Diseases Of Blood And Lymphoreticular System Notes and Short Essays

Diseases Of Blood And Lymphoreticular System Important Notes

1. Thalassemia

Diseases Of Blood And Lymphoreticular System Thalassemia

2. Types of leukemia

Diseases Of Blood And Lymphoreticular System Types Of Leukemia

3. Causes of DIC

  • Infections like E.coli, N.meningitis, strep. Pneumonia
  • Cancers of lung, prostrate, pancreas
  • Obstetric preeclampsia, amniotic fluid embolism

4. Complications of polycythemia vera

  1. Elevated red cells
  2. Splenomegaly
  3. Leukocytosis
  4. Thrombosis

5. Components that are destroyed quickly from stored blood are

  • WBC
  • Clotting factors
  • Platelets

6. Types of hemophilia

Diseases Of Blood And Lymphoreticular System Type Of Hemophilia

7. Bleeding tests

Diseases Of Blood And Lymphoreticular System Bleeding Tests

8. Platelets

  • Normal count 1.54 lakhs/mm3
  • Increased in thrombocytosis
  • Decreased in thrombocytopenic purpura

9. Anaemia

Diseases Of Blood And Lymphoreticular System Anaemia

10. Anticoagulants

Diseases Of Blood And Lymphoreticular System Anticoagulants

11. Erythroblastosis foetalis

  • When a Rh ve mother carries in a Rh +ve fetus, usually first child escapes the complication of the Rh incompatibility
  • When the mother conceives for the second time and carries an Rh +ve fetus, the Rh agglutinins enter the fetus and cause agglutination of fetal RBC and hemolysis
  • Complications
    • Hydrops fetalis
    • Kernicterus

Diseases Of Blood And Lymphoreticular System Short Essays

Question 1. Sickle cell anaemia

Answer:

Sickle cell anaemia

  • Hb S is abnormal haemoglobin which gets polymerise and distorts the cell membrane to form abnormal sickle-shaped cell

Sickle cell anaemia Clinical features

  1. Chronic anaemia features
    • Fatigue
    • Lassitude
    • Breathlessness
    • Cardiomegaly
    • Increased susceptibility to infection
    • Hyperplasia of bone marrow producing frontal bossing and malar prominence
    • Mild jaundice
    • Splenomegaly
    • Poor healing ulcers
  2. Other features
    • Pain due to blockage of small or large vessels
    • Large swelling, pain, and tenderness of fingers and toes
    • Acute abdominal colic, renal infarction
    • Painful hematuria
    • Aseptic necrosis of head of femur
    • Fever, malaise
    • Microembolisation of pulmonary vessels occurs in late pregnancy

Read And Learn More: General Medicine Question and Answers

Sickle cell anaemia Diagnosis

  • Haemoglobin low
  • Unconjugated bilirubin increases
  • Peripheral blood smear shows
    • Sickle cell, target cells, and Howell Jowel bodies
  • Positive sickling test
  • Presence of abnormal hemoglobin – HbS

Management

Diseases Of Blood And Lymphoreticular System Sickle Cell Anaemia Management

Question 2. Causes of megaloblastic anaemia

Answer:

Causes of megaloblastic anaemia

  • Inadequate dietary intake
  • Malabsorption
    • Intrinsic factor deficiency
      • Pernicious anaemia
      • Gastrectomy
      • Congenital lack of factor
    • Intestinal causes
      • Tropical sprue
      • Ileal resection
      • Crohn’s disease
    • Removal of B12 from intestine
      • Bacterial proliferation in intestinal blind loop syndrome
      • Fish tapeworm infestations
      • Drugs ex: PAS, neomycin

Question 3. Oral manifestations of leukemia

Answer:

Gingiva

  • Gingivitis
  • Gingival hyperplasia
  • Enlargement of interdental papilla
  • Swollen gingival tissue
  • Cyanotic bluish discoloration of gingiva
  • Thrombosis of gingival vessels

Teeth

  • Rapid loosening of teeth
  • Alteration in developing tooth crypts
  • Destruction of lamina dura
  • Displacement of teeth

Oral mucosa

  • Thinning of oral mucosa
  • Petechiae and ecchymosis over oral mucosa
  • Development of multiple large irregular necrotic ulcers

Other

  • Large hematomas over lower lip
  • Oral infections
  • Palatal ulcerations
  • Mental nerve neuropathy
  • Prolonged postoperative bleeding
  • Osteomyelitis of jaw

Question 4. Iron deficiency anaemia

Answer:

Iron deficiency anaemia

  • It is A chronic, microcytic, hypochromic anacmia that occurs either due to inadequate absorption or excessive loss of iron from the body

Iron Deficiency Anaemia Clinical Features:

  1. Anaemia:
    • Usual symptoms are weakness, fatigue, dyspnoea on exertion, palpitations, pallor of skin, mucous membranes, and sclera.
    • Older patients may develop angina and congestive cardiac failure.
    • Womenmenorrhagia is common symptom.
  2. Epithelial tissue changes:
    • Nails (koilonychia or spoon-shaped nails)
    • Tongue (Atrophic glossitis)
    • Mouth (angular stomatitis)

