Heart Failure Causes and Treatment PDF

Heart failure Ahmed Rashad Mashaal  Left sided heart failure 1 (causes) 1. Valve disease: Aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation. 2. Hypertension 3. Myocardial disease: myocardial infarction, myocardi...

Heart failure Ahmed Rashad Mashaal  Left sided heart failure 1 (causes) 1. Valve disease: Aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation. 2. Hypertension 3. Myocardial disease: myocardial infarction, myocarditis and cardiomyopathy ( weakness and hypocontractility of unknown reason)  Left sided heart failure 2 (symptoms) ❑ Symptoms due to pulmonary congestion: dyspnea on exertion dyspnea at rest orthopnea paroxysmal nocturnal dyspnea. Acute pulmonary edema where the patient becomes distressed (cannot breathe). Sweaty and cough frothy blood stained sputum. ❑ Symptoms due to decease in cardiac output Fatigue due to poor perfusion of skeletal muscles Cold extremities with peripheral cyanosis due to poor perfusion of skin. Oliguria due to poor perfusion of kidneys. Syncope  Right sided heart failure 1 (causes) 1. Secondary to left sided heart failure 2. Chronic obstructive pulmonary disease as emphysema causing pulmonary hypertension followed by right sided failure. This called Cor – pulmonale 3. Pulmonary embolism. 4. Pulmonary and tricuspid valve disease ( stenosis or regurge) 5. Rarely: Myocardial disease: myocardial infarction, myocarditis and cardiomyopathy  Right sided heart failure 2 (Symptoms)  Congested neck veins  Enlarged congested and tender liver  Edema of ankles in ambulant patients and edema over the sacrum in bed ridden patients and ascites occurs later.  Ascites may precedes lower limb oedema in cases of tricuspid regurge (TR).  Mal-digestion due to congestion of the viscera.  Treatment of heart failure 1- Treatment of the underlying causes e.g. surgical valve replacement. 2-Rest in bed reduces the work of the heart, better in semi-setting position. 3-Diet: light diet given in small frequent meals. Salt restriction. 4-Diuretics: they decrease the blood volume and the preload on the heart e.g. frusemide and spironolactone. 5-Vasodilators: they reduce the preload due to venodilation and also reduce the arterial resistance (after load) due to arteriolar dilation. Angiotensin-converting enzyme inhibitors (ACE inhibitors) are the drugs commonly used as vasodilators. 6-Digitalis: it increases the force of systolic contraction and decrease the heart rate. 7-Beta-blockers: they are now used in patients with chronic stable heart failure.  Shock (Acute peripheral circulatory failure) Ahmed Rashad Mashaal  Shock  Definition: Shock or acute circulatory failure is a case of inadequate tissue perfusion resulting in tissue hypoxia.  Causes: 1. Hypovolaemic shock. 2. Septic shock. 3. Cardiogenic shock. 4. Anaphylactic shock. 5. Obstructive shock. 6. Neurogenic shock.  1- Hypovolaemic shock 1. The blood volume is reduced as in: o Haemorrhage (bleeding). o Extensive burn with loss of plasma. o Loss of fluid as in severe vomiting and diarrhea e.g. cholera infection. 2. Clinically, these patients are: o Pale. o Cold clammy sweat. o Irritable and confused. o There is rapid weak pulse, hypotension. o If the blood volume is not corrected, oliguria & anuria may be present. 3. Treatment: replacement of the lost blood, fluid or plasma, guided by measuring the CVP & auscultation of lung bases (to avoid overload).  2- Septic shock (A- definitions & causes)  Septic shock is the last and most severe stage of sepsis. A. Sepsis occurs when your immune system has an extreme reaction to an infection. B. Severe sepsis: This is when sepsis causes your organs to malfunction. This is usually because of low blood pressure. C. Septic shock: Septic shock is the last stage of sepsis and is defined by extremely low blood pressure, despite lots of IV (intravenous) fluids.  