General Medicine

Diseases Of The Gastrointestinal System Short Essays

Question 1. Gingival

Answer:

Gingival Causes:

1. Inflammation
   • Acute
   • Chronic
2. Drug-induced
   • Phenytoin
   • Cyclosporins
3. Systemic diseases
   • Conditioned
     • Puberty
     • Pregnancy
     • Non-specific
   • Systemic diseases
     • leukemia
4. Neoplastic
   • Benign tumors
   • Malignant tumors
5. False enlargements
6. idiopathic

Gingival Features

1. Color – Reddish
2. Surface – Smooth and shiny
3. Symptoms – Painful, expanding lesion
4. Sign – Bleeding on probing
   • Tender on percussion
   • Exudation of purulent material
5. Size – Swollen gums

Question 2. Glossitis.

Answer:

Glossitis

Glossitis is an inflammation of the tongue that causes is to enlarge and change in color.

Glossitis Types:

1. Acute glossitis – Appears suddenly
2. Chronic glossitis – Appears very often
3. Idiopathic glossitis – Leads to loss of papillae.

Glossitis Causes:

1. Allergic reactions.
2. Immunological diseases
3. Oral herpes simplex infection.
4. Iron deficiency
5. Dry mouth
6. Trauma

Glossitis Clinical Features:

1. Pain or tenderness in the tongue.
2. Swelling in the tongue.
3. Redness of tongue.
4. Difficulty in speech, eat or swallowing.
5. Loss of papillae.

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Glossitis Treatment:

1. Dietary changes – to treat anaemia.
2. Avoid irritants.
3. Uses of antibiotics, antifungal, corticosteroids.
4. Regular tooth brushing.
5. Flossing of teeth.
6. Improve oral hygiene.

Glossitis Complications:

1. Discomfort.
2. Airway blockage.

Question 3. Difference between gastric/peptic ulcer and duodenal ulcer.

Answer:

Difference between gastric/peptic ulcer and duodenal ulcer

Question 4. Plummer-Vinson syndrome.

Answer:

Plummer-Vinson syndrome

It is characterized by dysphagia, iron deficiency anemia, dystrophy of nails, and glossitis.

Plummer-Vinson syndrome Clinical Features:

1. Age – middle-aged women.
2. Dysphagia.
3. Angular chelitis.
4. Spasms in throat.
5. Sore throat.
6. Smooth, red, and enlarged tongue.
7. Pale and painful oral mucosa.
8. Dry mouth.
9. Spoon-shaped nails.

Plummer-Vinson syndrome Diagnosis:

1. Atrophy of epithelium
2. Atrophy of lamina propria.
3. Atrophy of muscles.

Plummer-Vinson syndrome Treatment:

1. Treat anaemia.
2. Oesophageal dilatation.

Question 5. Acute gastritis.

Answer:

Acute gastritis

Gastritis refers to inflammation of the stomach.

Acute Gastritis:

Acute gastritis is usually erosive and hemorrhagic.

Acute Gastritis Causes:

1. Aspirin and other NSAIDs.
2. Antimitotic drugs.
3. Renal failure.
4. H. Pylori infection,
5. Alcohol abuse
6. Iron therapy.
7. Stress
8. Following burns.
   • Postoperative.

Acute Gastritis Clinical Features:

1. Abdominal pain.
2. Nausea and vomiting.
3. Haematemesis.
4. Anorexia.

Acute Gastritis Treatment:

1. Avoid NSAIDs
2. Avoid alcohol.
3. Removal of causative agents.
4. Misoprostol – 100 – 200 jig four times a day.
5. Ranitidine – 10 mg twice daily.
6. In mild cases, antacids 30 ml 4 – 6 hourly.

Question 6. Diarrhea.

Answer:

Diarrhea

It refers to frequent loose stools i.e., more than 3 loose stools in a day.

Diarrhea Types:

1. Acute diarrhea – Rapid in onset.
2. Chronic diarrhea – Insidious onset.

Diarrhea Causes:

1. Infective diarrhea.
   • Viral – Norwalk and rotavirus.
   • Bacterial.
     • Staphylococcal.
     • Salmonella.
     • Cholera
     • E. Coli.
     • Clostridium.
   • Traveler’s diarrhea.
2. Non-infective diarrhea.
   • Crohn’s disease.
   • Drugs – cholinergic, antacids, ampicillin.
   • Irritable bowel syndrome.
   • Foecal impaction.
   • Stress.
   • Consumption of fish, shellfish.

Diarrhea Clinical Features:

1. Large number of loose watery stools.
2. Rapid loss of fluids and electrolytes.
3. Dehydration.
4. Hypotension.
5. Lower abdominal pain.
6. Fever

Diarrhea Treatment:

1. Rest.
2. Oral rehydration solution administration.
3. 4 fluid administration.
4. Oxytetracycline – 500 mg after every 6 hours.
5. Ciprofloxacin – 500 mg BID.
6. Metronidazole – 400 mg TID.
7. Antimotility agents – loperamide or codeine is used.

Question 7. Constipation.

Answer:

Constipation

Constipation refers to bowel movements that are infrequent or hard to pass.

Constipation Causes:

1. Insufficient dietary fiber intake.
2. Inadequate fluid intake.
3. Decreased physical activity.
4. Side effects of medication.
5. Hypothyroidism.
6. Obstruction by cancer.

Constipation Clinical Feature:

1. Infrequent bowel movements.
2. Difficulty during defecation.
3. Sensation of incomplete bowel evacuation.

Constipation Treatment:

1. Removal of the causative agent.
2. Changes in dietary habits.
3. Uses of laxatives – milk of magnesia.
4. Surgery
5. Increased intake of water and fibers.

Constipation Prevention:

1. Adequate exercise.
2. Adequate fluid intake.
3. High fiber diet.

Constipation Complication:

1. Hemorrhoids
2. Anal fissures
3. Rectal prolapsed
4. Fecal impaction.

Question 8. Oesophageal varices.

Answer:

Oesophageal varices

Oesophageal varices are extremely dilated submucosal veins in the lower third of the esophagus.

Oesophageal varices Causes:

1. Portal hypertension.
2. Cirrhosis.
3. Splenic vein thrombosis.

Oesophageal varices Symptoms:

1. Vomiting of blood.
2. Black tarry or bloody stools.
3. Shock
4. Signs of liver disease.
   • Jaundice
   • Spider nevi
   • Palmar erythema
   • Shrunken testicles
   • Swollen spleen.
   • Ascites.
5. Treatment:
   1. Intravenous administration of blood and fluids.
   2. Endoscopy is done to identify the site of bleeding
   3. Sclerotherapy
   4. Surgery – to reduce pressure in varies.

Question 9. Hypersplenism.

Answer:

Hypersplenism

It is clinical condition in which spleen removes excessive quantities of erythrocytes, granulocytes, and platelets from circulation.

Hypersplenism Clinical Features:

1. Splenomegaly.
2. The accelerated destruction of formed elements of blood.
3. Pancytopenia.
4. Infections.
5. Easy disability.
6. Increased bleeding tendencies.

Hypersplenism Diagnosis:

1. Splenomegaly.
2. Hypercellular bone marrow, a Reticulocytosis.
3. Sequestration of radioactively labelled RBCs.

Hypersplenism Treatment:

1. Removal of causative agent,
2. Splenectomy.
3. Blood transfusion.

Diseases Of The Gastrointestinal System Short Answers

Question 1. Causes of gum bleeding

Answer:

Causes of gum bleeding

1. Local causes
   • Toothbrush trauma
   • Food impaction
   • Presence of plaque and calculus
   • Biting into solid foods
   • Acute necrotizing ulcerative gingivitis
   • Gingival burns
2. Systemic causes
   • Scurvy
   • Vitamin K deficiency
   • Purpura
   • Haemophilia
   • Leukemia
   • Drug-induced like salicylates, heparin

Question 2. Stomatitis.

Answer:

Stomatitis

Stomatitis is the inflammation of the mouth.

Etiology:

1. Local causes.
   • Poor oral hygiene
   • Excessive use of tobacco, alcohol & spices.
   • Use of broad-spectrum antibiotics.
2. General causes.
   • Infections.
   • Mucocutaneous diseases
   • Drug toxicity.
   • Diabetes

Stomatitis Treatment:

1. Eliminate causative agent.
2. Use of mouthwash.
3. Vit. B complex.
4. Topical steroids.

Question 3. Melaena.

Answer:

Melaena

• Malaena refers to the black, tarry feces that are associated with upper gastrointestinal bleeding.
• Black color is caused by the hemoglobin in the blood being altered by digestive chemicals and intestinal bacteria.

Melaena Causes:

1. Peptic ulcer.
2. Bleeding from upper GIT.
3. Drug overdose n Tumours
4. Gastritis
5. Oesophageal varices
6. Iron supplements

Melaena Diagnosis:

1. Anaemia.
2. Low blood pressure.
3. Rectal examination
4. Stool examination.
5. Endoscopy.

Question 4. Melaena.

Answer:

Melaena

Dietary fiber can be defined as these parts of food that are not digested by human enzymes.

High Fibre Diet Significance:

1. Lowers blood sugar
2. Reduces cholesterol.
3. Prevent colon cancer.
4. Avoids hemorrhoids.
5. Relieves constipation.
6. Reduces absorption of bile salts.
7. They are digested more slowly and this slows the rise in blood glucose after eating.
8. Examples:
9. Pure or unprocessed brans, cereals.
10. Beans, legumes.
11. Plant foods, root vegetables.

Question 5. Ulcerative colitis.

Answer:

Ulcerative colitis

Ulcerative colitis is an inflammatory disease affecting mainly the large intestine.

Ulcerative colitis Causes:

1. Genetic factors
2. Stress
3. High intake of unsaturated fat
4. Autoimmune disease

Ulcerative colitis Clinical Features:

1. Diarrhea – bloody stools.
2. Abdominal cramps.
3. Tenesmus.
4. Fever
5. Loss of appetite
6. Weight loss
7. Dehydration
8. Anaemia.

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Ulcerative colitis Treatment:

1. Intake of high protein & low residue diet
2. Blood and plasma infusion.
3. Correction of dehydration.
4. Medications.
   • Corticosteroids – For immunosuppression.
   • Loperamide – For diarrhea
   • Sulphasalazine – To prevent relapse
5. Surgical Management – Surgical removal of the large intestine.

Question 6. Intestinal nematodes.

Answer:

Intestinal nematodes

1. Ascaris lumbricoides.
   • The adult worm lives in the jejunum.
   • It is elongated, rounded in shape, and tapers at both ends.
   • It passes its life cycle only in one host.
   • It causes ascariasis.
2. Hookworm.
   • Ancylostoma duodenale.
     • It is small, greyish-white, and cylindrical.
     • Man is the only definitive host
     • Causes hookworm disease.
     • Characterized by microcytic, hypochromic anemia.
   • Necator americanus.
     • It is smaller and more slender.
     • It is less pathogenic.

Question 7. H₂ antagonists.

Answer:

H₂ antagonists

H₂ antagonists competitively inhibit the action of histamine on H₂ receptors.

1. It reduces gastric secretion.
2. Hastens healing of peptic ulcer.
3. They are.
   • Cimetidine – 400 mg BD
   • Ranitidine – 150 mg BD
   • Famotidine – 20 mg BD
   • Roxatidine – 75 mg BD

H₂ antagonists Use:

1. Peptic ulcer
2. Gastritis
3. Reflux oesophagitis.
4. As pre-anesthetic medication.

Question 8. Leukoplakia.

Answer:

Definition: It is a whitish patch or plaque that cannot be characterized clinically or pathologically, as any other disease and which is not associated with any other physical or chemical causative agent except the use of tobacco.

Leukoplakia Clinical Features:

1. Older age males are commonly affected.
2. Represents solitary or multiple white patches.
3. Lesions are thick, fissured, indurated, or papilloma.
4. The surface may be smooth wrinkled or rough.
5. They are usually white or greyish-white in color.
6. Thickness varies.
7. Causes pain and a burning sensation in the mouth.

Question 9. Oral ulcers.

Answer:

Oral ulcers

It is a common disease characterized by the development of painful, recurrent, solitary ulceration of the oral mucosa.

Etiology:

1. Immunological abnormalities
2. Genetic abnormalities
3. Microbes – α hemolytic streptococci
4. Systemic diseases
   • Nutritional deficiency
   • Cyclic neutropenia.

Oral ulcers Types:

1. Minor aphthae ulcer- less than 1 cm in diameter.
2. Major aphthae ulcer-over 1 cm in diameter
3. Herpetiform ulcer – small ulcers throughout mucosa.

Oral ulcer Treatment:

• Symptomatic treatment.

Question 10. Complications of peptic ulcers.

Answer:

Complications of peptic ulcers are

1. Gastrointestinal bleeding.
2. Perforation.
3. Gastric outlet obstruction H Pancreatitis
4. Gastric malignancy.

Question 11. Barium swallow.

Answer:

Barium swallow

Barium swallow is used to study the gastrointestinal tract

Barium swallow UsVisualizelise a break in the gut mucosa.

1. Detects mucosal abnormalities.
2. Detects motility disorders.
3. Shows filling defect caused by varices or tumors
4. Detects hiatus hernia or diverticulum.

Question 12. Gastritis.

