoea ᴥ Inside of chest obstruction ->expiratory dyspnoea peripheral airway obstruction-> expiratory dyspnoea
49. HOW DO THE BLOOD GASES CHANGE DURING RESPIRATORY FAILURE? RF is characterized by dysfunction of lung ventilation and dysfunction of gas-exchange o Lung dysfunction -> decrease of PO2 and increase in PC02 o Gas exchange dysfunction -> decrease in PCO2 but PCO2 may be normal, decreased or increased.
50. WHAT KIND OF ACID-BASE IMBALANCES MAY HAPPEN TO PATIENTS WITH RESPIRATORY FAILURE? PLEASE EXPLAIN THEIR MECHANISMS. Acid-Base Imbalance and Electrolyte Disturbance during Respiratory Failure
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PATHO-PHYSIOLOGY EXAM REVIEW 2015
Metabolic Acidosis Hypoxia Respiratory Acidosis carbon dioxide retention Respiratory Alkalosis hyperventilation Metabolic Alkalosis iatrogenic Mixed Disorder of Acid-Base Balance OR
There are four kinds of acid base imbalance: >Metabolic Acidosis: Both type 1 and type 2 respiratory failure have hypoxemia. In the case of hypoxia the percentage of anaerobic metabolism rises, as a result acid products increase and lead to metabolic acidosis. >Respiratory Acidosis: At the presence of type 2 respiratory failure, respiratory acidosis develops because there is massive carbon dioxide retention. >Respiratory Alkalosis: At the presence of type 1 respiratory failure, hypoxia may cause hyperventilation so that too much carbon dioxide expire out of the lung. This lead to respiratory alkalosis. >Metabolic Alkalosis: If breathing apparatus, excess diuretic or NaHCO3 (sodium bicarbonate)is used iatrogenic metabolic alkalosis can be produced. 51. WHAT ARE THE CHANGES IN RESPIRATORY SYSTEM DURING RESPIRATORY FAILURE? o PO2 between 60mmHg-30mmHg stimulated peripheral chemoreceptor’s and enhances respiratory movement. PO2 below depress respiratory function. o PCO2 -> between up to 80mmHg stimulate the central chemoreceptors and enhance respiratory movement. Above 80mmHg represses the respiratory centre and respiration. Respiration is maintained by the peripheral activation by the low PO2. o Some RF diseases can cause characteristic respiration Central respiratory failure -> slow, shallow and periodic breathing Restrictive hypoventilation -> increased respiratory rate and shallow breathing Central airway obstruction outside the chest -> inspiratory dyspnoea Central airway obstruction inside the chest-> expiratory dyspnoea
EXTRA-QUESTIONS 1. What are corpumonale mechanisms? Corpomonale is the involvement of RF with the heart, mainly hypertrophy and right side failure. Mechanisms are o Contraction of lung arterioles -> caused by hypoxia ad CO2 retention o Thickening and hardening of lung vessel walls -> caused by prolonged contraction o Primary lung disease o High blood viscosity o Hypoxia and acidosis -> inhibit excitation and contraction of myocytes o Abnormal intra-thoracic pressure 2. What is carbon dioxide narcosis?
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PATHO-PHYSIOLOGY EXAM REVIEW 2015
When PCO2 reaches above 80mmHg it causes headaches, delirium, dizziness, drowsiness and depresses respiratory function 3. What are pulmonary encephalopathy and its mechanisms? Pulmonary encephalopathy is brain disorder caused by RF. There are two types of encephalopathy mechanisms o Effects of acidosis and hypoxia on the brain vessels ->they dilate blood vessels and induce cephalemia. They also cause vessel damage which increases its permeability which causes brain edema. Cephalemia and brain edema increase intracranial pressure and can lead to herniation. o Effects of hypoxia and acidosis on the brain cells ->acidosis increases glutamate decarboxylase which produces more Gamma-amino butyric acid (GABA) which is an inhibitory neurotransmitter. So cerebral function is inhibited. Acidosis causes an increase in phospholipase activity and increase lysosomal hydrolase release, this damages nerve cells and tissue. 4. Why is high concentration of O2 not good for type 11 RF in O2 therapy Type II RF causes decrease in PO2 and increase in PCO2. When PCO2 is above 80mmHg it represses the respiratory centre and respiration, respiratory movement is maintained by the peripheral chemoreceptorâ&#x20AC;&#x2122;s that are being activated by the low Po2. High concentration of O2 would cause respiratory depression because the hypoxia will be resolved
PREVIOUS YEAR QUESTION PAPER 2012 BATCH Questions 1. SHOCK 2. HIGH AND LOW OUTPUT HEART FAILURE. ITS DIFFERENCES 3. METABOLIC ACIDOSIS 4. AMMONIA
<CHECK SECOND PDF :: REVIEW QUESTIONS FROM PROF II. >
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