Caused usually by severe bacterial infection associated with toxemia → trigger an overreacting inflammatory response (SIRS) resulting in vasodilatation, increased capillary permeability and blood clots inside the capillaries causing (tissue hypoxia).  Fungi and (rarely) viruses may also cause the condition. 2- Septic shock (B- clinical picture)  Early signs of sepsis can include: o Fast heart rate. o Fever or hypothermia (low body temperature). o Shaking or chills (rigors). o Warm, clammy or sweaty skin. o Nausea & vomiting.  Signs of severe sepsis (sepsis + multi organ failure): o Low blood pressure. o Confusion & disorientation (brain damage). o Oliguria or anuria (renal failure). o Hyperventilation (rapid breathing) due to associated lactic acidosis → respiratory failure. o Cool and pale limbs. o Skin rash (e.g. as in meningococcaemia ). o Septic shock (severe sepsis associated with exteremly low blood pressure in spite of aggressive IV fluid therapy).  2- Septic shock (C- risk factors & treatment)  Risk factors include: o Extreme of ages. o Pregnant females. o Addicts, AIDS patients and organ transplant recipients. o Immune compromised patients (as in diabetes & malignancy). o Patients with artificial heart valves or artificial joints.  Mortality in septic shoch with treatment ranges between 30-50%.  Treatment lines include: o Rapid installation of the specific antibiotics, later adjusted by the culture and sensitivity tests. o correction of the vital parameters (e.g. hypoxia, hypovolaemia). o Vasopressors is commonly used in resistant hypotension. o Modulation of the host response (e.g. anti inflammatory agents as hydrocortisone). 3- Cardiogenic shock 1. Caused by acute affection of the contractility of the heart muscle; as in myocardial infarction and arrhythmias where the heart is unable to maintain adequate circulation. 2. Abrupt onset of heart failure signs include: o Raised jugular venous pressure (congested neck veins). o Gallop rhythm. o May end by pulmonary oedema. 3. Management according to the etiology + inotropics.  4-Anaphylactic shock 1. Anaphylaxsis = severe allergic reaction. 2. It usually follows injections (e.g as penicillin hypersensitivity) or may be secondary insect bites or nut ingestion. 3. Due to fixation of the allergen on the surface of the mast cells by IgEs→ degranulation of the mast cell → secretion of histamine, leukotrienes and other mediatiors → rapid & dramatic with marked peripheral vasodilatation: o Facial and laryngeal oedema o Bronchospasm causing dyspnca. o hypotension. o Abdominal pain, nausea, vomiting & diarrhea. 4. Treatment: o Lay patient down with feet raised. o Ensure free airway and give oxygen o Monitor blood pressure. o Drugs: adrenaline, Antihistamine and/or Hydrocortisone.  5-Obstructive shock 1. It occurs secondary to: pulmonary embolism, tension pneumothorax, cardiac tamponade. 2. There is elevated JVP (congested neck vein), weak heart sounds and low cardiac output.  5- Neurogenic shock  it usually follows severe pain (e.g. fracture femur or perforating peptic ulcer) where there is reflex vasodilatation & pooling of blood into the capillaries decreasing the venous return to the heart.  