Patho phy prof 2 (16 questions) by Medicos 143

PATHOPHYSIOLOGY PROF . II REVIEW QUESTIONS

MBBS 2013 BATCH BHAGATH M S

RAJEEV BISWAS

PATHOPHYSIOLOGY REVIEW 2013 BATCH

REVIEW QUESTIONS FROM PROF. II HEART FAILURE 1. What is low-output heart failure? What is high-output heart failure? What are the differences between lowand high-output heart failure? 2. What are the mechanisms for dysfunction of myocardial energy metabolism? 3. What are the mechanisms for dysfunction of myocardial excitation-contraction coupling? 4. What is concentric myocardial hypertrophy? What is eccentric myocardial hypertrophy? What are differences between concentric and eccentric myocardial hypertrophy?

1. What is low-output heart failure? What is high-output heart failure? What is difference between low- and high-output heart failure?  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.  Difference between LOW AND HIGH OUTPUT HEART FAILURE In the case of low output heart failure, cardiac output is lower than the normal level and In the high output heart failure, the cardiac output is higher than the normal level.

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2. What are the mechanisms for dysfunction of myocardial energy metabolism? THE MECHANISM FOR DYSFUNCTION OF MYOCARDIAL ENERGY METABOLISM ARE :: o Disorder of Myocadial Energy PRODUCTION o Disorder of Myocardial Energy STORAGE o 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.

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ď&#x192;&#x2DC; 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.

3. What are the mechanisms for dysfunction of myocardial excitation-contraction coupling? THE MECHANISM FOR DYSFUNCTION OF MYOCARDIAL EXITATION-CONTRACTION COUPLING ARE :: o Dysfunction of Extracellular đ??śđ?&#x2018;&#x17D;2+ Influx o Dysfunction of Sarcoplasmic Reticulum Handling đ??śđ?&#x2018;&#x17D;2+ o Dysfunction of đ??śđ?&#x2018;&#x17D;2+ Binding to Troponin OR There are three mechanisms for dysfunction of myocardial excitation contraction coupling. o 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.

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o DYSFUNCTION OF SARCOPLASMIC RETICULUM HANDLING CALCIUM IONS: There are three causes below. I. II. III.

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.

o 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.

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4. What is concentric myocardial hypertrophy? What is eccentric myocardial hypertrophy? What is difference between concentric & eccentric myocardial hypertrophy?

o 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. o 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. o 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.

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RESPIRATORY FAILURE 5. What is respiratory failure? What are the mechanisms of restrictive hypoventilation? 6. What kind of acid-base imbalances may happen to patients with respiratory failure? Please explain their mechanisms. 7. What are corpulmonale and its mechanisms? (What is corpulmonale? Please explain the mechanisms by which chronic respiratory failure causes right heart failure.) 8. What is pulmonary encephalopathy? Please explain the mechanisms by which respiratory failure causes encephalopathy.

5. What is respiratory failure? What are the mechanisms of restrictive hypoventilation? 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 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 Chronic RF-> occurs slowly over months and years, allows for compensation.

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Mechanisms of Restrictive Hypoventilation

o Dysfunction of Respiratory Muscular Activity Cerebral trauma, Brain tumor, Cephalitis, Central myelitis, Polyneuritis, Myasthenia gravis, Hypokalemia, Hypoxia, Acidosis

o Degraded Compliance of the Chest Wall Severe thoracic deformity, Pleural fibrosis

o Degraded Compliance of the Lungs Severe pulmonary fibrosis, Reduced alveolar surfactant

o 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: o 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. o 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. o 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. o 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

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

6. 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 o Metabolic Acidosis Hypoxia o Respiratory Acidosis carbon dioxide retention o Respiratory Alkalosis hyperventilation o Metabolic Alkalosis iatrogenic o Mixed Disorder of Acid-Base Balance P a g e 7 | 19

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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.

7. What are corpulmonale and its mechanisms? (What is corpulmonale? Please explain the mechanisms by which chronic respiratory failure causes right heart failure.) Respiratory failure that can involve heart mainly causes hypertrophy and right heart failure. It is called corpulmonale. Mechanism: The mechanisms are:: o Contraction of Lung Arteriole o Thickening and Hardening of Lung Vessel Wall o Primary Disease of Lung o Heightening of Blood Viscosity o Hypoxia and Acidosis o Abnormal Level of Intra-Thoracic Pressure OR The mechanisms of corpulmonale are very complex, including six kinds of causes. > First, the mechanism of corpulmonale is CONTRACTION OF LUNG ARTERIOLE. High level of H+ (hydrogen ion) in the blood caused by hypoxia and CO2 retention can make lung arteriole contract, and increase pulmonary arterial pressure and the after-load of right heart.