Answer:

Gastritis

It refers to inflammation of the stomach

Gastritis Types:

1. Acute gastritis.
2. Chronic gastritis.

Gastritis Causes:

1. Clinical Features:
2. Aspirin and other NSAIDs
3. Renal failure
4. Autoimmune
5. H. Pylori infection
6. Alcohol abuse n Iron therapy
7. Stress
8. Following burns
9. Postoperative.

Question 13. Diarrhea.

Answer:

Diarrhea

Diarrhea refers to frequent loose stools i.e., more than 3 loose stools in a day.

Question 14. Amoebiasis.

Answer:

Amoebiasis

A disease caused by entamoeba histolytica is called amoebiasis.

Amoebiasis Types:

1. Intestinal amoebiasis.
2. Extraintestinal amoebiasis

Amoebiasis Clinical Features:

1. Frequent motions with blood and mucus
2. Abdominal pain
3. Diarrhea alternating with constipation

Amoebiasis Management:

1. Oral metronidazole – 800 mg hourly for 5 days.
2. Tinidazole – 2 g daily for 3 days.
3. Diloxanide furoate 500 mg hourly for 10 days.

Question 15. Causes of upper gastrointestinal bleeding.

Answer:

Causes of upper gastrointestinal bleeding

1. Oesophageal causes.
   • Oesophagitis.
   • Oesophageal ulcers
   • Oesophageal varices
   • Oesophageal cancer
2. Gastric causes.
   • Gastric ulcer
   • Gastric erosion
   • Gastric cancer
3. Duodenal ulcers
4. Vascular malformation.

Question 16. Lactose intolerance.

Answer:

Lactose intolerance

Lactose intolerance occurs due to a deficiency of the enzyme lactase.

Lactose intolerance Types:

1. Primary – racial.
2. Secondary – due to abnormal intestinal biopsy.

Lactose intolerance Clinical Features:

1. Abdominal colic.
2. Abdominal distension.
3. Increased flatus
4. Diarrhea after ingesting milk or milk products.

VIVA Voce

1. Haematemesis is red or black-colored vomiting of blood
2. Malena is the passage of black, tarry stools containing altered blood
3. Odynophagia is pain during swallowing
4. Dysphagia is difficulty in swallowing
5. Aphagia is a complete esophageal obstruction
6. Phagophobia is fear of swallowing
7. Foul breath from the mouth – halitosis
8. Excessive salivation – sialorrhoea
9. Reduced salivation – xerostomia
10. Loperamide in children may lead to toxic dilatation of the bowel.

Diseases Of The Gastrointestinal System Important Notes

1. Barium swallow
   • Uses
     • To study the gastrointestinal tract
     • Visualize break in gut mucosa
     • Detects mucosal abnormalities
     • Detects motility disorders
     • Shows filling defect caused by varices or tumor
     • Detects hiatus hernia or diverticulum
2. Stool examination
3. Dental caries
   • It is progressive destruction of mineral and organic constituents of both enamel and dentin
   • Fluoride is used to protect it
   • Etiological agent
     • Bad oral hygiene
     • Staph. Aureus responsible for initiation of caries activity
     • Lactobacillus leads to acid formation
   • Progression of disease
     • Dental caries → acute pulpitis → periapical granuloma → periapical cyst
4. Ludwig’s angina
   • It is a subcutaneous infection involving all three salivary glands – parotid, submandibular and sub lingual
   • Clinical features
   • Swelling on floor of mouth
   • Elevation of tongue
   • Difficulty in breathing or chewing
5. Periodontal disease
   • Progression of disease
     • Gingivitis → involvement of alveolar bone and periodontal ligament → bone resorption → loss of attachment of periodontal ligament → pocket formation
   • Result
     • Mobile teeth
     • Recurrent abscess formation
     • Poor prognosis
6. Acute necrotizing ulcerative gingivitis (ANUG)
   • Etiology
     • Fusiform spirochaetes
   • Clinical features
     • Gingival bleeding
     • Gingival necrosis
     • Ulceration
     • Halitosis
     • Regional lymphadenopathy
7. Changes in gingiva in different diseases
8. Causes of stomatitis
   • Infective
     • Bad oral hygiene
     • Low immunity
   • Nutritional
     • Iron deficiency
     • Vitamin B complex deficiency
9. Drugs used in different diseases of oral cavity
10. Dysphagia
    • It is defined as a sensation of obstruction of the passage of food through the mouth, pharynx, or esophagus
    • Causes
      • Extrinsic pressure – mediastinal glands, goiter, enlarged left atrium
      • Intrinsic lesion – foreign bodies, stricture, lower oesophageal rings, pharyngeal pouch
      • Oesophageal motility disorders – scleroderma, diabetes mellitus
11. Plummer Vinson syndrome
    • It is characterized by dysphagia, iron deficiency anemia, dystrophy of nails and glossitis
12. Upper gastrointestinal bleeding
    • Characterised by haematemesis and melaena
    • Causes
      • Peptic ulcer
      • Gastric erosion
      • Varices
      • Oesophagitis
      • Cancer of stomach or esophagus
13. Mallory Weiss tear
    • It is one of the cause of acute upper gastrointestinal bleeding
    • It occurs at the oesophagogastric junction
14. GERD
    • Burning pain is produced by bending, stooping, or lying down
    • Pain seldom radiates to arm
    • Pain precipitates by drinking hot liquids or alcohols
    • Relieved by antacids
15. Dyspepsia or peptic ulcer
    • It means an ulcer in the wall of stomach or duodenum caused by the digestive action of gastric juice
    • Types
      • Gastric ulcer
    • It is peptic ulcer occurring in stomach
    • In it pain occurs while eating or drinking and is relieved by vomiting
    • It is associated with anorexia and weight loss
      • Duodenal ulcer
    • It is peptic ulcer found in the duodenum
    • In it pain is felt 1-2 hours after food intake and during night
    • Pain is relieved by taking food
16. Gastritis
    • It is acute or chronic inflammation of stomach
    • Types:
17. Diarrhea
    • It refers to frequent loose stools
    • Bacteria causing it are
      • Staph. Aureus
      • Bacillus cereus
      • CI. perfringens
      • Cl. Botulinum
      • Salmonella
      • Vibrio cholera
    • Treatment
      • Fluid replacement
      • Antibiotics
        • Oxytetracycline, ciprofloxacin, metronidazole
18. Traveller’s diarrhea
    • Acute diarrhea seen in tourists
    • May resolve spontaneously
    • Drug used is loperamide in adults

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1. Malabsorption syndrome
   • Refers to defective absorption of one or more essential nutrients through the intestine
   • Etiology
     • Disorders of maldigestion
     • Deficiency of bile acids
     • Genetic abnormality
     • Metabolic defects
   • Treatment
     • Gluten-free diet
     • Vitamin and mineral supplements
     • Corticosteroids
2. Lactose intolerance
   • Occurs due to a deficiency of lactose
   • Clinical features
     • Intestinal colic
     • Distension of abdomen
     • Increased flatus
       • After ingestion of milk
     • Followed by diarrhoea
   • Treatment
     • Intake of lactose-restricted diet
3. Amoebiasis
   • Caused by entamoeba histolytica
   • Clinical features
     • Fever, nausea, vomiting
     • 2-4 loose stools per day mixed with blood and mucous
     • Pam in abdomen
     • Necrotizing colitis with mucosal sloughing, ulceration, and bleeding
   • Drugs used
     • Oral metronidazole 800 mg TID for 5 days or
     • Oral tinidazole 2 g daily for 3 days or
     • Oral secnidazole 2 g single dose
4. Hematemesis and hemoptysis

Aims Of Medicine Important Notes:

1. Auscultatory areas
2. Clubbing
   • Definition
     • Bulbous enlargement of soft parts of terminal phalanges with both transverse and longitudinal curving of nails
   • Causes
     • Pulmonary – bronchogenic carcinoma, lung abscess, bronchiectasis
     • Cardiac – infective endocarditis, cyanotic congenital heart disease
     • Alimentary – ulcerative colitis, Crohn’s disease, biliary cirrhosis
     • Endocrine – myxedema, Grave’s disease, acromegaly
     • Miscellaneous – hereditary, heroin addicts
   • Grading
     
     
3. Pseudoclubbing
   • In hyperparathyroidism, excessive bone resorption may result in the disappearance of the terminal phalanges with telescoping of soft tissues and a drumstick appearance of the fingers resembling clubbing
   • However, the curvature of the nail is not present
4. Scliamrotli’s sign
   • Normally when two fingers are held together with nails facing each other, a space is seen at the level of the proximal nail fold
   • This is lost in clubbing
5. Jugular venous pressure
6. Different sounds and their significance
7. Important terms

Aims Of Medicine Short Essays:

Question 1. Jugular venous pulse.

Answer:

Jugular venous pulse

It is an important sign of cardiovascular disease

Jugular venous pulse Procedure:

1. Patient is placed in a reclining position at 45° angle with neck muscles relaxed.
2. Upper level of pulsation of an internal jugular vein is seen.

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Jugular venous pulse Significance:

1. Fall in pressure during inspiration.
2. Rise in pressure in constrictive pericarditis & cardiac tamponade.

Jugular venous pulse Waves:

1. Positive waves
   • a wave
     • Cause – Atrial contraction.
     • Absent in atrial fibrillation.
     • Prominent in tricuspid stenosis.
   • c wave
     • Small positive wave.
   • v wave
     • Cause: Passive filling of blood from veins into the right atrium.
2. Negative waves
   • x wave
     • Cause: Descent of tricuspid valve.
   • y wave
     • Cause: Rapid flow of blood from right atrium to right ventricle when the tricuspid valve is open.
     • Prominent y wave – seen in tricuspid regurgitation.

Question 2. Clubbing.

Answer:

Clubbing Definition:

It is an enlargement of distal segment of fingers and toes due to an increase in soft tissues.

Clubbing Causes:

1. Disorders of heart.
   • Cyanotic heart disease.
   • Subacute bacterial endocarditis
2. Disorders of lungs.
   • Suppuration of lung
   • Tumours of lung
3. Disorders of GI tract St liver
   • Inflammatory bowel disease.
   • Cirrhosis of liver.
   • Malignancy of liver
4. Hereditary or idiopathic.

VIVA Voce

• The commonest cause of raised JVP is cardiac failure
• White-colored sputum is called mucoid
• Yellowish greenish lotid sputum is called purulent sputum
• Grade 3 clubbing gives nails shape of parrut’s beak.

Diseases Of The Gastrointestinal System Long Essays

Question 1. Describe the pathophysiology, clinical features, diagnosis & management of reflux oesophagitis.

Answer:

Reflux oesophagitis

Gastro-oesophageal reflux disease (GERD)

Definition:

• It is defined as reflux of gastric contents into the esophagus resulting in inflammation of esophagus caused by H+ ions, pepsin & bile salts.

Pathophysiology

Clinical Features:

1. Heartburn
2. Acid eructation.
3. Painful swallowing.
4. Transient dysphagia, n Strictures.
5. Iron deficiency anaemia. b Hoarseness of voice.
6. Acid erosion of incisors.
7. Pneumonia.

Diagnosis:

1. General Measures
   • Weight reduction
   • Avoid alcohol & smoking.
   • Avoid sleeping immediately after large meals.
   • Avoid use of analgesics & anti-inflammatory drugs.
   • Use of small volumes & frequent meals.
2. Medical Measures:
   • In mild cases.
     • Liquid antacid – 10 – 15 ml 1 – 3 hours after meals.
   • In moderate cases – H2 antagonists are used.
     • Cimetidine – 400 mg.
     • Ranitidine – 150 mg BD or QID with meals. & before bed for 6 weeks.
   • In severe cases – proton pump inhibitors are used.
     • Omeprazole – 20 – 40 mg/ day.
     • Lansoprazole – 15 – 30 mg/ day.
     • Pantaprazole – 40 mg/ day.
     • Rabiprazole – 10 – 20 mg/day.
   • Other
     • Metoclopramide 10 mg TID increases lower oesophageal sphincter.
3. Surgical treatment:
   • Repair of the sphincter.
   • Construction of additional valve mechanism.

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Question 2. Describe etiology. Clinical features, diagnosis & management of peptic ulcer.

Answer:

Peptic Ulcer:

1. It is defined as the presence of an ulcer in the lower esophagus, stomach or duodenum, in the jejunum after surgery to the stomach.
2. It is a breach in the mucosa.

Etiology:

1. Hereditary.
2. Helicobacter pylori infection.
3. Smoking.
4. Corticosteroids
5. Acid-pepsin versus mucosal resistance.
6. Alcohol consumption.

Pathogenesis:

Peptic Ulcer Clinical Features:

1. It is chronic condition
2. Epigastric pain.
3. Hunger pain – occurring in an empty stomach.
4. Night pain – wakes the patient from sleep.
5. Episodic pain.
6. Excessive salivation.
7. Heart bum.
8. Loss of appetite.
9. Nausea, vomiting anorexia.
10. Haematemesis.
11. Weight loss.