Caused by sudden loss of the sympathetic nervous system control. Thank you Gastroesophageal reflux disease and Peptic ulcerations DR Dina Attia Associate Professor of Tropical Medicine Faculty of Medicine, Beni-Suef University 2018-2019  Gastroesophageal reflux disease GERD Definition: Gastroesophageal reflux: Reflux of gastric contents into the esophagus due to insufficient closure of the LES. Physiological reflux: in normal persons after fatty meals or increased alcohol intake Gastroesophageal reflux disease: Causes disturbed the quality of life  Protecting mechanisms preventing reflux 1. Intraabdominal esophagus 2. Angle between esophagus and stomach 3. High pressure in the lower part of the esophagus 4. Rosette shape arrangement of the esophageal mucosa 5. Proper opening of the diaphragm  Types: −Endoscopic negative reflux disease NERD (non-erosive disease reflux): Typical complaint in absence of evidence of the reflux esophagitis −Endoscopic positive reflux disease ERD: Typical complaint with macroscopic or microscopic mucous membrane inflammation. Etiology Primary due to improper relaxation of the lower esophageal sphincter Secondary due to other known causes: −Impaired esophageal peristalsis. −Delayed gastric emptying −Hiatus hernia aggravating the condition e.g. late pregnancy, abdominal obesity, progressive sclerosis, after operative treatment of achalasia. Clinically: Heartburn in 75% of cases Pressure sensation behind the sternum Regurgitation and belching Epigastric pain with burning sensation Salty tasting of the mouth with dental caries and damage of the enamel Nausea and vomiting Extraesophageal manifestations −Reflux bronchitis with new onset or aggravating bronchial asthma, chronic bronchitis −Posterior laryngitis, hoarseness and dry cough −Disturbance in sleeping  Complications Chest pain simulating angina/infarction Aspiration of the stomach content Esophageal ulceration, stenosis rarely bleeding Barrett’s esophagus Adenocarcinoma of the esophagus Diagnosis History Proton pump inhibitor trial Upper endoscopy and biopsy diagnostic of reflux esophagitis and/or Barrett’s esophagus Magnification endoscopy, chromoendoscopy with methylene blue or acetic acid, virtual chromoendoscopy (NBI/FICE) and endomicroscopy. Los Angeles Classification of reflux disease Stage A: non-confluent erosions < 5mm Stage B: non-confluent erosions > 5mm Stage C: confluent erosions < 75% of the circumference Stage D: confluent erosions > 75% of the circumference 24-h-pH nasoesophageal manometry Oropharyngeal pH-manometry Treatment: 1. Conservative: Weight loss Avoidance of late meals Avoidance of foods that increase reflux ‘’sweets and alcohol’’ Stop smoking Elevate the head of the bed Avoidance of sleeping immediately after food intake 2. Medical therapy Proton pump inhibitors are the best choice; complete decrease of H/K ATPase leading to complete arrest of acid secretion − Omeprazole, rabeprazole, esomeprazole: 20 mg/d − Pantoprazole 40 mg/d, − Lansoprazole 30 mg/d. Weaker actions: − H2 blockers: Cimetidine, ranitidine, famotidine − Antacids 3. Operative / endoscopic fundoplication in some cases 4. Regular follow up in Barrett’s esophagus  Peptic ulcer disease I. Definition Damage of the epithelial mucosa (erosions) or muscularis mucosa (ulcers) of the lower esophagus, stomach, duodenum or jejunum caused by acid pepsin. Role of HCL in the stomach: Keeps the stomach PH 1-2 Destroys foreign microorganisms and prevents infection Denatures proteins and converts pepsinogen into pepsin (-ve feedback) Prevents diseases e.g. anemia Mechanism of HCL secretion: HCL is secreted from parietal cells in the stomach under the activity of H-K- ATPase at the parietal cell membrane Gastrin secreted from G cells in the antrum stimulates HCL secretion Somatostatin secreted from D cells all over the stomach inhibits HCL secretion Pepsin inhibits HCL secretion. Imbalance between gastroduodenal mucosal defense forces and the aggressive forces 1. Chronic H pylori gastritis: −Most common cause of gastric and duodenal ulcerations, −Source is oro-oral or feco-oral transmission −Prevalence increases with age. −Gastritis at the antrum/corpus causing with achlorhydria and intestinal metaplasia. 