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> Second, the mechanism of corpulmonale is THICKENING AND HARDENING OF LUNG VESSEL WALL. Long time of lung arteriole contraction can cause hyperplasy of smooth muscle cells and fibroblasts, and increase synthesis of collagen and stress proteins so that lung vessel wal is thickened and hardened. > Third, the mechanism of corpulmonale is SOME PRIMARY DISEASES OF LUNG such as lung arteriolitis, great damage of pulmonary capillary bed, lung embolism. All of them can cause pulmonary artery hypertension. > Fourth, the mechanism of corpulmonale is heightening of blood viscosity. > Fifth, the mechanism of corpulmonale is HYPOXIA AND ACIDOSIS. > Last, the mechanism of corpulmonale is ABNORMAL LEVEL OF INTRA-THORACIC PRESSURE.

8. What is pulmonary encephalopathy? Please explain the mechanisms by which respiratory failure causes encephalopathy. Brain disorder caused by respiratory failure is defined as pulmonary encephalopathy. Mechanism: o Effects of Acidosis and Hypoxia on Brain Vessels o Dilation of Brain Vessels and Induction of Cephalemia o Blood Vessel Original Brain Edema o Cellular Brain Edema o Effects of Acidosis and Hypoxia on Brain Cells o Increase of ÉŁ â&#x20AC;&#x201C; Aminobutyric Acid (GABA) o Glutamate Decarboxylase o Release of Lysosomal Hydrolase o Phosphlipase OR There are two kinds of mechanisms. o The first one is effects of acidosis and hypoxia on brain vessels. Both acidosis and hypoxia dilate brain vessels and induce cephalemia. Both acidosis and hypoxia damage brain vessel endothelium and increase its permeability. That induces blood vessel original brain edema. Hypoxia reduces ATP production. Deficiency of ATP influences function of Na+-K+ pump (sodium and potassium pump) and increases the content of Na+ and water to form cellular brain edema. o The second one is effects of acidosis and hypoxia on brain cells. In nerve cells, acidosis increases glutamate decarboxylase activity in the brain to produce more g-aminobutyric acid. Because gaminobutyric acid is inhibitory neurotransmitter, the cerebral function is inhibited. Acidosis also stimulates phospholipase activity to release lysosomal hydrolase. The lysosomal hydrolase can damage nerve cells and tissues.

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HEPATIC ENCEPHALOPATHY 9. What is hepatic encephalopathy? What are differences between endogenous and exogenous hepatic encephalopathy? 10. What are mechanisms by which ammonia level increases in the blood of patients with hepatic failure? (What are mechanisms for increased ammonia in the blood?) 11. What are toxic effects of ammonia on the brain? Please explain their mechanisms. (What is intoxication of ammonia on the brain?) 12. What are precipitating factors of hepatic encephalopathy? Please explain the mechanisms by which the precipitating factors promote development and progression of hepatic encephalopathy.

9. What is hepatic encephalopathy? What are differences between endogenous and exogenous hepatic encephalopathy? HEPATIC ENCEPHALOPATHY is a complex, potentially reversible disturbance in the central nervous system that occurs as a consequence of severe liver diseases. o DIFFERENCE BETWEEN ENDOGENOUS AND EXOGENOUS HEPATIC ENCEPHALOPATHY ENDOGENOUS H E

EXOGENOUS H E

COMMON CAUSE

Fulminant hepatic failure (25%)

Hepatocirrhosis with the portal-systemic shunt (75%)

PRECIPITATION FACTOR

YES

DURATION

Acute

Chronic & Recurrent

NH3 IN BLOOD

HEPATIC FUNCTION RESPONSE TO REDUCTION OF AMMONIA

OR 

 

25% of patients with hepatic encephalopathy are endogenous. Their common cause is fulminant hepatic failure. While 75% of patients with hepatic encephalopathy are exogenous. Their common cause is hepatocirrhosis with the portal-systemic shunt. Endogenous hepatic encephalopathy has no obvious precipitating factors, but exogenous hepatic encephalopathy has some precipitating factors. Endogenous hepatic encephalopathy is acute and exogenous hepatic encephalopathy is chronic and recurrent. P a g e 10 | 19

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 

Plasma ammonia level is uncertain in the endogenous hepatic encephalopathy, but exogenous hepatic encephalopathy has high level of plasma ammonia. The reduced hepatic function is found in both endogenous and exogenous hepatic encephalopathy, especially in endogenous hepatic encephalopathy.