Iron Deficiency Anaemia  Diagnosis:

  • Serum iron and ferritin are low.
  • Total iron binding capacity is increased Transferrin saturation is below 16%.
  • Stool examination for parasites and occult blood is useful.
  • Endoscopic and radiographic examination of GI tract is needed to detect the source of bleeding.
  • Hematological findings: Examination of peripheral blood picture.
  • Size: Microcytic anisocytotic a Chromicity: Anisochromia is present.
  • Shape: Poikilocytosis often present, pear-shaped tailed variety of RBC, elliptical form common.
  • Reticulocytes: Present, either normal/reduced
  • Osmotic fragility: slightly decreased
  • ESR: Seldom elevated
  • Absolute value: MCV, MCH, and MCEIC are reduced.

Bone marrow findings:

  • Marrow cellularity increased due to erythroid hypoplasia micronormoblast.
  • Marrow ironreduce reticuloendothelial iron stores and absence of siderotic iron granules from developing normoblasts.

Iron Deficiency Anaemia  Management:

  • Iron supplement
  • Ferrous sulphate 300 mg 34 times/day for 6 months only
  • Iron sorbitol 1.5 mg/kg body weight given parentally

Question 5. Aplastic anaemia clinical features

Answer:

Aplastic anaemia

  • Aplastic anemia is characterized by
    • Anaemia
    • Leukopenia
    • Thrombocytopenia
    • Hypocellular bone marrow

Aplastic Anaemia Clinical Features:

  • Anaemia
  • Excessive tendency to bleed
  • Easy bruising
  • Epilaxis
  • Gum bleeding
  • Heavy menstrual flow
  • Petechiae
  • Predisposition to infections

Question 6. Megaloblastic anaemia

Answer:

Megaloblastic anaemia

  • It is macrocytic anaemia with megaloblasts in the bone marrow

Etiology:

  1. Inadequate dietary intake
  2. Malabsorption
    • Intrinsic factor deficiency
      • Pernicious anaemia
      • Gastrectomy
      • Congenital lack of factor
    • Intestinal causes
      • Tropical sprue
      • Ileal resection
      • Crohn’s disease
    • Removal of B12 from the intestines
      • Bacterial proliferation in intestinal blind loop syndrome
      • Fish tape worm infestation
    • Drugs for example, PAS, neomycin

Megaloblastic anaemia Clinical Features:

  • Anemia,
  • Glossitis
  • Neurological manifestations numbness, paraesthesia, weakness, ataxia, diminished reflexes
  • Others mild jaundice, angular stomatitis, purpura, malabsorption, anorexia

Megaloblastic anaemia Management:

  1. Vitamin B12 deficiency
    • Parenteral administration of hydroxocobalamin 1000 microgram twice a week during first week
    • followed by 1000 microgram weekly for 6 weeks
    • Maintenance therapy includes hydroxocobalamin 1000 microgram intramuscular every 3 months for rest of life
  2. folate deficiency
    1. Daily dose of 5 mg of folic acid as initial dose
    2. Dose of 5 mg of folic acid once a week as a maintenance dose

Question 7. Plummer Vinson syndrome

Answer:

Plummer Vinson syndrome

  • It is characterised by dysphagia, iron doccie anaemia, dystrophy of nails and glossits

Plummer Vinson syndrome Clinical Features:

  • Common in middle age females
  • Dysphagia
  • Angular chelitis
  • Spasm in throat
  • Sore mouth
  • A smooth, red, and enlarged tongue
  • Oral mucosa is pale and painful
  • Dry mouth
  • Spoon shaped nails

Plummer Vinson syndrome Diagnosis

  • Biopsy shows:
  • Atrophic epithelium
  • Atrophy of lamina propria and muscles

Plummer Vinson syndrome Management:

  • Correction of anaemia
  • Esophageal dilation

Question 8. Eosinophilia

Answer:

Eosinophilia Clinical features:

  • Dysponea
  • Orthopnoca
  • Wheezing
  • Cough with mucoid expectoration
  • Chest pain

Eosinophilia Management:

  • DiethvlrarbamaZine2 mg/kg three firms a day for 2 weeks
  • Antihistamines are given to treat allergic reations

Question 9. Tropical eosinophilia

Answer:

Tropical eosinophilia

  • It is characterised by the presence of hypereosinophilia, circulating filarial antibodies, microfilaria in tissues
  • Commonly seen in tropical countries like India, and Sri Lanka. Indonesia, Pakistan and Southeast Asia
  • Patient may have lymphadenopathy, splenomegaly,chronic, cough, nocturnal bronchospasm

Tropical eosinophilia Diagnosis:

  • History of prolong stay in endemic area
  • Lack of microfilaria in peripheral blood
  • Peripheral eosinophilia
  • IgE levels of atleast 1000 units/ ml

Tropical eosinophilia Management:

  • Diethylcarbamazine-2 mg/kg three times a day for 2 weeks
  • Antihistamines are given to treat allergic reactions