Peptic Ulcer Investigations:

Peptic Ulcer Treatment:

1. General measures:
   • Avoid smoking
   • Avoid alcohol consumption
   • Avoid NSAIDs
2. Medical treatment:
   • Antacids
     • 15 – 30 ml liquid, 1 – 3 hours after food and before bedtime for 4-6 weeks.
   • H2 receptor antagonists.
     • Cimetidine – 400 mg BD
     • Ranitidine – 150 mg BD
   • Proton pump inhibitor.
     • Omeprazole – 20 mg daily for 4 – 8 weeks.
     • Lansoprazole – 15 – 30 mg daily for 4-8 weeks.
     • Pantaprazole – 40 mg daily for 4-8 weeks.
   • Prostaglandin analogs.
     • Misoprostol – 200 mg 4 times daily.
3. Surgical treatment:
   • Truncal vagotomy + pyloroplasty.
   • Partial gastrectomy.
   • Elective surgery.

Question 3. Discuss the etiology, clinical features and management of malabsorption syndrome.

Answer:

Malabsorption syndrome:

• It refers to the defective absorption of one or more essential nutrients through the intestine.

Etiology:

1. Pancreatic disorders.
   • Chronic pancreatitis
   • Cystic fibrosis
   • Malignancy pancreas.
2. Disorders causing deficiency of bile acids.
   • Interruption of enterohepatic circulation.
   • Abnormal bacterial proliferation in small intestine.
   • Drugs like neomycin.
   • Inadequate absorptive surface.
   • Mucosal defects.
     • Mucosal defects.
     • Tropical sprue.
     • Lymphoma.
     • Amyloidosis.
3. Biochemical or genetic abnormalities.
   • Disaccharidase deficiency.
   • Hypogammaglobulinaemia.
4. Metabolic defects.
   • Diabetes mellitus
   • Addison’s disease
5. Specific malabsorption.
   • Lactose deficiency.
   • Vitmai B₁₂ malabsorption.

Malabsorption syndrome Clinical Features:

1. General Features:
   • 3 health
   • Loss of weight
   • Lazziness, lassitude
   • Fatigue, weakness.
2. GIT symptoms
   • Diarrhea
   • Abdominal pain, distension.
   • Stomatitis, glossitis, cheilosis.
3. Genitourinary.
   • Nocturia.
   • Loss of libido.
4. Hematopoietic.
   • Anaemia.
5. Skeletal
   • Bone pain
   • Tetany
   • Muscle wasting
6. Nervous system
   • Night blindness
   • Xerophthalmia.
   • Peripheral neuropathy.
7. Skin
   • Purpura.
   • Hyperkeratosis
   • Edema of legs

Malabsorption syndrome Management:

1. Use of gluten-free diet.
2. Use of a low-fat diet and cholestyramine.
3. Replacement therapy for anemia, bone disease, and coagulation defects.
4. Vitamins and minerals supplementation.
5. Oral administration of folic acid & iron.
6. Intravenous fluid administration for dehydration.
7. Use of corticosteroids to suppress immunological responses.

Question 4. How will you investigate a case of dysphagia? Enumerate conditions causing dysphagia.

Answer:

Dysphagia:

• It is defined as difficulty in swallowing.

Dysphagia Causes:

1. Mechanical narrowing of the esophagus.
   • Intrinsic causes.
     • Congenital atresia.
     • Stomatitis, glossitis, tonsillitis, pharyngitis.
     • Benign or malignant tumors.
     • Oesophageal stricture or ulceration.
   • Extrinsic causes.
     • Retropharyngeal abscess.
     • Enlarged thyroid gland.
     • Aortic aneurysm.
2. Motor dysphagia.
   • Lower motor neuron paralysis.
   • Neuromuscular paralysis.
   • Oesophageal muscle weakness.
   • Paralysis of the oesophageal sphincter.

Dysphagia Investigations:

Diseases Of Cardiovascular System Important Notes

1. Cyanosis
   • It is a bluish discoloration of skin and mucous membrane
   • Types: central and peripheral
   • Causes:
     • Pulmonary – high altitude, pneumonia, pneumothorax, COPD, severe acute asthma
     • Cardiovascular causes – acute pulmonary edema, cyanotic heart disease
     • Blood disorders-methemoglobin
2. CPR (Cardiopulmonary resuscitation)
   • Rescues breathing in adult 12 times/min
   • Compression to ventilation ratio in two people is 5:1
   • Compression to ventilation ratio in one person is 15:2
   • Compression should be 60-80 minute in adults and 100/minute in children
   • Depth of compression should be 1 1/2 -2 inches at the lower half of the sternum at an average of each second
3. Starling’s law
   • It states that an increase in the force of contraction is directly related to cardiac output
   • It states that the force of ventricular contraction is directly related to the end-diastolic volume
4. Co pulmonale
   • It is an enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs
   • It is a condition where there is right ventricular hypertrophy with or without failure resulting from diseases affecting the structure or function of the lungs.
5. Rheumatic fever
   • It is an acute inflammatory disease that occurs as a sequel of infection caused by group A streptococci
   • Jone’s criteria is used for its features
   • Diagnostic features
     • Leucocytosis
     • Raised ESR
     • Raised CRP
     • Raised ASO titre
     • Cardiomegaly
6. Jone’s criteria
   • Used for diagnosis of rheumatic fever
   • Major manifestations:
     • Carditis
     • Polyarthritis
     • Chorea
     • Erythema marginatum
     • Subcutaneous nodules over bones or tendons
   • Minor manifestations:
     • Fever
     • Arthralgia
     • Previous history of rheumatic fever
     • Raised ESR
     • Leucocytosis
     • First or second-degree AV block
7. Mitral stenosis
   • Symptoms:
     • Breathlessness
     • Oedema, ascites
     • Palpitation
     • Hemoptysis
     • Cough
   • Signs:
     • Atrial fibrillation
     • Mitral facies
     • Auscultation
       • Loud first heart sound
       • Opening snap
       • Mid diastolic murmur
     • Pulmonary hypertension
     • Pulmonary edema
8. Endocarditis prophylaxis
   • AJ STANDARD PROPHYLAXIS:
     • Amoxycillin
     • Dose= Adult-2 gm
     • Child- 50 mg 1 hour before surgery
   • BJ Patient unable to take orally:
     • Ampicillin
     • Dose: Adult – 2 gm IM/IV
     • Child- 50 mg 1 hour before surgery
   • CJ Patient allergic to penicillin
     • Clindamycin
     • dose: Adult – 600 mg
     • Child- 300 mg 1 hour before surgery
9. Infective endocarditis
   • Etiology
   • Clinical features
     • Roth spots
     • Cerebral emboli
     • Petechial hemorrhages of skin and mucous membrane
     • Splinter hemorrhages and clubbing of nails
     • Osier’s nodes
     • Splenomegaly
     • Haematuria
     • Murmurs
     • Arrhythmias
     • Cardiac failure
10. Myocardial infarction
    • Lab investigations
11. Heart sounds
12. Risk factors of atherosclerosis
    • Cigarette smoking
    • Hypertension
    • Low HDL cholesterol
    • Diabetes mellitus
    • Family history of CHD
    • Old age
    • Life style
      • Obesity
      • Physical inactivity
      • Atherogenic diet
13. ECG waves

Diseases Of Cardiovascular System Short Essays

Question 1. Risk factors of IHD

Answer:

Risk factors of IHD

1. Age: Occurs in middle and old age
   • Sex: More common in males than in females
   • Family history – Hyperlipidaemia and hyperfibrinogenemia are genetically determined
2. Smoking – Related to IHD
3. Hypertension
   • Systolic and diastolic blood pressure increases the risk of IHD
4. Hypercholesterolaemia
   • HDL cholesterol is a protective
   • LDL cholesterol increases the risk of IHD
5. Hyperfibrinogenaemia
   • Increases risk of IHD
6. Hyperhomocysteinaemia
   • Elevated levels of homocysteine in blood may promote thrombosis
7. Sedentary habits
   • Regular exercise for 20 min 2-3 times a week increases HDL cholesterol, lowers BP, reduces blood clotting, and promotes collateral formation
8. Diabetes mellitus
   • Diabetes is associated with coronary atherosclerosis, obesity, and physical inactivity which further increases the risk of coronary heart disease
9. Obesity
   • It is associated with hypertension, diabetes, physical inactivity
10. Alcohol
    • A moderate quantity of alcohol has a protective effect, while heavy drinking is considered a risk factor
11. Mental stress
    • It aggravates symptoms of pre-existing heart disease
12. Diet
    • A deficiency of polyunsaturated fatty acids increases the risk of IHD
    • Low levels of vitamins A, C, and E increase the production of oxidized LDL

Read And Learn More: General Medicine Question and Answers

Question 2. Clinical features of acute rheumatic fever Jone’s criteria

Answer: Used for diagnosis of rheumatic fever

Major manifestations:

• Carditis
• Polyarthritis Chorea
• Erythema marginatum
• Subcutaneous nodules over bones or tendons

Minor manifestations:

• Fever
• Arthralgia
• Previous history of rheumatic fever
• Raised ESR
• Leucocytosis
• First or second-degree AV block

Question 3. Cyanosis.

Answer:

Cyanosis

Bluish discoloration of skin and mucous membranes is called cyanosis.

Sites involved:

• Lips n Nail beds a Finger’s tip Ear lobule.
• The undersurface of the tongue,
• Malar eminences
• Creases of plans.

Cyanosis Types of Causes:

1. Central cyanosis.
   • Pulmonary causes.
     • High altitude
     • Pneumonia.
     • Pneumothorax
     • COPD
     • Severe acute asthma
     • Respiratory failure.
   • Cardiovascular causes.
     • Acute pulmonary edema
     • Cyanotic heart diseases
     • Corpulmonale,
   • Blood disorders,
     • Methemoglobin.
2. Peripheral cyanosis,
   • Decreased cardiac output
   • Congestive cardiac failure
   • Cold exposure
   • Arterial obstruction
   • Venous obstruction.

Cyanosis Features:

1. Peripheral cyanosis.
   • Occurs due to extraction of 02 from blood.
   • Occurs in healthy persons due to cold exposure.
   • Seen on lips, nails, tip of nose, ear lobule
2. Central cyanosis.
   • Occurs due to poor oxygenation of blood in the lungs.
   • Seen on the undersurface of the tongue, mucous membrane of the oral cavity, and palate.
3. Mixed cyanosis.
   • It is a combination of peripheral and central cyanosis.

Question 4. Right ventricular failure.

Answer:

Right ventricular failure

It is defined as heart failure due to right ventricular outflow or inflow tract obstruction leading to passive congestion of the viscera.

Right Ventricular Failure Causes:

• Acute corpulmonale.
• Chronic corpulmonale.
• Pulmonary valve disease.
• Tricuspid valve disease
• Mitral valve disease
• Isolated right ventricular cardiomyopathy.

Right Ventricular Failure Clinical Features:

• Fatigue.
• Dyspnoea.
• Hypochondria pain.
• Protuberant abdomen.
• Swelling of leg.
• Distended neck veins.
• fender, soft, smooth hepatomegaly,
• Pitting edema.
• Ascites
• Pleural edema.
• Ascites
• Pleural effusion.

Right Ventricular Failure Treatment:

• Salt restriction
• Diuretics
• ACE inhibitors.

Question 5.Congenital cardiac disease.

Answer:

Congenital cardiac disease

Congenital heart disease may present in early childhood or remain asymptomatic till adult life.

Congenital Cardiac Disease Classification:

1. Acyanotic.
   • Acyanotic with left to right shunt.
     • Atrial septal defect
     • Ventricular septal defect.
     • Patent ductus arteriosus.
   • Acyanotic without shunt.
     • Pulmonary stenosis.
     • Aortic stenosis.
     • Coarctation of aorta.
2. Cyanotic.
   • Complete transposition of great vessels.
   • Persistent trances arteriosus.
   • Tetralogy of Fallot.
   • Common atrium.

Etiology:

• Infections – rubella infection.
• Chromosomal defects – Down’s syndrome, Turner’s syndrome.
• Connective tissue disorders
• Alcohol abuse.
• Teratogenic drugs.

Congenital Cardiac Disease Clinical Features:

• Breathlessness.
• Central cyanosis.
• Clubbing.
• Growth retardation.
• Syncope.
• Short stature.

Question 6. Tetralogy of Fallot.

Answer:

Tetralogy of Fallot Components:

• Pulmonary stenosis.
• Ventricular septal defect.
• Over-riding of the aorta at the level of ventricular septal defect.
• Right ventricular hypertrophy.

Pathogenesis:

Tetralogy of Fallot Clinical Features:

• Cyanosis – develops after 1 year of age.
• Grade 4 dubbing of fingers and toes
• Stunted growth.

Tetralogy of Fallot Diagnosis:

• ECG – shows right ventricular hypertrophy.
• The second heart -sound – shows delayed splitting.
• Echocardiography – demonstrates aorta.
• X-ray chest – Boot-shaped heart.

Question 7. Angina pectoris — clinical features.

Answer:

Angina pectoris Clinical Features:

• Common in 40 – 60-year-old males, n Retrosternal pain.
• Pain radiates to the left arm or the right arm, throat, back, chin, and epigastrium.
• It gets precipitated by exertion and relieved by rest.
• The patient feels heaviness, pressure, squeezing, or choking sensation.
• Nocturnal angina.

Question 8. Hypertensive encephalopathy.

Answer:

Hypertensive encephalopathy

It is a neurological symptom occurring due to high blood pressure.

Hypertensive encephalopathy Clinical Features:

• Transient abnormalities in speech or vision.
• Paraesthesia.
• Disorientation
• Fits.
• Loss of consciousness.
• Papilloedema.