 Responses to reduction of ammonia are uncertain in endogenous hepatic encephalopathy, but in exogenous hepatic encephalopathy reponses are good.

10. What are mechanisms by which ammonia level increases in the blood of patients with hepatic failure? (What are mechanisms for increased ammonia in the blood?) Causes of Increased Ammonia in Blood :: o Reduction of Ammonia Detoxification  Dysfunction of Kerbs-Henseleit Ornithine Cycle in the Liver Portosystemic Shunting o Increase of Ammonia Production  Increased Production of Ammonia in the GASTRO-INTESTINAL TRACT  Increased Production of Ammonia in the KIDNEY  Increased Production of Ammonia in the MUSCLES I. DYSFUNCTION OF KERBS- HENSELEIT ORNITHINE CYCLE IN THE LIVER

“Under catalysis of CPS I, enzyme, ammonia reacts with CO2 (carbon dioxide) and produces carbamyl phosphate. Under catalysis of OTC enzyme, reaction of carbamyl phosphate with ornithine produces citrulline. Under catalysis of ASS enzyme, citrulline combines aspartic acid and produces argininosuccinic acid. Under catalysis of AS enzyme, arginosuccinic acid decomposes into arginine and fumaric acid. Then, under catalysis of arginase, arginine decomposes into ornithine and urea. So this cycle is called ORNITHINE CYCLE or UREA CYCLE. P a g e 11 | 19

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Normally, ammonia is detoxified in the liver by conversion to urea through this cycle. However, ever the liver is damaged, three reasons lead to the cycle impairment.â&#x20AC;?

o The first reason is DECREASE OF ATP ATP is required for this cycle. The liver dysfunction causes decrease of ATP and then cycle impairment. So, ammonia can not be detoxified in the liver and will increase in the blood. o Reason is DECREASE IN ORNITHINE CYCLE RELATED ENZYMES When the liver is damaged, the enzymes decrease. This must impair this cycle and cause high level of ammonia in the blood. o Decrease in ORNITHINE CYCLE-RELATED COMPONENTS. This cycle contains many kinds of essential components, including orthinine, citruline, arginine and so on. However, when the liver is damaged, these components will decrease. So, Ammonia can not be detoxified in the liver and will increase in the blood. So, the first cause for reduction of ammonia detoxification is dysfunction is dysfunction of KerbHenseleit ornithine cycle in the liver. (This is the first cause of reduced ammonia detoxification in severe liver dysfunction.) The second cause is PROTOSYSTEMIC SHUNTING. o Protosystemic shunting The portal blood form the gastrointestinal tract will bypass the liver and directly flow into systemic circulation. So, the ammonia in the blood can not be effciently converted to urea.

II. Increased Production of Ammonia in the GASTRO-INTESTINAL TRACT o Too many amino acids enchance amino production o Increase activities of amino acid oxidase and urease o Impairment of urea excretion from kidneys o Hepatocirrhosis cause patient often esophageal varies. P a g e 12 | 19

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III. & IV Increased Production of Ammonia in the MUSCLE and KIDNEY Besides, ammonia is also produced in the kidneys and the skeletal muscles. In the case of severe hepatic dysfunction, the kidneys and the skeletal muscles also increase ammonia production.