Question 10. Discuss an approach to bleeding disorders

Answer:

  1. Investigations of disordered vasiular hemostasis
    • Bleeding time
      • It is based on the principle of formation of hemostatic plug following a standard incision on the ulnar aspect of the forearm and the time from incision to when bleeding stops is measured
      • Normal-3-8 minutes
    • Hess capillary resistance test
      • This test is done by tying the sphygmomanometer cuff to the upper arm and raising the pressure in it between diastolic and systolic for 5 minutes
      • After deflation, the number of petechiae appear in the next 5 minutes in 3 camera over the cubital fossa are counted
      • Piesence of more than 20 petechiae is considered a positive test
  2. Investigation of blood coagulation
    • Screening test
      • Whole blood coagulation time
        • The estimation of whole blood coagulation time done by various capillary and tube method
        • Normal value-4-9 minutes
      • Activated partial thromboplastin time (PTTK)
        • This test is used to measure the intrinsic system factors as well as factors common to both intrinsic and extrinsic factors
        • One stage prothrombin time measures the extrinsic system factor 6 as well as factors in the common pathway
    • Special tests
      • Coagulation factor assays
        • These are based on the results of PTTK or prothrombin time tests
      • Quantitative assays
        • Done by immunological and other chemical methods

Question 11. Clinical features and management of acute myeloid leukemia

Answer:

  • Acute myeloid leukemia is a heterogenous disease charaterised by the infiltration of malignant myeloid cells into the blood, bone marrow, and other tissues

Acute Myeloid Leukemia Clinical Features:

  • Anemia-producing pallor, lethargy, dyspnoea
  • Thrombocytopenia
  • Spontaneous bruises
  • Petechiae, bleeding from gums, and other bleeding tendencies
  • Infections
  • Fever
  • Pain and tenderness of bones
  • Lymphadenopathy
  • Splenomegaly
  • Hepatomegaly
  • Leukemic infiltration of the kidney
  • Gum hypertrophy
  • Testicular swelling

Acute Myeloid Leukemia  Management:

  • Regular platelet transfusion
  • Prophylaxis against infections
  • Combination of three drugs is used
    • Cytosine arabinoside
    • Anthracyclines
    • 6-thioguanine
  • Bone marrow transplantation

Question 12. Clinical features and management of chronic myeloid leukemia

Answer:

Chronic Myeloid Leukemia Clinical Features:

  • Onset is usually slow, initial symptoms are often nonspecific.g: weakness, pallor, dyspnoea, and tachycardia.
  • Symptoms due to hypermetabolism such as weight loss, anorexia, night sweats.
  • Splenomegaly is almost always present and is frequently massive. In some patients, it may be associated with acute pain due to splenic infarction.
  • Bleeding tendencies such as bruising, epistaxis, menorrhagia, and heamatomas may occur.
  • Visual disturbance, neurologic manifestations.
  • Juvenile CML is more often associated with lymph node enlargement than splenomegaly.

Chronic Myeloid Leukemia Management:

  • Imatinib oral therapy
  • Allogenic bone marrow transplantation
  • Interferon-alpha
  • Chemotherapy drugs used are busulfan, cyclophosphamide, and hydroxyurea

Question 13. Oral manifestations of hematological disorders transfusion

Answer:

Oral manifestations of hematological disorders transfusion

  • Gingivasevere hemorrhage
  • Soft tissue hematoma formation
  • Jawrecurrent subperiosteal hematoma
  • Tumourlike malformation B Teethhigh caries index
  • Severe periodontal disease
  • Oropharyngeal bleeding
  • Severe bleeding at the injection site

Question 14. Complications of blood transfusion

Answer:

Complications of Blood Transfusion

  1. Transfusion reactions
    • Incompatibility due to
      • Incompatible transfusion
      • Transfusion of hemolysed blood
      • Transfusion of expired blood
    • Pyrexia reactions characterized by
      • Pyrexia
      • Chill
      • Rigor
      • Restlessness
      • Headache
      • Increased pulse rate
      • Nausea and vomiting
    • Allergic reactions
      • Mild tachycardia
      • Urticarial rash
      • Fever
      • Dyspnoea
    • Sensitization to leucocytes and platelets
  2. Transmission of diseases like
    • Hepatitis
    • AIDS
    • Bacterial infections
  3. Reactions caused by massive transfusion
    • Acid base imbalance
    • Hyperkalaemia
    • Citrate toxicity
    • Hypothermia
    • Failure of coagulation
  4. Complication of general intravenous fluid transfusion
    • Congestive cardiac failure
  5. Complication of general intravenous fluid transfusion
    • Thrombophlebitis
    • Air embolism

Question 15. Idiopathic thrombocytopenic purpura investigations and treatment

Answer:

. Idiopathic thrombocytopenic purpura

  • Idiopathic thrombocytopenic purpura is an autoimmune disorder due to antibodies directed against platelet membrane glycoprotein resulting in the premature clearance of these cells by the immune system

Idiopathic Thrombocytopenic Purpura  Investigations:

  • Chronic history of bleeding
  • Bleeding time is prolonged
  • Reduced platelet count
  • Bone marrow shows increased megakaryocytes indicating peripheral destruction of platelets

Idiopathic Thrombocytopenic Purpura  Management:

  • Self-limiting in children
  • Moderate to severe ITP is treated with prednisolone 2 mg/ kg daily orally
  • In adults prednisolone 60 mg dialysis started and then continued for 24 weeks and then slowly withdrawn
  • In severe cases, intravenous immunoglobulin IgG should be given in a dose of 1 g/kg

Diseases Of Blood And Lymphoreticular System Short Answers

Question 1. Sickle cell anaemia

Answer:

Sickle cell anaemia

  • Hb S is abnormal haemoglobin which gets polymerise and distort the cell membrane to form abnormal sickle-shaped cell

Sickle cell anaemia Clinical features

  • Chronic anaemia features
    • Fatigue
    • Lassitude
    • Breathlessness
    • Cardiomegaly
    • Increased susceptibility to infection
    • Hyperplasia of bone marrow producing frontal bossing and malar prominence
    • Mild jaundice
    • Spleenomegaly
    • Poor healing ulcers
  • Other features
    • Pain due to blockage of small or large vessels
    • Large swelling, pain and tenderness of fingers and toes
    • Acute abdominal colic, renal infarction
    • Painful hematuria
    • Aseptic necrosis of head of femur
    • Fever, malaise
    • Microembolisation of pulmonary vessels occurs in late pregnancy

Question 2. Von Willebrand disease

Answer:

Von Willebrand disease

  • It is coagulation disorder

Von Willebrand disease Causes and related features

  • Platelet dysfunction leads to
    • Superficial bruising
    • Epitaxis
    • Menorrhagia
    • GI bleeding
  • Low levels of von Willebrand factor
    • Depending on the level of vWF, 3 types of disease occurs

Von Willebrand disease Diagnosis:

  • Abnormal platelet function
  • Increased bleeding time
  • Normal prothrombin time
  • Decreased factor 8
  • Reduced vWF

Question 3. Causes of pancytopenia

Answer:

Pancytopenia

  • Pancytopenia is a simultaneous presence of anaemia, leucopenia, and thrombocytopenia
  • pancytopenia Causes
    • Aplastic anaemia
    • Paroxysmal nocturnal hemoglobinuria
    • Megaloblastic anaemia
    • Bone marrow infiltration

Question 4. Peripheral smear in iron deficiency anaemia

Answer:

Peripheral smear in iron deficiency anaemia

  • Hematological findings: Examination of peripheral blood picture.
  • Size: Microcytic anisocytosis
  • Chromicity: Anisochromia is present.
  • Shape: Poikilocytosis is often present, pear-shaped tailed variety of RBC, elliptical form common.
  • Reticulocytes: Present, either normal/reduced
  • Osmotic fragility: slightly decreased
  • ESR: Seldom elevated
  • Absolute value: MCV, MCH, and MCHC are reduced.

Question 5. Treatment of iron deficiency anaemia

Answer:

Iron supplement

  • Ferrous sulphate 300 mg 34 times/day for 6 months only
  • Iron sorbitol 1.5 mg/kg body weight given parentally

Question 6. Iron therapy

Answer:

Iron Preparations:

  1. Oral iron preparations
    • It is the preferred route of administration
    • Preparations:
      • Ferrous sulfate 200 mg tab
        • Contains 20% hydrated salt and 32% dried salt
        • It is inexpensive
        • Produces metallic taste in mouth
      • Ferrous gluconate 300 mg tab
        • Contains 12% of iron
        • Causes less gastric irritation
      • Ferrous fumarate 200 mg tab
        • Contains 33% iron
        • It is less water soluble and tasteless
      • Ferrous succinate 100 mg tab, 35% iron
        • Better absorbed and expensive
      • Iron calcium complex 5% iron
        • Better absorbed and expensive
      • Ferric ammonium citrate 45 mg tab
        • Better absorbed and expensive
    • Dose:
      • Total 200 mg given daily in 3 divided doses
      • Prophylactic dose 30 mg daily
    • Indications:
      • Iron deficiency anaemia
    • Adverse Effects:
      • Nausea, vomiting, epigastric pain
      • Heart bum
      • Staining of teeth
      • Metallic taste
      • Constipation
  2. Parenteral iron preparations
    • Intramuscular injection of iron is given deep in the gluteal region using Z technique
    • Intravenous is given slowly over 510 minutes
    • Preparations:
      • Iron dextran
        • It is colloidal solution containing 50 mg elemental iron
        • It is given intravenously and Intramuscularly
      • Iron sorbitol citric acid complex
        • Contains 50 mg elemental iron
        • Can be given only IM
        • If given 4 it quickly saturates transferrin stores
        • Due to it free iron levels in the plasma rises and causes toxicity
    • Dose:
      • It is calculated using formula:
      • Iron requirement ( in mg) = 4.4 * body weight (in kg) * Hb deficit (in g/ dl)
    • Indications:
      • When oral iron is not tolerated
      • Failure of absorption of oral iron
      • Noncompliance
      • In presence of severe deficiency with chronic bleeding
      • Along with erythropoietin
    • Adverse Effects:
      • Pain at the site of injection
      • Pigmentation of skin
      • Sterile abscess
      • Fever
      • Headache
      • Joint pain, flushing, palpitation
      • Chest pain, dyspnoea
      • Anaphylactic reaction