Hypertensive encephalopathy Treatment:

• Bed rest
• Sedation
• Intravenous sodium nitroprusside – 0.3 – 1 mcg/kg/min.
• Diuretics.
• Parenteral use of labetalol, hydralazine, or nitroglycerine.

Question 9. Complications and management of hypotension.

Answer:

Hypotension Complications:

• Headache
• Dizziness
• Fainting,
• Risk of accidents.
• Deprive of oxygen to vital organs, n Damage to the brain and heart.

Hypotension Treatment:

• Fluid administration – to treat dehydration,
• Use of compression stockings.
• Change body positions slowly,
• Increase salt intake.
• Fludrocortisone is used.

Question 10. Beta-blockers.

Answer:

Beta-blockers

Bela blockers are drugs that block the actions of catecholamines mediated through beta receptors.

Beta-blockers Classification:

1. Non-selective.
   • Propranolol, timolol, satalol.
2. Cardio-selective.
   • Metoprolol, atenolol, esmolol, betaxolol.
3. Partial agonists.
   • Pindolol, oxprenolol, carteolol.
4. With additional alpha-blocking properties.
   • Labetalol, carvedilol.
5. β₁ blockers β₂ agonist.
   • Celiprolol.

Beta-blockers Uses:

• Hypertension.
• Angina pectoris,
• Cardiac arrest
• Myocardial infarction.
• Congestive cardiac failure,
• Obstructive cardiomyopathy,
• Pheochromocytoma.
• Thyrotoxicosis.
• Glaucoma.
• Prophylaxis of migraine.
• Anxiety.

Beta-blockers Adverse Reactions:

• Bradycardia.
• Precipitates CCF and acute pulmonary edema,
• Cold extremities.
• Precipitates asthma.
• Insomnia, depression, hallucination, fatigue.
• Weakness, dizziness. a Rebound hypertension.

Question 11. Digoxin.

Answer:

Digoxin

Digoxin is a cardiac glycoside.

Digoxin Uses:

• Congestive cardiac failure.
• Cardiac arrhythmia.
• B Atrial fibrillation
• Atrial flutter
• Paroxysmal supraventricular tachycardia.

Digoxin Adverse Effects:

• Inhibits Na⁺/K⁺ – ATPase.
• Anorexia, nausea, vomiting, diarrhea.
• Directly stimulates chemoreceptor trigger zone (CTZ)
• Weakness.
• Confusion, hallucination.
• Blurred vision.
• Gynaecomastia.
• Cardiac toxicity.

Digoxin Contraindications:

• Hypokalemia.
• Myocardial infarction.
• Thyrotoxicosis.
• Acid-base imbalance.

Question 12. Anti-platelet drugs.

Answer:

Anti-platelet drugs

Antiplatelet drugs are drugs that interfere with platelet function.

Anti-platelet drugs Classification:

1. PG synthesis inhibitor – Aspirin.
2. Phosphodiesterase inhibitor – dipyridamol.
3. ADP antagonists – ticlopidine, clopidogrel.
4. Glycoprotein 2b/3a receptors antagonist – Abciximab.
5. Others – PGI₂.

Anti-platelet drugs Uses:

• Myocardial infarction.
• Unstable angina.
• In patients with prosthetic heart valves, valvular hediseaseaand and se, coronary artery-bypass surgery.
• Cerebral thrombosis.
• Atrial fibrillation.

Diseases Of Cardiovascular System Short Answers

Question 1. Coronary vasodilators

Answer:

Coronary vasodilators

They reduce the mortality in patients with cardiac failure

They are:

• Arteriolar dilators – hydralazine, minoxidil
  • They relax arterial smooth muscles thus reducing peripheral vascular resistance and afterload
• Venodilators – nitrates
  • They reduce the venous return to the heart
  • This reduces the stretching of the ventricular walls and myocardial oxygen requirements
• Arteriolar and venular dilators – sodium nitro- pride, ACE inhibitors, prazosin, calcium channel blockers
  • They reduce both preload and afterload

Question 2. Four causes of acute left ventricular failure

Answer:

Four causes of acute left ventricular failure

1. Left ventricular outflow obstruction
   • Systemic hypertension
   • Coarctation of aorta
   • Aortic valvular stenosis
2. Left ventricular inflow obstruction
   • Mitral stenosis
3. Left ventricular volume overload
   • Mitral valve prolapsed
   • Mitral regurgitation
   • Aortic regurgitation
   • Ventricular septal defect
4. Reduced left ventricular contractility
   • Cardiomyopathy
   • Anterior wall myocardial infarction

Question 3. Cyanosis.

Answer: Cyanosis

Definition: Bluish discoloration of skin and mucous membrane is called cyanosis.

Cyanosis Sites Involved:

• Lips a Nail beds
• Fingertips
• Ear lobule.
• The undersurface of the tongue.
• Malar eminence
• Creases of palms.

Cyanosis Types:

1. Peripheral cyanosis.
2. Central cyanosis.

Question 4. Causes of central cyanosis.

Answer:

Causes of central cyanosis

1. Pulmonary causes
   • High altitude
   • Pneumonia
   • Pneumothorax
   • COPD
   • Severe acute asthma
   • Respiratory failure.
2. Cardiovascular causes.
   • Acute pulmonary edema.
   • Cyanotic heart disease.
3. Blood disorders.
   • Methaemoglobin.

Read And Learn More: General Medicine Question and Answers

Question 5. Mid-diastolic murmur.

Answer:

Mid-diastolic murmur

Mid-diastolic murmur is a trembling murmur heard at the apex.

• It is a flow murmur.

Mid-diastolic murmur Causes:

• Dilatation of left ventricle,
• Functional mitral regurgitation.

Question 6. Bradycardia – causes.

Answer:

Sinus node dysfunction:

• Myocardial infarction.
• Hypothermia.
• Hypothyroidism.
• Obstructive jaundice.
• Raised intracranial pressure
• Typhoid fever
• Drugs like digoxin, calcium channel blockers, and beta-blockers.

Question 7. Tachycardia.

Answer:

Tachycardia

A heart rate of more than 100 per minute due to any cause is called tachycardia.

Tachycardia Causes:

1. Physiological
   • Exercise
   • Emotion
   • Fear
   • Smoking.
   • Excessive consumption of tea, coffee, etc.
2. Pathological.
   • Anxiety.
   • Fever
   • Thyrotoxicosis.
   • Anaemia.
   • Heart failure
   • Hypo or hypertension
   • Pheochromocytoma.
   • Drugs – bronchodilators.

Tachycardia Types:

1. Supraventricular tachycardia.
2. Ventricular tachycardia.

Question 8. Atrial fibrillation.

Answer:

Atrial fibrillation

Atrial fibrillation is the most common cardiac arrhythmia.

• The atrial rate is more than 350 beats/min.

Atrial fibrillation Causes:

• Coronary artery disease
• Rheumatic valvular disease
• Idiopathic
• Cardiomyopathy
• Thyro toxicosis.
• Alcoholism.
• Congenital heart disease.
• Pulmonary embolism.

Atrial fibrillation Treatment:

• Treat the cause
• Anti-arrhythmic drugs,
• Anti-coagulant.
• Defibrillation.

Question 9. Cardiac arrest.

Answer:

Cardiac arrest

Definition: It is defined as the sudden complete arrest of heart function.

Cardiac arrest Causes:

• Ventricular fibrillation
• Ventricular asystole.
• Electromechanical dissociation.

Cardiac Arrest Clinical Features:

• Absence of pulses.
• Cold extremities.
• Loss of consciousness.
• Cessation of respiration.
• No heartbeat.

Cardiac arrest Management:

• ABC support.

1. A – airway.
   • Clear mouth and airway.
   • Extend neck and raise chin.
2. B-breathing.
   • Direct mouth-to-mouth breathing.
   • Indirect mouth-to-mouth breathing.
3. C-circulation.
   • Cardiac massage.

Question 10. Heart failure.

Answer:

Heart failure

Heart failure denotes a pathophysiologic state when the heart is not able to maintain its cardiac output to meet the demands of metabolizing tissues.

Heart failure Types:

• Acute and chronic.
• Compensated and decompensated
• Right, left, and biventricular heart failure.
• Forward and backward heart failure.
• Systolic and diastolic heart failure.
• High and low output failure.

Question 11. Treatment of cardiac failure.

Answer:

Treatment of cardiac failure

1. General measures.
   • Bed rest
   • Regular isotonic exercises
   • Low-calorie intake.
   • Salt restriction.
2. Drug therapy.
   • Digitalis – digoxin – 0.25 – 0.5 mg/ day
   • Sympathomimetic amine – dopamine, dobutamine.
   • Diuretics – thiazides, loop diuretcis, potassium sparing.
   • Vasodilators – ACE inhibitors – captopril – 12.5 – 25 mg TID.
3. Cardiac transplantation.

Question 12. Complications of heart failure.

Answer:

Complications of heart failure

• Acute renal failure.
• Hypokalemia.
• Hyponatraemia.
• Jaundice.
• Deep vein thrombosis.
• Arrhythmias.
• Systemic embolism.

Question 13. Congenital heart disease.

Answer:

Congenital Heart Disease Clinical Features:

• Central cyanosis.
• Growth retardation.
• Syncope
• Stature

Etiology:

• Infections – rubella infection.
• Chromosomal defects – Down’s syndrome.
• Connective tissue disorders,
• Alcohol abuse.

Question 14. Classification of congenital heart disease.

Answer:

Classification of congenital heart disease

1. Acyanotic.
   • Acyanotic with left to right shunt.
     • Atrial septal defect.
     • Ventricular septal defect.
     • Patent ductusarteriosus.
   • Acyanotic without shunt.
     • Pulmonary stenosis.
     • Aortic stenosis.
     • Coarctation of aorta.
2. Cyanotic.
   • Complete transposition of great vessels.
   • Tetralogy of Fallot
   • Persistent truncus arteriosus.

Question 15. Atrial septal defect.

Answer:

Atrial septal defect

It is a cyanotic heart disease with a left to right shunt through a defect in the interatrial septum.

Atrial Septal Defect Types:

1. Ostium secundum defect – Involves fossa ovalis.
2. Ostium primum defect.
   • Lies in the common atrioventricular canal.

Atrial Septal Defect Features:

• Asymptomatic.
• Good volume pulse
• Systolic murmur.
• Diastolic flow murmur.
• Wide and fixed splitting of the second heart.
• Chest X-ray – shows an enlargement of the heart.
• ECG – shows incomplete or complete right bundle branch block.
• Echocardiogram – shows right ventricular dilatation, hypertrophy.
• Color Doppler – measures flow velocities.

Atrial Septal Defect Treatment:

• Surgical closure of the defect.

Question 16. Fallor tetralogy.

Answer:

Fallot Tetralogy Components:

• Pulmonary stenosis.
• Ventricular septal defect.
• Over-riding of the aorta.
• Right ventricular hypertrophy.

Fallot Tetralogy Clinical Features:

• Cyanosis – develops after 1 year of age.
• The child may become apnoeic and may fall unconscious.
• Growth retardation.
• Grade 4 clubbing.
• Polycythaemia.
• Ejection systolic murmur.

Question 17. Rheumatic fever/Jone’s criteria.

Answer:

Rheumatic fever/Jone’s criteria

It is an acute inflammatory disease that occurs as a complication of group A streptococcal infection.

Rheumatic Fever Clinical Features:

• Jone’s criteria.
• Major criteria.
• Carditis
• Polyarthritis
• Chorea
• Erythema marginatum
• Subcutaneous nodules.
• Minor criteria.
• Fever
• Arthralgia.
• Raised ESR
• Previous history of rheumatic fever.
• Positive CRP.

Question 18. Aortic regurgitation – signs.

Answer:

Collapsing or good volume pulse:

• Bounding peripheral pulses.
• Corrigan’s sign-dancing carotids.
• Quincke’s sign-capillary pulsation in nail beds.
• Duroziez’s sign.
• Pistol shots sound.
• De Musset’s sign – head nodding with a carotid pulse.
• Cyanosis.
• Pitting ankle oedema.
• Tender hepatomegaly.

Question 19. Infective endocarditis.

Answer:

Infective endocarditis

It is a microbial infection of the mural endocardium a heart valve or valves or lining of blood vessels.

• Clinical Features:

Question 20. Complications of infective endocarditis.

Answer:

Complications of infective endocarditis

If not treated, infective endocarditis may lead to.

• Stroke
• Organ damage
• Spread of infection to other body parts
• Heart failure.
• Septic embolization
• Mycotic aneurysm.
• Neurologic complications.
• Renal complications.
• Musculoskeletal complications.

Question 21. Complications of hypertension.

Answer:

Complications of hypertension

1. Central nervous system.
   • Cerebral atheroma
   • Transient cerebral ischaemic attacks
   • Stroke.
   • Hypertensive encephalopathy
   • Subarachnoid hemorrhage.
2. Retinopathy.
3. Heart
   • Left ventricular hypertrophy.
   • Cardiac failure.
4. Kidney
   • Proteinuria
   • Uraemia.

Question 22. Hypertensive retinopathy.

Answer:

Hypertensive retinopathy

It is an ophthalmic complication of hypertension.