11.What are toxic effects of ammonia on the brain? Please explain their mechanisms. (What is intoxication of ammonia in brain) Ammonia has three kinds of intoxication on the brain. I. AMMONIA CAN IMPAIR ENERGY METABOLISM IN THE BRAIN.  This is the process of glycolysis. Under the regulation of phosphofructokinase, PFK.  In anerobic metabolism, pyruvate will produce lactic acid.  When severe hepatic dysfunction occurs, there are 4 ways to decrease ATP level in brain. o High level of ammonia in the brain inhibits activity of Pyruvate decarboxylase, coenzyme A, & Acetyl CoA and DECREASE ATP PRODUCTION. o Increased ammonia produce glutamate and decreases α-ketoglutarate. α-Ketoglutarate is required for TCA cycle and less α-ketoglutarate cause DECREASE IN ATP. o This reaction also needs NADH. NADH is required for the production of ATP from mitochondria. So lack of NADH cause disorder for mitochondrial respiratory chain and DECREASES ATP PRODUCTION. o High concentration of Ammonia also react with Glutamate to produce Glutamine. This reaction directly consume ATP and results in LOW ATP PRODUCTION IN BRAIN

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II. HIGH CONCENTRATION OF AMMONIA CAUSES ALTERATIONS OF NEUROTRANSMITTERS IN THE BRAIN.  Reduce Acetyl Choline production  Glutamate decreases because α-Ketoglutarate lacks  High concentration of Ammonia increases glutamine and cause inhibition of CNS  Increased γ-GABA will cause inhibition of CNS III. HIGH CONCENTRATION OF AMMONIA CAUSES INHIBITION OF THE NERVE CELL MEMBRANE.

12. What are precipitating factors of hepatic encephalopathy? Please explain the mechanisms by which the precipitating factors promote development and progression of hepatic encephalopathy. Precipitating Factors of Hepatic Encephalopathy o GASTROINTESTINAL BLEEDING Intestinal tract will have blood and bloodhave many proteins and amino acid, This will cause accumulation of proteins and amino acid in intestinal tract. Amino acid produces amonia, since the accumulation of protein and amino acid occurs they stimulate proliferation of bacteria and they increases amino acid oxidase and uriase in GI tract. In addition, GI Bleeding cannot be stopped easily. This often cause Hypovolemia, shock or hypoxia which induce hepatic encephalopathy. o HIGH PROTEIN DIET It can induce accumulation of proteins and amino acid in intestinal tract. So it cause hepatic encephalopathy. P a g e 14 | 19

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o ABUSE OF SEDATIVES AND NARCOTIC  This often affect neurons.  The membrane hyperpolarization and post synaptic inhibition occur. So it precipitating factor for hepatic encephalopathy. o ALKALOSIS 

When alkalosis occurs ammonium in blood turns to ammonia.



So ammonium can easily cross Blood-Brain Barrier and cause high level of ammonia in brain and encephalopathy.



It also causes Respiratory Alkalosis

o MASSIVE PARACENTESIS  It will decrease intra-abdominal pressure  It will increase the absorption of ammonia by intestinal tract, So plasma Ammonia increases.  It also cause dehydration and hypovolemia.  So this three can induce encephalopathy. o INFECTIONS  They result in fever and tissue break down.  Increase Nitrogenous Load

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RENAL FAILURE 13. What are prerenal, intrarenal and postrenal acute renal failures? 14. What are the metabolic and functional alterations during oliguric stage in the oliguric type of acute renal failure? Please explain the mechanisms of those alterations. 15. Why does hyperkalemia represent a life-threatening complication of acute renal failure? 16. What are the mechanisms of polyuria during polyuric stage in acute renal failure?

13. What are prerenal, intrarenal and postrenal acute renal failures? According to the position of cause, Acute Renal Failure can be divided into 3 types including :: 1. PRE-RENAL ACUTE RENAL FAILURE 2. INTRA-RENAL ACUTE RENAL FAILURE 3. POST-RENAL ACUTE RENAL FAILURE

o PRE-RENAL ACUTE RENAL FAILURE Itâ&#x20AC;&#x2122;s a condition in which functional components of the kidney are intact but inadequate blood flow to the kidney leads to reduced GFR and oliguria. Because the functional components of the kidney are intact, the pre-renal acute failure is functional renal failure.

o INTRA-RENAL ACUTE RENAL FAILURE The main cause of intra-renal acute renal failure is direct damage of nephrons.

o POST-RENAL ACUTE RENAL FAILURE Obstruction of urinary tract distal to the kidney results in elevated renal pelvic pressure which impedes, glomerular filtration and causes post renal acute renal failure.