Question 7. Megaloblastic anaemia

Answer:

Megaloblastic anaemia

  • It is macrocytic anaemia with megaloblastosis in the bone marrow

Etiology:

  1. Inadequate dietary intake
  2. Malabsorption
    • Intrinsic factor deficiency
      • Pernicious anaemia
      • Gastrectomy
      • Congenital lack of factor
    • Intestinal causes
      • Tropical sprue
      • Ileal resection
      • Crohn’s disease
    • Removal of B12 from the intestines
      • Bacterial proliferation in intestinal blind loop syndrome
      • Fish tape worm infestation
    • Drugs, for example, PAS, neomycin

Megaloblastic anaemia Clinical Features:

  • Aneamia
  • Glossitis
  • Neurological manifestations numbness, paraesthesia, weakness, ataxia, diminished reflexes.
  • Othersmild jaundice, angular stomatitis, purpura, malabsorption, anorexia

Question 8. Four causes of anaemia

Answer:

Four causes of anaemia

  1. Anaemia due to increased blood loss
    • Acute posthaemorrhagic anaemia
    • Chronic blood loss
  2. Anaemias due to impaired red cell production
    • Cytoplasmic maturation defects
      • Deficient haem synthesis:
        • Iron deficiency anaemia
      • Deficient globin synthesis:
        • Thalassaemic syndromes
    • Nuclear maturation defects
      • Vitamin B12 and/or folic acid deficiency:
      • Megaloblastic anaemia
    • Defect in stem cell proliferation and differentiation
      • Aplastic anaemia
      • Pure red cell aplasia
    • Anaemia of chronic disorders
    • Bone marrow infiltration
    • Congenital anaemia
  3. Anaemias due to increased red cell destruction (Haemolytic anaemias).
    • Extrinsic (Extracorpuscular) red cell abnormalities
    • Intrinsic (Intracorpuscular) red cell abnormalities

Question 9. Causes of iron deficiency anaemia

Answer:

Causes of iron deficiency anaemia

  • Inadequate intake of iron in diet
  • Malabsorption of iron due to diarrhea
  • Increased requirement in growing child and in pregnanacy
  • Increased loss of iron due to injury, epitaxis, and peptic ulcer
  • Gastrotomy

Question 10. Hemolytic anaemia

Answer:

Hemolytic anaemia Definition:

  • It is an abnormal exessive destruction of red cells that overwhelms the compensatory capacity of the bone marrow

Etiology:

  1. Congenital
    • Abnormalities of red cell membrane
    • Disorders of haemoglobin
    • Red cell enzyme defects
  2. Acquired
    • Immune defects
    • Nonimmune defects

Question 11. Two drugs used in eosinophilia

Answer:

Two drugs used in eosinophilia

  • Drugs used in eosinophilia are;
  1. Prednisolone
  2. Diethylcarbamazine

Question 12. Classification of leukemia

Answer:

leukemia

  1. Based on cell types predominantly involved.
    • Myeloid
    • Lymphoid.
  2. Based on natural history of disease:
    • Acute
    • Chronic.

WHO classification of myeloid neoplasm:

  1. Myeloproliferative Diseases:
    • Chronic myeloid leukaemia (CML), {Ph chromosome t(9;22), BCR/ABLpositive}
    • Chronic neutrophilic leukaemia
    • Chronic eosinophilic leukaemia/ hypereosinophilic syndrome
    • Chronic idiopathic myelofibrosis
    • Polycythaemia vera (PV)
    • Essential thrombocythaemia (ET)
    • Chronic myeloproliferative disease, unclassifiable
  2. Myelodysplastic/Myeloproliferative Diseases:
    • Chronic myelomonocytic leukaemia (CMML)
  3. Myelodysplastic Syndrome (MDS):
    • Refractory anaemia (RA)
    • Refractory anaemia with ring sideroblasts (RARS)
    • Refractory cytopenia with multilineage dysplasia (RCMD)
    • RCMD with ringed sideroblasts (RCMD-RS)
    • Refractory anaemia with excess blasts (RAEB-1)
    • RAEB-2
    • Myelodysplastic syndrome unclassified (MDS-U)
    • MDS with isolated del 5q
  4. Acute Myeloid Leukaemia (AML):
    • AML with recurrent cytogenetic abnormalities
      • AML with t(8;21)
      • AML with abnormal bone marrow eosinophils
      • Acute promyelocytic leukaemia (t(15;17)
      • AML with 11q23 abnormalities (MLL)
    • AML with multilineage dysplasia
      • With prior MDS
      • Without prior MDS
    • AML and MDS, therapy-related
      • Alkylating agent related
      • Topoisomerase type 2 inhibitor-related
      • Other types
    • AML, not otherwise categorised
      • AML, minimally differentiated
      • AML without maturation
      • AML with maturation
      • Acute myelomonocytic leukaemia (AMML)
      • Acute monoblastic and monocytic leukaemia
      • Acute erythroid leukaemia
      • Acute megakaryocytic leukaemia
      • Acute basophilic leukaemia
      • Acute panmyelosis with myelofibrosis
      • Myeloid sarcoma
  5. Acute Biphenotypic Leukaemia