Grades:

1. Cardiac causes
   • Malignant arrhythmias.
     • Ischaemic heart disease
     • Heart blocks
     • Valvular heart disease
     • Infective endocarditis
     • Myocarditis
     • Cardiomyopathy.
   • Thromboembolism.
2. Idiopathic.

Question 23. Causes of sudden death in myocardial infarction.

Answer:

Causes of sudden death in myocardial infarction

• Noncardiac causes
  • Cerebral hemorrhage.
  • Ruptured aortic aneurysm.

Question 24. Risk factors for coronary artery disease.

Answer:

Old age:

• Sex – common in males
• Family history
• Smoking, alcohol.
• Hypertension.
• Mental stress Hypercholesterolemia.
• Diabetes mellitus.
• Sedentary habits
• Obesity
• Polyunsaturated fatty acid deficiencies
• Hyperfibrinogenaemia.
• Low levels of anti-oxidant vitamins
• Protein S and C deficiency.

Question 25. Aspirin.

Answer:

Aspirin

Aspirin is a non-selective COX inhibitor.

Aspirin Uses:

• As analgesic
• Fever
• Arthritis, fibromyositis
• Acute rheumatic fever
• Rheumatoid arthritis
• Osteoarthritis.
• Postmyocardial infarction.
• Inflammatory bowel disease.

Aspirin Adverse Effects:

• Nausea, vomiting, epigastric distress.
• Headache, dizziness, confusion.
• Allergic reactions – rashes, urticaria, photosensitivity.
• Hemolysis.
• Nephrotoxicity.
• Hepatotoxicity.
• Reye’s syndrome.
• Salicylism.

Question 26. Oral anticoagulants.

Answer:

Oral anticoagulants

Oral anticoagulants are drugs given orally to reduce the coagulability of blood.

Oral Anticoagulants Classification:

1. Coumarin derivative.
   • Bishydroxycoumarin, warfarin sodium, acenocoumarol.
2. Indanedione derivative.
   • Phenindione.

Oral Anticoagulants Uses:

• Venous thrombosis
• Pulmonary embolism.
• Post-operative, post-stroke patients.
• Rheumatic valvular disease.
• Unstable angina.
• Vascular surgery.

Question 27. Beta-blockers – uses.

Answer:

Hypertension:

• Angina pectoris.
• Cardiac arrest
• Myocardial infarction.
• Congestive cardiac failure.
• Obstructive cardiomyopathy.
• Pheochromocytoma.
• Thyrotoxicosis.
• Glaucoma.
• Prophylaxis of migraine.
• Anxiety.

Question 28. Nitrates.

Answer:

Nitrates.

Nitrates are vasodilators. They are

• Nitroglycerin
• Isosorbide dinitrate
• Isosorbide mononitrate
• Pentaerythritol tetranitrate.

Nitrates Uses:

• External angina
• Vasospastic angina
• Unstable angina
• Cardiac failure.
• Myocardial infarction.
• Cyanide poisoning.
• Relieves oesophageal spasm.
• Spasmolytic.

Question 29. Anti-anginal drugs.

Answer:

Anti-anginal drugs

Anti-anginal drugs are used to improve the balance between oxygen supply and demand.

• Drugs used in the treatment of angina are as follows.

1. Nitrates
   • Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.
2. Calcium channel blockers.
   • Verapamil, diltiazem, amlodipine, nifedipine.
3. Beta-blockers
   • Propranolol, atenolol.
4. Potassium channel openers.
   • Nicorandil, pinacidil.
5. Miscellaneous.
   • Dipyridamole, aspirin, ivabradine.

Question 30. Calcium channel blockers (CCB).

Answer:

Calcium channel blockers (CCB) are.

1. Dihydropyridines.
   • Nifedipine.
   • Nimodipine.
   • Amlodipine.
   • Nicardipine.
   • Felodipine.
2. Others.
   • Verapamil.
   • Diltiazem.

Calcium channel blockers Use

• Angina pectoris
• Hypertension.
• Arrhythmia.
• Peripheral vascular disease.
• Hypertrophic cardiomyopathy.
• Migraine.
• Subarachnoid hemorrhage.
• Preterm labor.

Question 31. ESR, erythrocyte sedimentation rate.

Answer:

ESR, erythrocyte sedimentation rate

It was first demonstrated by Edmund Beirnacki in 1897.

Erythrocyte Sedimentation Rate Definition:

The rate at which the erythrocytes settle down in a vertical tube is called ESR.

Erythrocyte Sedimentation Rate  Normal values:

• According to Westergren’s method.
  • Males -3-7 mm in 1 hour.
  • Females – 5 – 9 mm in 1 hour.
  • Infants – 0 – 2 mm in 1 hour.

Erythrocyte Sedimentation Rate  Significance:

• Confirms diagnosis.
• Helps to assess the patient’s response to treatment for certain chronic inflammatory diseases.

Factors Affecting ESR:

• The specific gravity of RBC ais  Rouleaux formation.
• Size of RBC
• Viscosity of blood.
• RBC count.

Question 32. Heart sounds.

Answer:

Heart sounds

Mechanical activities of the heart during each cardiac cycle produce some sounds called heart sounds.

Heart sounds Types

Question 33. Pericarditis.

Answer:

Etiology:

• Infection.
• Immunological reaction.
• Trauma
• Neoplasm.
• Idiopathic.

Pericarditis Clinical Features:

• Retrosternal pain.
• Pain radiates to the shoulder and neck.
• Aggravated by deep breathing, movement, changes of position, exercise, and swallowing.

Pericarditis Management:

• Aspirin – 600 mg 4 hourly.
• Indomethacin – 25 mg 8 hourly.
• Paracentesis.
• Surgical drainage.

Question 34. Collapsing pulse.

Answer:

Collapsing pulse

It is a pulse characterized by a rapid upstroke, rapid downstroke, and a high volume.

Factors Effecting it:

• Increased stroke volume.
• Diastolic leak back into left ventricle
• Low systemic vascular resistance

Collapsing pulse Significance:

• It occurs in.
  • Aortic regurgitation
  • Patent ductusarteriosus
  • Ruptured sinus of Valsalva
  • Large arteriovenous fistula
  • Hyperkinetic circulatory states,

Question 35. Treatment of deep vein thrombosis.

Answer: Bed rest with legs elevated to 15 degrees

• Physiotherapy
• Graduated elastic stockings.
• Use of heparin.
• Thrombolysis with streptokinase.
• Thrombectomy.

Question 36. Corrigan’s sign.

Answer:

Corrigan’s sign

Described by Sir Dominic John Corrigan.

• It is a sign of severe aortic valve regurgitation.
• It is a jerky carotid pulse characterized by full expansion followed by quick collapse.
• It appears in the advanced form of the disease.
• By this time, the patient is usually symptomatic.

Corrigan’s sign Causes:

• Rheumatic fever.
• Infective endocarditis,
• Marfan’s syndrome.
• Ehlers – Danlos syndrome.
• Collagen vascular disease.

Question 37. Cardiopulmonary resuscitation.

Answer:

Cardiopulmonary resuscitation

Position the patient on a firm surface such as the floor.

• The heel of the hand should be placed over the lower end of the sternum and with the other hand above it depress the sternum for 3-4 cm,
• It should be maintained at the rate of 60 per minute.
• It should be continued as long as cardiac resuscitation remains feasible and cerebral function is intact.
• It may take a few minutes or even a few hours.

Question 38. Intermittent claudication.

Answer:

Intermittent claudication

It is a symptom occurring due to chronic arterial occlusion.

Intermittent claudication Features:

• Pain occurs during exertion and gradually disappears within minutes upon cessation of activity.
• The group of muscles which will be affected depends on the site of arterial occlusion.

Boyd’s Classification:

VIVA VOCE

1. The most common congenital heart disease is a ventricular septal defect
2. The commonest cause of ventricular tachycardia is acute myocardial infarction
3. The commonest cyanotic heart disease is tetralogy The commonestRheumatic fever mostly results in mitral regurgitation
4. Markers the commonesfirstst in myocardial infarction is CPK-MB
5. The pacemaker of the heart is the SA node
6. The first symptom of heart failure is dyspnoea
7. In atrial flutter P wave of ECG sarees a saThe pacemaker appearance
8. Preload is the first diastolic filling pressure of the ventricle just before,e contraction
9. The force against which the ventricular contracts is termed  as afterload
10. Kussumaul’s sign is an increase of jugular venous pressure during inspiration.

Disease Of The Hepatobiliary System Important Notes

1. Hepatic carcinoma
   • It is cancer of the liver
   • Hepatic carcinoma Etiology
     • Hepatitis B and C
     • Cirrhosis of liver
     • Wilsons disease
     • Haemochromatosis
     • Estrogen and androgen
     • Anabolic steroids
     • Alcohol
   • Hepatic carcinoma Clinical features
     • Yellow skin
     • Bloating from fluid in the abdomen
     • Easy bruising
     • Loss of appetite
     • Weight loss
     • Abdominal pain
     • Nausea, vomiting
     • Fatigue
     • Polycythemia
     • Hypoglycaemia
     • Hypercalcemia
2.  Liver abscess
   • It is a pus-filled mass inside the liver
   • Liver abscess Etiology
     • Portal vein bacteremia
     • Systemic bacteremia
     • Ascending cholangitis
     • Penetrating trauma
     • Direct extension from focus of infection
   • Liver abscess Clinical features
     • Jaundice
     • Abdominal pain
     • Nausea, vomiting
     • Dark urine
     • Clay-colored stools
     • Fever with chills
     • Loss of appetite
     • Weight loss
     • Weakness
3. Jaundice
   • The yellow pigmentation of the skin, mucous membrane & deeper tissues due to increased bilirubin levels in blood is called jaundice
   • It occurs when the bilirubin level exceeds 2 mg%
   • Jaundice Types:
4. Cirrhosis of the liver – features
   • Jaundice
   • Hepatomegaly
   • Ascites
   • Spider telangiectasia
   • Loss of libido
   • Gynaecomastia
   • Bruises, epistaxis
   • Portal hypertension
   • Clubbing
5. Ascites
   • It is an abnormal collection of fluid in the peritoneum
   • Clinical features
     • Abdominal enlargement
     • Stretching sensation
     • Low back pain
     • Indigestion
     • Heart bum
     • Dyspnoea or tachypnoea
     • Abdominal or inguinal hernia
     • Hepatosplenomegaly
6. Ascitic fluid in different diseases
7. Hepatic Encephalopathy
   • It is a neuropsychiatric syndrome caused by liver disease
   • Precipitating factors
     • Infection
     • Hypokalaemia
     • Constipation
     • GI bleeding
     • Dehydration
     • Drug
     • Trauma
8. Hepatomegaly
   • Hepatomegaly Cause
     • Hepatomegaly Vascular
       • Congestive cardiac failure
       • Hepatic vein thrombosis
       • Hemolytic anemia
     • Hepatomegaly Bile duct obstruction
       • Stone
       • Tumour
     • Hepatomegaly Infiltrative
       • leukemia
       • Lymphoma
       • Fatty liver
       • Fat storage disease
       • Amyloidosis

Read And Learn More: General Medicine Question and Answers

1. • • Parasitic
       • Malaria
       • Kala-azar
       • Hydatid disease
     • Inflammatory
       • Hepatitis
       • Typhoid fever
     • Tumor
     • Rare
       • Polycystic disease of the liver
2. Types of liver enlargement
   
3. Splenomegaly
   • Splenomegaly Causes
     • Infection
       • Bacterial – endocarditis, tuberculosis
       • Viral – hepatitis, AIDS
       • Protozoal – malaria
       • Spirochaetal – syphilis
       • Fungal – Histoplasmosis
     • Inflammatory
       • Rheumatoid arthritis
       • Sarcoidosis
     • Congestive splenomegaly
       • Portal hypertension
       • Hepatic vein thrombosis
       • Pericardial effusion
     • Hemolytic disorders
       • Spherocytosis
       • Thalassaemia
     • Infiltrative diseases
       • Amyloidosis
       • Acute leukemia
     • Miscellaneous
       • Iron deficiency anemia
       • Idiopathic
       • Sarcoidosis

Disease Of The Hepatobiliary System Short Essays

Question 1. Hepatitis A.

Answer:

Hepatitis A

It is caused by the Hepatitis A virus.

Hepatitis A Mode of Transmission:

• Faeco-oral route.
• Contaminated water and milk.
• Blood transfusion.
• Homosexual activity.

Hepatitis A Clinical Features:

1. Incubation period 15-45 days.

• • Prodromal symptoms – Anicteric phase.
  • Icteric phase.
  • Recovery phase.

Hepatitis A Investigations:

1. Serum transaminases – Rises.
2. Serum bilirubin – Rises (5 – 20 mg %)
3. Leucocytosis, neutropenia.
4. Prothrombin time – normal or prolonged.
5. Scrum alkaline phosphatase – normal.
6. Urine urobilinogen – Increased.
7. Bile salts and bile pigments – Appears in urine.
8. Ultrasound – shows an enlarged liver.

Hepatitis A Treatment:

• Bed rest.
• High protein and high carbohydrate intake.
• 4 glucose administration. n Avoid hepatotoxic drugs.
• Use of H₂ blockers and antacids.

Question 2. Hepatitis E.

Answer:

Hepatitis E

It is caused by hepatitis E virus.