2. Other H pylori negative gastritis causes a) Non-steroidal anti-inflammatory (NSAIDS) intake NSAIDS decreases cyclo-oxygenase enzyme (COX) which consequently decreases prostaglandins in the stomach and duodenum abolishing their cytoprotective effect and causing erosions and ulcerations. b) Smoking: Reduce response to standard therapy by decreasing ulcer healing, increases recurrence rate and risk of complications. c) Zollinger-Ellison syndrome or hyperparathyroidism d) Hereditary: positive family history, patients with blood group O e) GERD: ulcers in lower esophagus f) Cirrhotics: ↓↓ mucosal resistance due to ↓↓gastrin & histamine destruction g) Physiological and diet 3. Acute stress II. Location: Commonly the lesser curvature and antrum Atypical site: greater curvature, body and fundus and is associated with suspicion of malignancy Multiple erosions/ulcerations are associated with NSAIDS and Zollinger Ellison syndrome. Duodenal ulcers: are commonly at the duodenal bulb I. Diagnosis 1. Clinical − Pain (ulcer like-dyspepsia): 50% of patients − Type: burning, stabbing or dull aching a) Duodenal: epigastric, nocturnal, awakening the patient at night, relieved by food intake b) Gastric: immediate after meals relieved by antacids, H2 blockers and PPIs. c) NSAIDS associated ulcers are often painless and manifests by bleeding II. Complications: − Bleeding: hematemesis and melena − Perforation: sudden diffuse severe pain (acute abdomen). Subacute with localized epigastric pain − Associated with backpain not relieved by acid lowering medications: penetration of pancreas associated with acute pancreatitis − Associated with repeated vomiting: pyloric stenosis / hour glass stomach. − Malignancy in gastric ulcers. 2. Investigations: 1. Upper endoscopy with biopsy of the antrum/body with histology for H pylori, rapid urease test. Diagnose ulcerations, differentiate benign from malignant ulcers Follow up gastric ulcers after treatment 2. Diagnosis of H pylori 1. H pylori antigen in stool 2. Serum antibodies in recent and old infections 3. Rapid urease test 4. Histological identification in the endoscopic biopsy 5. Culture and sensitivity 3-7 days 6. Breath test: for successful eradication 3. In H pylori negative ulcers 1. Exclusion of Zollinger-Ellison syndrome: raised basal gastrin and after IV secretin 2. Exclusion of hyperparathyroidism: raised serum calcium and parathormone and decreased serum phosphate.  Treatment: I. Treatment of the cause 1. H pylori eradication PPI (2x1 standard dose/d) Clarithromycin 500mg (2x 1/d) Amoxicillin 500 mg (2x 2/d) Or PPI (2x1 standard dose/d) Clarithromycin 250mg (2x 1/d) Metronidazole 400mg (2x1 /d) 2. In H pylori negative ulcers Use of PPI in Zollinger-Ellison syndrome. Avoid combination of steroids and NSAIDS, stop smoking, alcohol and caffeine, reduce stress Prophylaxis use of PPI in case of NSAIDS use or need for combination with steroids. Jaundice and viral hepatitis Medicine in Dentistry DR Dina Attia Professor of Tropical Medicine Faculty of Medicine, Beni-Suef University Faculty of Dentistry, Al Ahram Canadian University 2024  Jaundice (Icterus) Normal serum values of total bilirubin typically are 0.2-1 mg/dL Definition: Yellowish discoloration of sclera, skin and mucous membrane due to raised the level of serum bilirubin abover 2 mg/dL  Heamolytic Hepatocellular Obstructive Conjugated and Type of raised bilirubin Unconjugated Conjugated unconjucated Normal Normal to dark Dark Urine color Darken on standing Choluric Choluric Acholuric Urine ✓ Conjugated bilirubin Absent ++ +++ ✓ Urobilinogen +++ + early, obstr. dec Absent ✓ Bile salt Absent + ++ Stool color Dark colored Normal to clay Clay colored ✓ Stercobilinogen +++ ̶ ̶ Cholestatic parameters Serum bilirubin ✓ Total ++ ++ +++ ✓ Direct (conjugated) Normal ++ +++ ✓ Indirect (unconjugated) +++ ++ AST + + Normal ALT + +++ ALP Normal 2-3 times raised 10-12 times raised Prolonged not corrected Prolonged corrected INR Normal with IM vit K with IM vit K  Heamolytic Jaundice Etiology: Hemolytic anemias ▪ hereditary spherocytosis, thalassemia, G6PD deficiency, immune mediated hemolytic anemia Clinical presentation ▪ Onset in young age with exacerbations and remissions with symptoms suggestive of hemolytic crises ▪ History of repeated blood transfusions and positive family history. During crises ▪ Jaundice is usually mild (lemon yellow), Dark stool, normal urine. ▪ Leg ulcers, mongoloid facies, splenomegaly is common. Investigations: During crises ▪ Serum bilirubin ▪ Urobilinogen and stercobilinogen ▪ Blood picture anemia with reticulocytosis ▪ Investigation of cause.  During heamolysis  Hepatocellular jaundice Etiology: Acute ▪ Acute viral hepatitis Hepatotropic viruses: HAV, HEV, HBV, HDV less common HCV Non-hepatotropic viruses: EBV, CMV, HSV and rarely Ebola virus ▪ Other infections: toxoplasmosis, leptospirosis ▪ Toxic hepatitis: acute alcoholic hepatitis acute drug hepatitis e.g. halothane, paracetamol ▪ Acute fatty liver of pregnancy ▪ Reye’s syndrome Chronic ▪ All causes of liver cirrhosis ▪ All causes of chronic active hepatitis ▪ Advanced cases of obstructive jaundice ▪ Extensive hepatic malignancy ▪ Familial non-hemolytic hyperbilirubinemia ▪ Gilbert’s disease, Crigler-Najjar syndrome, Lucey-Driscoll syndrome, breast milk jaundice  Hepatocellular jaundice Clinical presentation ▪ Jaundice is usually orange yellow ▪ Urine ▪ Stools ▪ Liver failure may be present ▪ Features of the cause Investigations ▪ Synthetic functions of the liver: ✓S. bilirubin ✓S. albumin decreased in cirrhosis ✓Prothrombin time prolonged and not corrected after IV vitamin K. ▪ Transaminases are raised in chronic active hepatitis. ▪ Abdominal Ultrasonography: liver cirrhosis, portal hypertension ▪ Upper endoscopy: esophageal varices. Unconjugated Bilirubin Conjugated Bilirubin Stercobilinogen  Cholestatic jaundice Etiology I. Extrahepatic ▪ Lumen : Stone in common bile duct or common hepatic duct, Ascaris or Fasciola worms ▪ In the wall : Congenital strictures or sclerosing cholangitis, tumors e.g. cholangiocarcinoma ▪ Pressure from outside the lumen: Cancer head of pancreas or ampullary carcinoma, Enlarged lymph node in the porta hepatis II. Intrahepatic ▪ Primary biliary cholangitis ▪ Primary or secondary sclerosing cholangitis ▪ Cholestatic viral hepatitis ▪ Drugs: chlorpromazine, tolbutamide, anabolic steroids, ▪ Pregnancy jaundice in the last trimester ▪ HCC or secondaries ▪ Long standing hemolytic anemias ▪ Dubin-Jonhson syndrome, Rotor syndrome  Cholestatic jaundice Clinical presentation Age of onset: middle to old Deep jaundice with dark urine and pale stools. Pruritis and bleeding tendency Symptoms of the cause. Investigations Urine Stool Raised cholestatic parameters Raised serum cholesterol Abdominal ultrasonography diagnoses the dilated biliary radicles, stone impaction, thickened wall of bile ducts in cholangitis, differentiate intra from extrahepatic causes. Diagnosis with MRCP, endosonography. Treatment: ERCP, PTD  Acute viral hepatitis Etiology: ▪ Hepatotropic viruses: HAV, HEV, HBV, HDV and less common HCV ▪ Non-hepatotropic viruses: EBV, CMV, HSV and rarely yellow fever virus Clinical presentation: I. Icteric hepatitis Pre-icteric phase (3-9 days) Non-specific constitutional and gastrointestinal symptoms Acute onset of fever, headache and malaise with anorexia, nausea and vomiting Pain the right hypochondrium and epigastrium Icteric phase: (1-3 weeks) Prodromal abate or disappear with onset of jaundice Acute onset of jaundice with darkening of urine and pale stools and mild transient pruritis. Enlarged tender