Question 13.Chronic myeloid leukemia

Answer:

Chronic myeloid leukemia Clinical Features:

  • Onset is usually slow, initial symptoms are often nonspecific.g: weakness, pallor, dyspnoea, and tachycardia.
  • Symptoms due to hypermetabolism such as weight loss, anorexia, and night sweats.
  • Splenomegaly is almost always present and is frequently massive. In some patients, it may be associated with acute pain due to splenic infarction.
  • Bleeding tendencies such as bruising, epistaxis, menorrhagia, and heamalomas may occur.
  • Visual disturbance, neurologic manifestations.
  • Juvenile CML is more often associated with lymph node enlargement than splenomegaly.

Question 14. Agranulocytosis

Answer:

Agranulocytosis

  • The term agranulocytosis is used to describe a stale of severe neutropenia.
  • A reduction in the number of granulocytes in blood is known as neutropenia.

Agranulocytosis Causes:

  • Neutropenia can be caused by following reasons.
    1. Drug induced: Anti-cancer, antibiotics, anticonvulsants, antithyroid drugs
    2. Haematological disease: Aplastic anaemia, acute leukaemia etc.
    3. Infections: Malaria, TB, typhoid,
    4. Autoimmune: Systemic lupus erythematosis
    5. Congenital: Cyclic neutropenia.

Agranulocytosis Clinical Features:

  • Initally patient develops malaise, chills, and fever, with subsequently marked weakness and fatiguability.
  • Massive growth of microorganisms due to inability to produce leukocyte response.
  • Infections are usually present as ulcerating, necrotizing lesions of gingiva, the floor of the mouth, buccal mucosa, and other sites within oral cavity known as agranulocytic angina.
  • Lymphadenopathy and hepatosplenomegaly may be present.

Agranulocytosis Treatment:

  • Patients with neutropenia and fever must be sent to the hospital.
  • In severe infections, neutrophil transfusion must be done.
  • Broad-spectrum antibiotics and antifungal drugs are to be given.

Question 15. Management of acute leukemia

Answer:

Management of acute leukemia

  • Regular platelet transfusion
  • Prophylaxis against infections
  • Combination of three drugs is used
    • Cytosine arabinosidc
    • Anthracyclines
    • 6thioguanine
  • Bone marrow transplantation

Question 16. Purpura

Answer:

Purpura Types:

  1. Nonthrombocytopenic purpura
    • It is due to defect of capillaries
  2. Thrombocytopenic purpura
    • It is due to decreased number of platelets

Purpura Clinical Features:

  • Antiplatelet globulin or antibodies to platelets in blood are present
  • Spleen is not palpable
  • Severe and profuse gingival bleeding
  • Platelet count is less than 60,000 per mm2
  • Increased bleeding time
  • Cessation of bleeding

Purpura Treatment:

  • Splenectomy

Question 17. Thrombotic thrombocytopenic purpura

Answer:

Thrombotic thrombocytopenic purpura

  • It is lethal disorder of vascular endothelial damage

Thrombotic thrombocytopenic purpura Cause:

  • Deficiency of a protease called ADAMTS 13

Thrombotic thrombocytopenic purpura Clinical Features

  • Florid purpura
  • Fibrin mierolhrombi
  • Thrombocytopenia
  • Macroangiopalhic hemolytic anaemia
  • Fever
  • Renal failure
  • Fluctuating levels of consciousness
  • Focal neurological signs

Thrombotic thrombocytopenic purpura Treatment:

  • Exchange transfusion
  • Plasmapheresis combined with infusion of fresh frozen plasma

Question 18. Idiopathic thrombocytopenic purpura

Answer:

Idiopathic thrombocytopenic purpura

  • It is characterized by Immunologic destruction of platelet and normal or increased megakaryocytes in the bone marrow

Idiopathic thrombocytopenic purpura Types:

  • Acute ITP
  • Chronic ITP

Idiopathic thrombocytopenic purpura Clinical Features:

  • Usual manifestations are petechial haemorrhage, purpura, easy bruising, epistaxis, mucosal bleeding such as menorrhagia in women, nasal bleeding, bleeding from gums, haematuria.
  • Intracranial haemorrhage is rare.
  • Splenomegaly, hepatomegaly may also occur.