Hepatitis E Etiology:

• Poor hygiene and sanitation.
• Mode of transmission – Faeco – oral route.

Hepatitis E Clinical Features:

• Incubation period – 3 – 8 weeks.
• It does not progress to chronicity.

Hepatitis E Diagnosis:

• Detection of anti-HEV antibodies,
  • IgM – during the early phase.
  • IgG – after recovery.

Question 3. Chronic active hepatitis.

Answer:

Chronic active hepatitis

Chronic hepatitis is defined as any hepatitis lasting 6 months or longer.

Chronic active hepatitis Causes:

1. Infective.
   • Hepatitis B, C, and D.
2. Toxic.
   • Drugs – alpha – methyldopa, isoniazid.
   • Alcohol.
3. Metabolic.
   • Hemochromatosis.
   • Wilson’s disease.
4. Other
   • Autoimmune hepatitis.

Question 4. Discuss the etiology and clinical features of ascites.

Answer:

Ascites: Abnormal collection of fluid in peritoneum e c.tll< d ascites.

Ascites Etiology:

1. Systemic causes.
   • Nephrotic syndrome.
   • Cirrhosis of liver
   • Hypoproteinaemia.
   • Congestive cardiac failure.
   • Malignancy of the liver.
2. Local causes.
   • Peritonitis
   • Tuberculosis.
   • Pancreatitis.

Ascites  Clinical features: 

• Abdominal enlargement.
• Stretching sensation
• Low back pain
• Indigestion, heartburn
• Dyspnoea or tachypnoea.
• Abdominal or inguinal hermia.
• Hepatosplenomegaly.

Question 5. Complications of hepatitis B 

Answer:

Complications of hepatitis B

• Cirrhosis of liver
• Liver cancer
• Liver failure
• Chronic renal diseases

Question 6. Obstructive jaundice – investigation.

Answer:

Obstructive jaundice – investigation

1. Hemoglobin level – normal.
2. Bile Salts and bile pigment.
   • Present in urine
   • Absent in stools
3. Bilirubin – raised, conjugated.
4. Serum cholesterol – raised.
5. Serum alkaline phosphate – raised
6. Serum transaminase – mildly raised.
7. USG – shows dilatation of intrahepatic and extra-hepatic biliary system.

Question 7. Hepatomegaly.

Answer:

Hepatomegaly

Enlargement of the liver is called hepatomegaly.

Hepatomegaly Causes:

1. Vascular changes.
   • Congestive cardiac failure.
   • hepatic vein thrombosis
   • hemolytic anemia.
2. Bile duct obstruction
   • Due to stone, tumour.
3. Infiltrative causes.
   • leukaemia.
   • Lymphoma
   • Fatty liver
   • Amyloidosis.
4. Parasitic infection.
   • Malaria
   • Kala-azar
   • Amoebic liver abscess
5. Inflammatory disease
   • hepatitis
   • Typhoid fever.
6. Tumors
   • Primary or secondary in River.

Question 8. Tender hepatomegaly – causes.

Answer:

Tender hepatomegaly Causes:

• Hepatitis
• Malignancy
• Hepatic vein thrombosis
• Congestive cardiac failure
• Constrictive pericarditis.

Question 9. Hepatitis B – prevention.

Answer:

Hepatitis B – prevention

Two HBV vaccines are available.

1. Recombivax HB
2. Engerix – B
   • 3 injections of it are administered over six months.

Hepatitis B – prevention Recommended for:

• All infants at birth
• Children – 18 years or above who have not been vaccinated previously.
• Anyone who is undergoing treatment for sexually transmitted disease.
• Injection drug users.
• People with chronic liver diseases
• Residents and staff for developmentally disabled individuals.
• Hemodialysis patients.
• People living with HIV.

Question 10.  Hepatitis C.

Answer:

Hepatitis C

Caused by hepatitis C, RNA virus.

Hepatitis C Route of Transmission:

• Blood transfusions.
• 4 drug user
• Sexual transmission.

Hepatitis C Clinical Features:

• Incubation period – 45 – 50 days.
• Insidious in onset.
• Produces moderate hepatitis.
• Occurs in all age groups.
• It leads to.
  • Vasculitis.
  • Arthritis
  • Glomerulonephritis.
  • Cryoglobulinaemia.
• Its chronicity leads to
  • Cirrhosis of liver
  • Hepatocellular carcinoma
  • Liver failure.

Question 11. Complications of cirrhosis of the liver.

Answer:

Complications of cirrhosis of the liver

• Portal hypertension
• Hepatic
• encephalopathy
• Hepatorenal syndrome.
• Hepatic cell carcinoma.
• Fulminant septicaemia.
• Fatal bleeding.
• Peritonitis.

Question 12. Portal hypertension.

Answer:

Complications of cirrhosis of the liver

It is defined as prolonged elevation of portal venous pressure above normal levels.

Portal hypertension Causes:

1. Prehepatic causes.
   • Portal vein thrombosis.
2. Intrahepatic causes.
   • Cirrhosis.
   • Congenital hepatic fibrosis.
   • Drugs.
   • Sarcoidosis.
   • Secondaries in the liver.
3. Post hepatic causes.
   • Budd-Chiari syndrome
   • Right heart failure.

Portal hypertension Clinical Features:

• Haemetemesis or malena.
• Ascites,
• Splenomegaly.
• Fetor hepaticus.
• Chronic hepatic encephalopathy.

Question 13. Hepatic encephalopathy.

Answer:

Hepatic encephalopathy

It is a syndrome of mental and neurological features that occur in patients with long-standing cirrhosis with or without portal hypertension.

Hepatic encephalopathy Clinical Features:

• Impaired celebration.
• Moderate to severe jaundice.
• Fetor hepaticus.
• Flapping tremors.
• Cirrhosis.
• Portal hypertension.
• Fever
• Tachycardia.
• Hyperventilation.
• Hypotension.

Question 14. Spider nevi.

Answer:

Spider nevi is one of the features occurring due to arteriolar changes induced hyperestrogenism.

• They are dilated central arterioles with radiating small vessels.

Spider nevi Parts involved:

• Parts drained by superior vena cava.
  • Head
  • Neck
  • Upper limbs
  • Front and back of the chest.
• Size: Varies from 1- 2 mm to 1 – 2 cm in diameter.
• Seen in:
  • Cirrhosis of liver
  • Chronic hepatic dysfunction.

Question 15. Splenomegaly-causes.

Answer:

Splenomegaly-causes

1.  Infective disorders.
   • Bacterial – Endocarditis, tuberculosis, septicaemia.
   • Viral – Hepatitis, AIDS.
   • Protozoal malaria.
   • Spirochaetal – syphilis.
   • Fungal – Histoplasmosis.
2. Inflammatory disorders.
   • Rheumatoid arthritis, sarcoidosis.
3. Congestive splenomegaly.
   • Portal hypertension.
   • Hepatic vein thrombosis.
   • Pericardial effusion.
4. Hemolytic disorders.
   • Spherocytosis, thalassemia.
5. Infiltrative diseases.
   • Amyloidosis.
   • Gaucher’s disease
   • Aclucleukemia.
6. Miscellaneous.
7. Iron deficiency anemia.
8. Idiopathic
9. Sarcoidosis.

VIVA VOCE

1. Glucose is stored in the liver in the form of glycogen
2. The liver utilizes amino acids for endogenous protein synthesis and plasma protein synthesis
3. Conjugation of unconjugated bilirubin occurs in liver cells with the help of glucuronyltrans- phrase
4. Kupffer cells are derived from blood monocytes and have immunological functions
5. Normal bilirubin level – 0.3-1.0 mg/dl
6. Normal alkaline phosphatase level – 25-115 U/L
7. Normal acid phosphatase level – 1-5 U/l
8. The normal prothrombin time index is 100%
9. Transudative ascites is seen in cirrhosis of the liver
10. Blood-stained ascites are seen in malignant infiltration of the peritoneum
11. Milky ascites is seen in ductal obstruction
12. Exudative ascites are seen in TB, malignancy, and hepatic vein obstruction
13. Serum bilirubin level more than 2.5 mg/dl leads to jaundice
14. Potassium-sparing diuretics are used in ascites
15. Budd Chiari syndrome occurs from occlusion of the hepatic vein
16. Collection of fluid more than 300 ml in the peritoneum leads to ascites

 

Disease Of The Hepatobiliary System Long Essays

Question 1. Describe etiopathogenesis, clinical features, diagnosis, and management of hepatic carcinoma.

Answer:

Hepatic Carcinoma:

• It is the most common type of liver cancer

Etiology:

• Hepatitis B and C infection.
• Alcoholism.
• Cirrhosis of the liver.
• Hemochromatosis.
• Wilsons disease.
• Oestrogen and androgen.
• Anabolic steroids.

Hepatic Carcinoma Clinical Features:

• Yellow skin.
• Bloating from fluid in the abdomen.
• Easy bruising.
• Loss of appetite n Weight loss
• Abdominal pain
• Nausea, vomiting
• Fatigue.
• Poly ischemia, hypoglycemia, hypercalcemia.

Hepatic Carcinoma Diagnosis:

• Serum alkaline phosphatase – high.
• Ultrasonography – shows carcinoma, lesion shows poorly defined margins.
• CT scan – detects small tumours.
• Angiography — shows tumor blushes.
• Liver aspiration – confirms tumour.

Hepatic Carcinoma Management:

• Liver transplantation.
• Surgical resection.
• Transcatheter arterial chemoembolization (TACE)
• Palliative therapy – use of cisplatin, and fluorouracil.
• Radiofrequency ablation.

Question 2. What are the causes of liver abscesses? Describe clinical features and complications of liver abscess.

Answer:

Liver Abscess:

• Liver abscess is a pus-filled mass inside the liver.

Etiology:

• Portal vein bacteremia from appendicitis, diverticulitis, and a perforated bowel.
• Systemic bacteremia via the hepatic artery.
• Ascending cholangitis.
• Penetrating trauma.
• Direct extension from focus of infection.

Liver Abscess Clinical Features:

• Subacute in onset.
• Jaundice
• Abdominal pain.
• Nausea, vomiting.
• Dark urine, clay-colored stools.
• Fever with chills.
• Loss of appetite.
• Weight loss.
• Weakness.

Liver Abscess Complications:

• Pleural effusion.
• Perforation of abscess with peritonitis
• Subphrenic abscess.
• Empyema,
• Hepatic coma.

Read And Learn More: General Medicine Question and Answers

Question 3. Classify jaundice. Describe etiology, clinical features, diagnosis, complications, and its management.

Answer:

Jaundice: Jaundice refers to yellow discoloration of skin, mucous membrane, sclera, and conjunctiva due to raised serum bilirubin.

Jaundice Classification:

1. Based on coloration of sclera.
   • Medical jaundice – yellow coloration.
   • Surgical jaundice – greenish-yellow coloration.
2. Based on etiology of jaundice.
   • Hemolytic.
   • Hepatic
   • Obstructive.
3. Based on chemical nature of bilirubin.
   • Unconjugated hyperbilirubinemia.
   • Conjugated hyperbilirubinemia.

Jaundice Causes:

1. Jaundice with predominantly unconjugated hyperbilirubinemia.
   • Hemolysis.
     • Intracorpuscular or extracorpuscular defects.
     • Drug-induced.
     • Infections.
   • Decreased uptake of bilirubin.
     • Drugs
     • Sepsis
     • Congenital
   • Decreased conjugation of bilirubin.
     • Neonatal jaundice.
     • Gilbert’s syndrome.
2. Jaundice with predominantly conjugated hyperbilirubinemia.
   • Intrahepatic cholestasis.
     • Congenital
     • Drugs and alcohol.
     • Hepatitis
     • Primary biliary cirrhosis.
     • Hodgkin’s lymphoma.
     • Postoperative.
   • Extrahepatic biliary obstruction.
     • Bile duct stone
     • Biliary stricture c Trauma
     • Tumour
     • Pancreatitis.

Jaundice Clinical Features:

Jaundice Diagnosis:

Jaundice Complications:

• Sepsis
• Biliary cirrhosis
• Pancreatitis
• Coagulopathy
• Renal and liver disease

Jaundice Management:

• Treat the causative agent.
• Discontinue the causative drug/toxin.
• Maintain adequate hydration and rest.
• Avoid alcohol.
• Use of analgesics to relieve pain, antibiotics for infections.
• Blood transfusion.

Question 4. Describe etiology, clinical features, complications diagnosis, and management of serum hepatitis B. Add a note on its prevention. (or) Enumerate the viruses causing acute hepatitis. Describe the clinical features and complications of viral hepatitis B. Add a note on the dental significance.

Answer:

Hepatitis: It is an acute parenchymal disease of liver.

Viruses Causing Acute Hepatitis:

1. Specific viruses.
   • Hepatitis A virus
   • Hepatitis B virus
   • Hepatitis C virus
   • Hepatitis D virus
   • Hepatitis E virus
2. Other viruses.
   • Cytomegalovirus
   • Epstein barr virus.
   • Herpes simplex virus.

Hepatitis B:

Etiology: It is caused by hepatitis B virus.