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14. What are the metabolic and functional alterations during oliguric stage in the oliguric type of acute renal failure? Please explain the mechanisms of those alterations. Functional and Metabolic Alterations during Oliguric Phase

o URINARY ABNORMALITIES PRERENAL ACUTE RENAL FAILURE

INTRARENAL ACUTE RENAL FAILURE

URINE SPECIFIC GRAVITY

> 1.020

< 1.015

URINE OSMOTIC PRESSURE

> 400 mOsm/L

< 350 mOsm/L

URINE NA+

< 20 mmol/L

> 40 mmol/L

URINE PROTEIN AND MICROSCOPIC EXAMINATION

Normal

Protein(+)、RBC(+)、WBC(+)、Cast(+)

REACTION TO FLUID THERAPY

Urine Volume↑ Symptom Improvement

Urine Volume↓ Symptom Deterioration

o WATER INTOXIFICATION    

Oliguria directly cause water intoxication. Increase endogenous water, cause water intoxication. Give too much water to patient with accute renal failure cause water intoxication. Low concentration of Na in blood cause water intoxication.

o HYPERKALEMIA   

Decrease in urine K+ excretion. Tissue injury- Patient with accute renal failure often have severe injury of the kidney and the other organs. This will cause much K+ release from intracellular space to extracellular space. Acidosis increases K+ efflux and decreases renal pottasium excretion.

o METABOLIC ACIDOSIS   

Reduced to GFR, When fixed acid, phosporic acid, sulfuric acid elimination is limited, there increases phosphate, sulphate, and H+ ions which lead to metabolic acidosis. Disorders in excretion of H+ and reabsorption of HCO3 in the renal tubule. Increased catabolism – patients with acute renal failure have high catabolism. P a g e 17 | 19

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o AZOTEMIA

Azotemia is a medical condition characterized by abnormal levels of nitrogen-containing compounds, such as urea, creatinine, uric acid, various body waste compounds, and other nitrogen-rich compounds in the blood. It is largely related to insufficient filtering of blood by the kidneys.

15. Why does hyperkalemia represent a life-threatening complication of acute renal failure? HYPERKALEMIA   

16. What are the mechanisms of polyuria during polyuric stage in acute renal failure? The mechanism of Polyuria during Polyuric Stage are :: Symbol : Urine Volume > 400 ml/ d o GRADUAL IMPROVEMENT OF RENAL BLOOD FLOW AND FILTRATION ABILITY 

Newly added

Improvement of renal blood flow and Filtration ability SHOULD INCREASE GFR AND URINE

o IMPERFECT FUNCTION OF REGULATION RENAL TUBULAR EPITHELIUM  It means that the tubular epithelium has normal barrier function.  The renal tubular passive backflow to the interstitium has stopped.  However at this time the tubules cannot condensate urine so that patient has more than 400 mL of urine per day.

o RELIEF OF RENAL TUBULAR OBSTRUCTION 

Obviously, relief of Renal tubular obstruction should increase urine.

o OSMOTIC DIURESIS  

Osmotic diuresis is increased urination caused by the presence of certain substances in the small tubes of the kidneys. The excretion occurs when substances of high molecular weight, such as glucose, enter the kidney tubules.

 The substances cause an increase in the osmotic pressure within the tubule, causing retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (ie. diuresis).

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2012 BATCH QUESTION PAPER 1. METABOLIC ACIDOSIS 2. MICROCIRCULATION THEORY 3. HEART FAILURE 4. AMMONIA

2013 BATCH QUESTION PAPER 17/06/2015 1. WHAT IS EDEMA? DESCRIBE THE MECHANISM OF EDEMA FORMATION IN RIGHT HEART FAILURE. 2. WHAT IS HYPER KALEMIA? WHAT IS ACIDOSIS? EXPLAIN THE MECHANISM OF RELATION BETWEEN THEM. 3. WHAT IS CONCENTRIC MYOCARDIAL HYPERTROPHY? WHAT IS ECCENTRIC MYOCARDIAL HYPERTROPHY? WHAT IS DIFFERENCE BETWEEN CONCENTRIC & ECCENTRIC MYOCARDIAL HYPERTROPHY? 4. WHAT ARE PRECIPITATING FACTORS OF HEPATIC ENCEPHALOPATHY? PLEASE EXPLAIN THE MECHANISMS BY WHICH THE PRECIPITATING FACTORS PROMOTE DEVELOPMENT AND PROGRESSION OF HEPATIC ENCEPHALOPATHY.

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