Question 19. Importance of hemophilia to dental surgeon

Answer:

Importance of hemophilia to dental surgeon

  • It is essential to prevent accidental damage to the oral mucosa when carrying out any procedure in the mouth
  • Blood loss can be controlled locally with direct pressure or periodontal dressings with or without topical anlifibrinolytie agents
  • Patients with bleeding disorders can be given dentures as long as they are comfortable
  • Fixed and removable orthodontic appliances may be used along with regular preventive advice and hygiene therapy
  • Endodontic treatment is generally low risk for patients with bleeding disorders
  • Aspirin should not be used

Question 20.Burkitt’s lymphoma

Answer:

Burkitt’s lymphoma

  • Burkitt’s lymphoma is a rare type of nonHodgkin’s lymphoma (NHL).
  • Epsteinbarr virus (EBV) and HIV are associated with the development of Burkitt’s lymphoma.
  • This is the most rapidly progressive tumour first described in African children.
  • Most patients present with lymphadenopathy and abdominal mass.
  • It has a tendency to metastasize to the CNS.
  • Treatment should be initiated promptly with intensive chemotherapy. Prophylactic chemotheiapy is also given. 70-80% patients may be cured.

Question 21. Drugs used in Hodgkin’s lymphoma

Answer:

Drugs used in Hodgkin’s lymphoma are

  1. Vinblastin sulfate
  2. Bleomycin
  3. Mustargen
  4. Chlorambucil
  5. Cyclophosphamide

Question 22. Hyperspleenism

Answer:

Hyperspleenism

  • It is defined as a clinical condition in which spleen removes excessive quantites of erythrocytes, granulocytes, and platelets from the circulation

Hyperspleenism Clinical Features:

  • Cirrhosis of liver with portal hypertension
  • Accelerated destruction of one or more elements of blood
  • Pancytopenia
  • Infections
  • Easy bruising
  • Excessive bleeding tendencies

Hyperspleenism Treatment:

  • Treatment of underlying disorder
  • Spleenectomy
  • Supportive antibiotics
  • Blood transfusion

Question 23. Spleenomegaly

Answer:

Spleenomegaly

  • Enlargement of spleen is called spleenomegaly

Spleenomegaly Causes:

  1. Infective disorders
    • Bacterial
      • Endocarditis
      • Tuberculosis
      • Septicaemia
      • Salmonella
    • Viral
      • Hepatitis
      • AIDS
      • Infectious mononucleosis
    • Protozoal
      • Malaria
      • Leishmaniasis
    • Spirochaetal
      • Syphilis
    • Fungal
      • Histoplasmosis
  2. Inflammatory disorders
    • Rheumatoid arthritis
    • SLE
    • Sarcoidosis
  3. Congestive splenomegaly
    • Hepatic vein thrombosis
    • Chronic congestive heart failure
    • Pericardial effusion
  4. Diseases associated with hemolysis
    • Spherocytosis
    • Sickle cell disease
  5. Infiltrative disease of spleen
  6. Miscellaneous
    • Iron deficiency anaemia
    • Idiopathic
    • Sarcoidosis

Question 24. Causes of massive spleenomegaly

Answer:

Causes of massive spleenomegaly

  • Hemolytic anaemia thalassaemia
  • Infectionsmalaria, kalaazar
  • Collagen vascular disorder rheumatoid arthritis
  • Congestionportal hypertension
  • Malignant infiltration leukemia

Question 25. Bone marrow aspiration

Answer:

Bone marrow aspiration

  • Bone marrow aspiration is used for bone marrow examination

Bone marrow aspiration Uses:

  • To study cell markers
  • Karyotyping
  • Accurate diagnosis
  • Assessment of malignant diseases
  • Assessment of cellularity
  • Details of developing blood cells
  • Detect ratio between erythroid and myeloid cells
  • Assess iron stores

Bone marrow aspiration Indications:

  • Infiltrative disorders
  • Parasitic diseases
  • Cytopenic disorders
  • Infective disorders

Question 26. ESR

Answer:

ESR

If a sample of blood with an anticoagulant is allowed to stand in a vertical tube, the RBC settles down due to gravity as compared to plasma with a clear supernatant layer of plasma. The rate at which the cells settle down is called ESR.

Method of Estimation of ESR:

There are two standard methods as follows:

  1. Wintrobe’s and Landsberg’s method: ESR is measured in undiluted blood in a hematocrit tube.
  2. Westergren’s method: ESR is measured in venous blood diluted accurately with 31.3 g/L trisodium citratein the proportion of 1:4 (1 volume of 3.8% sodium citrate and 4 volume of blood).

The conditions were ESR is markedly raised are as follows:

  1. Infective: Tuberculosis, kala-azar, in most of the chronic infections.
  2. Inflammation: Rheumatoid arthritis, rheumatic fever, other connective tissue disorders.
  3. Neoplastic: Multiple myeloma, lymphoma, paraproteinaemia.
  4. Miscellaneous: Aplastic anaemia, autoimmune disorders, mixed connective tissue disorders.

Question 27. Three causes of neutropenia

Answer:

Three causes of neutropenia

Neutropenia can be caused by following reasons.