Hepatitis B Clinical Features:

1. Prodromal symptoms – Anicteric phase.
   • Occurs before the development of jaundice.
   • Fever with chills, malaise
   • Headache.
   • Aches and pain.
   • Nausea, vomiting, distaste for food.
   • Disturbed smell.
   • Dark-colored urine, clay-colored stools.
   • It lasts for few days to 2 weeks.
2. Icteric phase.
   • Jaundice occurs.
   • Enlarged and tender liver
   • Dark-colored urine, clay-colored stools
   • Pruritus.
   • Weight loss
3. Recovery phase.
   • It takes 2-8 weeks.
   • Jaundice starts regressing.
   • Full recovery occurs within 1-2 months.

Hepatitis B Complications:

• Cirrhosis of liver.
• Liver cancer
• Liver failure.
• Chronic renal diseases.

Hepatitis B Diagnosis:

• Serum transaminases – Rises
• High serum alkaline phosphatase level
• Serum bilirubin – 5 – 20 mg %.
• Prothrombin time – normal.
• Urine urobilinogen – Increased
• Ultrasound of liver – shows enlarged liver.

Hepatitis B Treatment:

• Bed rest.
• High-calorie diet.
• Intravenous fluid administration,
• Avoid hepatotoxic drugs
• Used of H₂ blockers and antacids.
• Liver transplantation.

Hepatitis B Prevention:

• Recombinant hepatitis B vaccine containing. HBs Ag is used for active immunization.

Hepatitis B Dental Significance:

• A significantly higher incidence of HBV occurs among dental staff.
• Vectors of infection are blood, saliva, and nasopharyngeal secretion.
• Intraorally, the greatest concentration of hepatitis B infection is gingival sulcus,
• Also, periodontal disease, severity of bleeding, and bad oral hygiene are associated with the risk of HBV.
• All dental healthcare workers should receive vaccination against hepatitis B.

Question 5. Discuss the etiology, clinical features, complications, and treatment of cirrhosis of the liver.

Answer:

Cirrhosis of Liver:

1. It is end result of hepatocellular injury characterized by triad of pathological changes i.e.,
   • Degeneration of hepatocytes.
   • Hyperplasia of remaining hepatocytes.
   • Fibrosis.

Cirrhosis of Liver Causes:

1. Common causes.
   • Alcohol.
   • Hepatitis B, C, non-A, non-B, non-C, viruses.
2. Other causes.
   • Autoimmune hepatitis.
   • Drug induced.
   • Biliary cirrhosis.
   • Haemochromatosis
   • Wilson’s disease
   • Cardiac cirrhosis.
   • Glycogen storage disease
   • Idiopathic.

Cirrhosis of Liver Clinical Features:

1. General
   • Fever, jaundice, weakness, fatigue, weight loss.
2. GIT symptoms:
   • Ascites.
   • Nausea, vomiting, anorexia.
   • Abdominal distension.
   • Splenomegaly.
   • Haematemesis.
   • Portal hypertension.
   • Nodular and enlarged liver.
3. Circulatory symptoms.
   • Palmar erythema, spider angiomata, cyanosis, clubbing.
4. Endocrine changes.
   • Loss of axillary and pubic hair, loss of libido, gynaecomastia, amenorrhoea.
5. Blood changes.
   • Aneamia, pancytopenia, bruises, purpura, epitaxis.

Cirrhosis of Liver Complications:

• Portal hypertension.
• Ascites
• Upper G1 bleeding
• Bacterial peritonitis.
• Hepatic encephalopathy n Hepatorenal syndrome.
• Hepatocellular carcinoma.

Cirrhosis of Liver Treatment:

1. Removal of causative agent.
2. General measures.
   • Intake of high protein and high caloric diet.
   • Avoid alcohol.
   • Vitamin and minerals supplements.
   • Low sodium diet.
   • Use of diuretics.
   • Water restriction.
3. Treatment of complications.
4. Liver transplantation.

Question 6. Define and describe the clinical features of ascites. Describe the pathogenesis and treatment of ascites.

Answer:

Ascites: An abnormal collection of fluid in the peritoneum is called ascites.

Pathogenesis:

1. Inflammation of peritoneum.

↓

Increased capillary permeability.

↓

Transudation of fluid into peritoneum

↓

Ascites

2. Venous obstruction

↓

Transudation of fluid into peritoneum

↓

Ascites

↓

Lymphatic obstruction → Ascites

Ascites Clinical Features:

• Abdominal enlargement.
• Stretching sensation
• Low back pain
• Indigestion, heartburn
• Dyspnoea or tachypnoea.
• Abdominal or inguinal hermia.
• Hepatosplenomegaly.

Ascites  Treatment:

• Salt restriction
• Use of diuretics
• Therapeutic paraentesis.
• Cefotaxime – 1g 4 twice a day.
• Gentamicin – 60 – 80 mg 4 or IM 8 hourly.

Diseases Of Cardiovascular System Long Essays

Question 1. What are the signs and symptoms of cardiac failure? How do you treat it? (or) Define heart failure. Describe its pathophysiology, etiology, clinical features, and management.

Answer:

Heart Failure:

• It denotes a pathophysiologic state when the heart is not able to maintain its cardiac output to meet the demands of metabolizing tissues.

Pathophysiology:

1. Preload.
   • It is maintained by venous return that fills the ventricle during diastole and raises their pressure.
2. Afterload.
   • It is the resistance offered by blood vessels to stroke output.
3. Myocardial contractility.
   • It depends on the adrenergic nervous activity and the levels of circulating catecholamine.
   • It causes the emptying of the chambers of the heart.
   • Over-stretching of the myocardium due to an increase in afterload leads to ventricular dilatation.

Etiology:

1. Ventricular outflow obstruction.
   • Hypertension
   • Aortic stenosis
   • Pulmonary hypertension.
   • Pulmonary stenosis.
2. Ventricular inflow obstruction.
   • Mitral stenosis.
   • Tricuspid stenosis.
3. Ventricular volume overload.
   • Mitral regurgitation.
   • Aortic regurgitation.
   • Atrial septal defect.
   • Ventricular defect.
4. Depressed ventricular contractility.
   • Myocarditis.
   • Cardiomyopathy

Pathophysiology Clinical Features:

1. Due to low cardiac output.
   • Fatigue
   • Cold extremities
   • Low BP
   • Oliguria.
2. Features due to left heart failure.
   • Dyspnea
   • Cough
   • Orthopnoea.
   • Paroxysmal nocturnal dyspnoea.
   • Cardiac arrhythmia.
   • Cardiomegaly.
3. Features due to right heart failure.
   • Raised jugular venous pressure
   • Hepatic enlargement.
   • Peripheral edema.
   • Anorexia, nausea, vomiting.
   • Jaundice.
4. Features of chronic heart disease.
   • Valvular defects.
   • Congenital defects.

Pathophysiology Management:

1. General measures.
   • Bed rest
   • Regular isotonic exercises.
   • Low-calorie intake.
   • Salt restriction.
2. Drug therapy.
   • Digitalis – digoxin – 0.25 – 0.5 mg/day.
   • Sympathomimetic amine – dopamine, dobutamine.
   • Diuretics – thiazides, loop diuretics, potassium sparing.
   • Vasodilators – ACE inhibitors – captopril – 12.5 – 25 mg TID.
3. Cardiac transplantation.

Question 2. Describe the etiology, clinical features, and management of acute ventricular failure.

Answer:

Left Ventricular Failure:

• It is defined as failure to maintain an effective left ventricular output for a given pulmonary venous or left atrial pressure.

Left Ventricular Failure Causes:

1. Left ventricular outflow obstruction.
   • Systemic hypertension.
   • Coarctation of aorta.
   • Aortic valvular stenosis.
2. Left ventricular inflow obstruction.
   • Mitral stenosis.
3. Left ventricular volume overload,
   • Mitral valve prolapsed.
   • Mitral regurgitation.
   • Aortic regurgitation
   • Ventricular septal defect.
4. Reduced left ventricular contractility.
   • Cardiomyopathy.
   • Anterior wall myocardial infarction.

Read And Learn More: General Medicine Question and Answers

Left Ventricular Failure Clinical Features:

1. Progressive dyspnoea – occurs on exertion.
2. Orthopnoea.
   • It is dyspnoea occurring in a recumbent position.
3. Paroxysmal nocturnal dyspnoea.
   • It refers to dyspnoea occurring at height and awakens the patients from sleep.
4. Cheyne – stokes respiration.
   • It is periodic respiration with alternate periods of hypernoea and apnoea.
5. Cough and hemoptysis.
6. Oliguria and nocturia.
7. Tachypnoea and tachycardia.
8. Fatigue and weakness.

Left Ventricular Failure Treatment:

1. General measures.
   • Removal of causative factors.
   • Removal of precipitating factors.
   • Maintain a sitting position with legs hanging alongside.
2. Drugs.
   • Sedative – morphine 5-10 mg IV.
   • Antiemetic – Metaoclopramide – 10 mg IV
   • Oxygen – 60 % through a face mask.
   • Loop diuretics – frusemide – 400 -100 mg.
   • Intravenous sodium nitroprusside – 20 – 30 μ/ min.
   • Digoxin – 0.5 – 1 mg.
   • Bronchodilator – aminophylline – 250 – 500 mg IV
   • Inotropes – dopamine, dobutamine.
3. Intra-aortic balloon counterpulsation.

Question 3. Describe clinical features and treatment of ventricular septal defects.

Answer:

Ventricular septal defect:

• It implies a defect in the interventricular septum.
• The defect lies in the membraneous part or muscular part of the interventricular septum.

Ventricular septal defect Clinical Features:

• Common in pediatric age group.
• Remains asymptomatic for longer periods.
• Normal pulse, wide pulse pressure.
• Increased incidence of respiratory diseases.
• Systolic thrill.
• Pansystolic murmur.
• The apex beat is shifted down.

Ventricular septal defect Complication:

• Congestive cardiac failure.
• Pulmonary hypertension.
• Right ventricular outflow tract obstruction.
• Aortic regurgitation.
• Infective endocarditis.

Ventricular septal defect Treatment:

• Digoxin – 10 – 20 gg/ day.
• Frusemide – 1 – 3 mg/day.
• Small defects close spontaneously.
• Large defects require surgical repair.

Question 4. Describe etiology, clinical features, diagnosis, and treatment of rheumatic fever.
(or)
Rheumatic fever – etiology, pathology, clinical features, complications, and dental considerations.
(or)
Discuss in detail the clinical features, diagnosis, management, and prophylaxis of acute rheumatic fever.

Answer:

Acute Rheumatic Fever:

• It is an acute inflammatory disease that occurs as a sequel to infection caused by group A streptococci.

Etiology:

• Streptococcal infection.

Pathology:

1. Gross appearance.
   • Consists of small, uniformly sized thrombotic vegetations.
   • Chronically scared, inflamed, and neovascular-sized valve.
2. Microscopic appearance.

• • Vegetations show.
  • Surface thrombi.
  • Lack of underlying valve destruction
  • Mild edema.
  • Chronic inflammation.
  • Neo vascularisation.
  • Mild calcification.

Acute Rheumatic Fever Clinical Features:

• Jones’ criteria.

1. Major criteria.
   • Carditis
   • Polyarthritis
   • Chorea
   • Erythema marginatum
   • Subcutaneous nodules.
2. Minor criteria.
   • Fever
   • Arthralgia.
   • Raised ESR
   • Previous history of rheumatic fever.
   • Positive CRP.

Acute Rheumatic Fever Diagnosis:

Acute Rheumatic Fever Treatment:

1. Bed rest
2. Drugs.
   • Antibiotics.
     • To treat the streptococcal infection.
     • A single injection of benzathine penicillin 1.2 million IM.
     • Daily injection of procaine penicillin 6,00,000 units IM for 10 days.
     • Oral erythromycin – 20 40 mg/kg/day.
   • Salicylates.
     • For symptomatic relief in arthritis.
     • Aspirin – 60 mg/kg/day 4 hourly.
   • Corticosteroids.
     • Prednisolone – 1 – 2 mg/kg per day.

Prophylaxis:

1. Primary prevention.
   • Done by mass penicillin prophylaxis
   • Established cases treated by benzathine penicillin oral penicillin or erythromycin.
2. Secondary prevention.
   • IM injection of 1.2 million units of benzathine penciling G every 3 weeks.
   • Oral penicillin V- 250 mg twice daily.
   • Sulphadiazine – lg/ day orally as a single dose.
   • Erythromycin – 250 mg twice daily orally.
3. Dental Consideration:
   • Acute rheumatic fever is caused by group A streptococcus.
   • This causes pharyngitis and sore throat.
   • Good oral hygiene should be maintained as oral bacteria entering the bloodstream can increase the risk of complications.
   • Antibiotics are given before some dental procedures to prevent bacterial infection of the damaged areas of the heart.
   • Patients with rheumatic fever have an increased risk of developing bacterial endocarditis after a dental procedure.

Question 5. Describe clinical features, complications, diagnosis, and management of rheumatic mitral stenosis.
(or)
Describe the etiology, clinical features, investigations, and management of mitral stenosis.

Answer:

Mitral Stenosis:

• Mitral stenosis is chronic rheumatic heart disease.

Etiology:

• Rheumatic
• Congenital
• Atrial fibrillation.
• Lack of coordinated contractions of atria.