liver with mild splenomegaly and posterior cervical lymphadenopathy in some cases (15-20% of HBV) Convalescence phase Resolution of all symptoms and signs Jaundice may persist for longer duration II. Anicteric hepatitis May present with fever and anorexia  Diagnosis I. History and clinical presentation II. Investigations: 1. Peripheral blood count: Leucopenia with relative lymphocytosis 2. Raised level of ESR 3. Liver enzymes: marked elevation of AST and ALT, 500-5000 IU/L, ALT rise more than AST 4. Liver function tests: serum bilirubin is increased both direct and indirect, prothrombin time: normal or 1-3 seconds prolonged, albumin normal or slightly decreased. 5. Alkaline phosphatase: is normal or slightly raised. 6. Plasma proteins: elevated globulins 7. Urine: ▪ Bilirubin and urobilinogen are detected ▪ Bile salts may be present 8. Stools ▪ Decreased stercobilinogin ▪ Pale, frothy offensive and greasy 9. Viral markers ▪ HAV IgM for hepatitis A, HEV IgM for hepatitis E 10. Other non-hepatotropic viruses: IgM for EBV, CMV and HSV  Sequalae: 1. Spontaneous resolution: In most HAV and HEV infections HBV and HDV most adult patients 15%-45% of HCV in symptomatic cases and in children 2. Cholestatic hepatitis Mostly autoimmune trigger by acute virus infection (HAV, HEV) Pruritis is prominent. Jaundice persists 8-28 weeks. 3. Relapsing hepatitis Reappearance of symptoms with rerise of aminotransferases and bilirubin weeks after apparent resolution. 4. Fulminant and sub-fulminant hepatitis High mortality rate 5. Chronic hepatitis with post-viral cirrhosis and hepatocellular carcinoma HBV, HDV and HCV  Treatment Self-limited disease Supportive care in the outpatient clinic is usually enough unless severe vomiting and dehydration necessitating hospital admission. Maintenance of adequate caloric and fluid intake No specific dietary recommendation Limitations of the daily activity is dependent on the patients’ fatigue and malaise Avoidance of all unnecessary drugs and alcohol intake.  Chronic hepatitis Etiology: Viral infections: HBV, HDV, HCV Alcoholic steatohepatitis Non-alcoholic steatohepatitis Autoimmune hepatitis Hemochromatosis, Wilson’s disease and alpha-1 antitrypsin Drugs: Isoniazid, methyl dopa  Clinical presentation HCV Most chronic hepatitis patients in Egypt are secondary to HCV and > 90% are genotype 4. Most cases are asymptomatic, fatigue and reduced quality of life. Once cirrhosis established, manifestation of portal hypertension (ascites, SBP, hepatic encephalopathy) and hepatocellular carcinoma. Jaundice is a late symptom with hepatic decompensation. Serum ALT show persistent to intermittent rise in most patients. HBV: Chronic infection is 90% in infants, 30-50% in children 1-4 years old and only 5% in healthy adults. Symptoms are usually non-specific with fatigue and right upper quadrant pain Investigations 1. Peripheral blood picture: Thrombocytopenia, leukopenia and anemia 2. Liver enzymes: ALT and AST > two-fold rise above the normal level which indicates active inflammation. 3. Liver function tests: In advanced hepatocellular decompensation; bilirubin rise, albumin decreased and prothrombin time prolonged 4. Viral markers: ▪ HCV IgG, HCV RNA ▪ HBsAg, HBcIgG, HBeAg and HBV DNA 5. Autoantibodies in autoimmune hepatitis; antinuclear antibodies (ANA), anti- smooth muscle antibodies (ASMA), liver kidney microsomal antibodies (LKMA). 6. Causing etiology in NAFLD; fasting blood sugar and glycated hemoglobin level, serum cholesterol and triglycerides. 7. Abdominal ultrasonography ▪ From normal findings to hepatomegaly or fatty liver. ▪ Manifestations of liver cirrhosis, portal hypertension e.g splenomegaly, collaterals and ascites. 8. Liver biopsy/ transient elastography ▪ To evaluate the stage of hepatic fibrosis