Mitral Stenosis Clinical Features:

1. Symptoms due to low cardiac output.
   • Fatigue
   • Lethargy
   • Weakness.
2. Symptoms of pulmonary congestion.
   • Dyspnoea.
   • Orthopnoea
   • Paroxysmal nocturnal dyspnoea.
3. Symptoms of right heart failure.
   • Puffiness of face
   • Oedema of legs
   • Hepatomegaly.
4. Symptoms due to embolization.
   • Hemoptysis.
   • Chest pain
   • Hemiplegia.
   • Abdominal pain.
   • Loss of peripheral pulses.
   • Gangrenes.
5. Others.
   • Mitral facies
   • Low pulse pressure.
   • Raised jugular venous pressure.
   • Cold extremities.
   • Pitting edema.

Mitral Stenosis Complications:

• Pulmonary hypertension a Heart failure
• Cardiomyopathy
• Atrial fibrillation
• Pulmonary edema.

Mitral Stenosis Investigations:

Mitral Stenosis Management:

1. Salt restriction.
2. Medical treatment.
   • Digoxin – 0.25 – 0.25 mg/day
   • Diuretics – to reduce pulmonary congestion.
   • Anticoagulants – to prevent systemic embolization.
   • Antibiotic prophylaxis.
3. Surgical treatment.
   • Mitral balloon valvuloplasty.
   • Mitral valve replacement.

Question 6. Discuss the etiology, clinical features, diagnosis, and management of infective endocarditis.
(or)
Discuss the etiology, pathogenesis, and management of subacute bacterial endocarditis. Add a note on its prophylaxis.
(or)
Mention causative factors, clinical features, and management of bacterial endocarditis. Add on the note on dental considerations.

Answer:

Infective Endocarditis:

• Infective endocarditis is a microbial infection of the mural endocardium, heart valve, or lining of the blood vessel.

Etiology:

• Causative organisms are:

1. • Staphylococcus aureus.
   • Streptococcus pneumonia.
   • Neisseria gonococci.

Pathogenesis:

Persons with pre-existing heart disease.
↓
Transient bacteremia following dental procedures.
↓
Bacteria in circulation get deposited on the endocardium at sites of high blood flow.
↓
Develops sterile vegetation consisting of platelets and fibrin.
↓
Infective endocarditis

Infective Endocarditis Clinical Features:

1. General
   • Fever, weight loss, night sweats, weakness.
2. GIT disturbances.
   • Nausea, vomiting, anorexia.
3. CVS disturbances.
   • Tachycardia, conduction defects, cardiac failure.
4. CNS.
   • Headache, toxic encephalopathy, hemiplegia.
5. Lungs.
   • Hemoptysis, pleuritic pain.
6. Nails.
   • Clubbing, OsleTs nodes.
7. Skin – petechiae, purpuric spots.
8. Eyes.
   • Roth’s spot, subconjunctival hemorrhage, petechial hemorrhage.
9. Kidneys – hematuria.
10. Spleen – spleenomegaly.

Infective Endocarditis Diagnosis:

• Duke’s criteria.

1. Major criteria.
   • Positive blood culture.
     • Typical organisms from two cultures.
     • Persistent positive blood cultures taken more than 12 hours apart.
     • 3 or more positive cultures taken over more than 1 hour.
   • Endocardial involvement.
     • Positive ECG findings.
     • New valvular regurgitation.
2. Minor criteria.
   • Predisposing heart conditions
   • Fever ≥ 38° C
   • Intravenous drug misuse.
   • Vascular phenomena.
   • Immunologic phenomena

• Microbiologic evidence.
• Treatment:
• Antibiotics.
• Penicillin G – 2 – 4 million units IV 4 – hourly.
• Gentamicin -1 mg/kg TV or IM 8 hourly.
• Ceftriaxone – 2 g IV OD.
• Ampicillin- 2 gIV4 hourly.
• Cefazolin – 2g IV 8 hourly.
• Vancomycin-15 mg/kg IV12 hourly.
• Surgery.
• Valve replacement.

Prophylaxis:

Dental, considerations:

• Bacteria in the mouth may trigger endocarditis in people at higher risk.
• Bacteria found in tooth plaque may multiply and cause gingivitis.
• Gingiva becomes inflamed and often bleeds during tooth brushing or dental procedures.
• When gingiva bleeds, the bacteria can enter the bloodstream and infect other parts of the body.
• Antibiotic prophylaxis is required before any surgical procedures.

Question 7. Describe the signs and symptoms of angina and how would you manage the case.
(or)
Describe clinical features, investigations, management, and prevention of angina pectoris.

Answer:

Angina Pectoris:

• It is a clinical syndrome of episodic chest discomfort due to transient myocardial ischemia.

Angina Pectoris Clinical Features:

• Common in 40 – 60 years males.
• Retrosternal pain.
• It radiates to the left arm or the right arm, throat, back, chin, and epigastrium.
• It gets precipitated by exertion and relieved by rest.
• The patient feels heaviness, pressure, squeezing, or choking sensation.
• Nocturnal angina – characterized by.
• Nightmares.
• Dyspnoea.
• Palpitation.
• Skin flushing.
• Profuse sweating.
• Wide pulse pressure.

Angina Pectoris Investigations:

Angina Pectoris Management:

1. General measures.
   • Proper explanation of the disease.
   • Avoid walking after meals.
   • Avoid smoking and alcohol.
   • Avoid strenuous exercise
   • Reduction of risk factors.
   • Control of BP and diabetes
   • Treatment of co-existing diseases.
2. Drug therapy.
   • Aspirin – 75 – 150 mg, reduces the risk of infarction.
   • Sublingual glyceryl trinitrate – 500 pg relieves angina pain within 2-3 min.
   • Beta-blockers – atenolol – 50 – 100 mg orally/day.
   • Calcium channel blockers – nifedipine – 5 – 30 mg orally 8 hourly.
3. Surgical treatment.
   • Coronary angioplasty.
   • Coronary artery bypass grafting.

Angina Pectoris Prevention:

1. Acute prevention
   • Sublingual nitroglycerin given 15 min before exertion can prevent the attack.
   • Its effect lasts for 30 min.
2. Chronic prevention.
   • Long-acting nitrates, beta-blockers, or calcium channel blockers are used.

Question 8. Describe the etiology, clinical features, complications diagnosis, and management of acute myocardial infarction.
(or)
What are the risk factors for coronary artery disease? Describe clinical features, investigations, and management of acute myocardial infarction.

Answer:

Risk Factors For Coronary Artery Disease:

• Old age
• More prone in males
• Family history
• Smoking, alcohol.
• Hypertension
• Mental stress.
• Sedentary habits.
• Diabetes mellitus.
• Obesity

Coronary Artery Disease Myocardial Infarction:

• Myocardial infarction is myocardial necrosis, occurring as a result of a critical balance between coronary blood supply and myocardial demand.

Etiology:

• Formation of occlusive thrombus.
• Erosion of an atheromatous plaque in a coronary artery.

Coronary Artery Disease Clinical Features:

• Prolonged and severe chest pain.
• Anxiety
• Dyspnoea
• Nausea, vomiting
• Sweating
• Syncope
• Pallor
• Tachycardia
• Cold extremities
• Oliguria.
• Low pulse pressure
• Fever

Coronary Artery Disease Investigation:

Coronary Artery Disease Management:

1. Early treatment.
   • Aspirin treatment.
   • Sublingual glyceryl trinitrate – 0.4 – 1 mg.
   • Oxygen administration – 2 – 4 L/min.
   • Analgesic – 4 morphine 5 mg + antimetic metaclopramide 10gm.
   • Beta-blockers – 4 metoprolol 5 mg every 2 – 5 min for 3 doses.
   • Thrombolysis.
2. Late treatment.
   • Bed rest
   • 4 morphine sulphate 10 mg + 4 prochlorperazine. 12.5 mg
   • Aspirin – 75 – 150 mg.
   • Inhalation of oxygen.
   • Streptokinase – 1.5 million units in 100 ml of saline given in an intravenous infusion over 1 hour.
   • Alteplase.
     • Bolus dose 15 mg.
     • 50 mg over 30 min.
     • 35 mg over the next 60 min.
     • Angioplasty.
     • Anticoagulant – subcutaneous heparin – 7500 units twice a day for 7-10 days.
     • Beta-blockers – 4 atenolol – 5 – 10 mg over 5 min.
     • Nitrates – sublingual glyceryl trinitrate – 0.4 mg.
     • Sedative – diazepam – 5 mg – 3-4 times a day.

Coronary Artery Disease Complications:

1. Immediate:
   • Arrhythmia and conduction disturbances.
     • Sinus bradycardia.
     • Ventricular tachycardia.
     • Ventricular fibrillation.
     • Atrial fibrillation
     • Heart block.
   • Post-myocardial angina.
   • Acute circulatory failure.
   • Pericarditis.
   • Mechanical complications.
     • Papillary muscle dysfunction.
     • Rupture of the interventricular septum.
     • Rupture of the ventricle.
   • Mural thrombosis and embolism.
   • Sudden death.
2. Late Complication
   • Post myocardial infarction syndrome.
   • Ventricular aneurysm.

Question 9. Describe the etiology, clinical features, complications, and management of systemic hypertension.

Answer: It is defined as a level of blood pressure at which there is an increased risk for target organ damage.

Etiology:

1. Primary hypertension.
   • Idiopathic.
2. Secondary hypertension.
   • Renal diseases
     • Chronic pyelonephritis.
     • Acute and chronic glomerulonephritis.
     • Renal artery stenosis.
   • Endocrine disorders
     • Cushing syndrome
     • Hyperparathyroidism.
     • Pheochromocytoma.
     • Acromegaly.
   • Drug-induced
     • Oral contraceptives
     • Anabolic steroids
     • Corticosteroids
     • NSAIDs
   • Pregnancy.
   • collagen vascular disorders.
     • SALE
   • Miscellaneous.
     • Coarctation of aorta.

Etiology Clinical Features:

1. General
   • Headache
   • Dizziness
   • Palpitation
   • Fatigue.
2. Primary hypertension
   • Epistaxis.
   • Blurring of vision.
   • Hematuria.
   • Angina pectoris
   • Dyspnoea.
3. Secondary hypertension
   • Polyuria, polydipsia.
   • Weakness.
   • Weight gain.
   • Truncal obesity.
   • Episodic headache
   • Palpitation
   • Sweating.

Etiology Complication:

1. Central nervous system.
   • Cerebral, atheroma.
   • Transient cerebral ischaemic attacks.
   • Stroke
   • Hypertensive encephalopathy.
   • Subarachnoid hemorrhage.
2. Retinopathy.
3. Heart
   • Left ventricular hypertrophy.
   • Coronary artery disease.
   • Cardiac failure.
4. Kidneys.
   • Proteinuria.
   • Uraemia.

Etiology Management:

1. General measures.
   • Avoid unnecessary stress
   • Salt restriction
   • Obesity correction.
   • Regular exercise
   • Avoid smoking.
2. Drug therapy.

Question 10. What is hypertension? Classify hypertensive drugs. Describe complications of hypertension.

Answer:

Hypertension: It is defined as a level of blood pressure at which there is an increased risk for target organ damage.

Hypertension Classification:

1. Diuretics.
   • Thiazide s- hydrochlorothiazide, chlorthiali- done.
   • Loop diuretics – Frusemide, bumetanide.
   • Potassium-sparing diuretics – Spironolactone, amiloride.
2. Drugs acting on renin – angiotensin system.
   • ACE inhibitors – captopril, enalapril, lisinopril.
   • Angiotensin 2 receptor antagonists – losar- tan, candesartan.
   • Renin inhibitor – Aliskiren.
3. Sympatholytics.
   • Centrally blockers – trimethaphan.
   • Adrenergic neuron blockers – reserpine.
   • Adrenergic receptor blocers.
     • α blockers – prazosin, phenoxybenzamine.
     • β blockers – propranolol, atenolo.
     • α and β blockers – labetalol.
4. Calcium channel blockers.
   • Verapamil, nifedipine, amlodipine.
5. Vasodilators.
   • Arteriolar dilators – hydralazine, minoxidil.
   • Arteriolar and venular dilators – sodium ni- troprusside.

Question 11. Describe etiopathogenesis, clinical features, and treatment of chronic corpulmonale.

Answer:

Definition: Chronic corpulmonale is defined as a combination of hypertrophy and dilatation of the right ventricle secondary to pulmonary hypertension.

Etiology:

1. Diseases of the lung.
   • Chronic obstructive pulmonary disease, COPD.
   • Chronic bronchial asthma.
   • Pulmonary tuberculosis.
   • Cystic fibrosis.
   • Pleural fibrosis.
2. Diseases of pulmonary circulation.
   • Recurrent pulmonary thromboembolism.
   • Primary pulmonary hypertension.
   • Chronic liver disease.
3. Diseases of the thorax.
   • Neuromuscular disease.
   • Obesity.

Pathogenesis:

Increased pulmonary vascular resistance.
↓
Pulmonary hypertension
↓
Chronic corpulmonale.

chronic corpulmonale Clinical Features:

• Dyspnoea.
• Dry cough.
• Peripheral cyanosis, Anterior chest pain,
• Tachypnoea.
• Ankle oedema,
• Right heart failure.
• Respiratory failure.

chronic corpulmonale Treatment:

• Treat the cause
• Avoid smoking.
• Avoid strenuous exercise
• Avoid traveling to high altitudes.
• Oxygen therapy
• Use of anti-coagulants.
• Lung transplant.