  1. Drug-induced: Anti-cancer, antibiotics, anticonvulsants, antithyroid drugs
  2. Haematological disease: Aplastic anaemia, acute leukaemia etc.
  3. Infections: Malaria, TB, typhoid.
  4. Autoimmune: Systemic lupus erythematosis
  5. Congenital: Cyclic neutropenia.

Question 28. Folic acid deficiency

Answer:

Folic acid deficiency

  • Folic acid deficiency leads to:
  • Megaloblastic anaemia
  • Glossitis
  • Diarrhoea
  • Weakness

Question 29. Blood groups

Answer:

Blood groups Classification:

  • It is based on the presence or absence of a specific agglutinogen or antigen on the surface of the red cell membrane
  • Important blood groups are:
  1. ABO system
    • It is based on the presence or absence of antigen A and antigen B
  2. Rh blood group
    • Rh fator is an antigen present in RBC

Blood groups Uses:

  • In blood transfusion
  • For matching tissues in organ transplantation
  • Investing cases of paternity disputes
  • Helpful in emergency conditions
  • In pregnancy
  • For research purposes
  • Anthropological purposes

Question 30. Hematological and bone marrow findings of multiple myeloma

Answer:

Hematological and bone marrow findings of multiple myeloma

  1. Blood examination shows
    • Anaemia
    • Neutropenia
    • Thrombocytopenia
    • Raised ESR
    • Reversal of albumin globulin ratio
    • Presence of BenceJones proteins
  2. Bone marrow examination
    • Exhibits presence of at least 10% atypical plasma cells in the total marrow cell population

Question 31. Clotting time

Answer:

Clotting time

  • It is the time interval from oozing of blood after a cut or injury till arrest of bleeding

Normal Duration:

  • 3-8 minutes

Prolonged In:

  • Hemophilia

Question 32. Prothrombin time

Answer:

Prothrombin time

Prothrombin time measures the extrinsic system factor 7 as well as factors in the common pathway

  • In it, tissue thromboplastin and calcium are added to the test

Normal Time:

  • 10-14 seconds

Prolonged in:

  • Administration of oral Anticoagulants
  • Liver disease
  • Vitamin K deficiency
  • Disseminated intravascular coagulation

Question 33. DIC

Answer:

DIC

Disseminated intravascular coagulation is a complex thrombo-hemorrhagic disorder occurring as a secondary complication in some systemic diseases

Etiopathogenesis:

  • Pathogenesis of DIC includes following events
  1. Activation of coagulation
    • Etiological factors like massive tissue injury, presence of infections, endothelial damage causes activation of coagulation by release of tissue factor
  2. Thrombotic phase
    • Endothelial damage from various thrombogenic stimuli causes:
      • Generalized platelet aggregation
      • Platelet adhesion
      • Deposition of small thrombi and emboli throughout microvasculature
  3. Consumption phase
    • Consumption of coagulation factors and platelets occurs
  4. Secondary fibrinolysis
    • Fibrinolytic system is secondary activated
    • This causes the breakdown of fibrin resulting in formation of FDPs in circulation

Question 34. Folic acid

Answer:

Folic acid

Folic acid is important in one-carbon metabolism

Folic acid Sources:

  • Green vegetables, liver, yeast, egg, milk, and some fruits

Folic acid Functions:

  • The Coenzyme of it, tetrahydrofolate (THF), serves as an acceptor or donor of one carbon units
  • It is involved in the synthesis of important compounds like
  • PurinesIncorporated into DNA and RNA
  • Pyrimidine nucleotide-deoxy thymidylic acid involved in the synthesis of DNA
  • Aminoacids-Glycine, serine, ethaloamine, and choline
  • N-FormylmethionineInitiator of protein biosynthesis

Folic acid Deficiency Manifestations:

  • Megaloblastic anaemia
  • Glossitis
  • Diarrhoea
  • Weakness

VIVA VOCE

  1. Chlorambucil is drug of choice of chronic lym, phoid leukemia
  2. Busulfan, hydroxycarbamide are drug of choice in chronic myeloid leukemia
  3. Hemophilia is transmitted as X-linked recessive trait
  4. Von Willebrand’s disease is transmitted as autosomal dominant trait

Respiratory Diseases Short Essays

Diseases Of The Respiratory System Short Essays

Question 1. Complications of pneumonia

Answer:

Complications of pneumonia

Diseases Of The Respiratory System Complications Of Pneumonia

Question 2. Treatment of pulmonary tuberculosis

Answer:

Pulmonary Tuberculosis Principles

  • To administer multiple drugs
  • To add atleast 2 new drugs in case of failure
  • To provide safest and most effective therapy shortest period of time
  • To ensure compliance to treatment

Pulmonary Tuberculosis Drugs

  • Anti-tubercular drugs that are used for treating it are as follows:
  • Four or three drugs are choosen from the drugs meant for first-line treatment for new cases
  • Response to treatment is assessed by
    • Gain in body weight
    • Improved appetite
    • Improvement in general health – Fall in ESR
    • Conversion of sputum from positive to negative
  • Primary or secondary resistance to drugs may develop when patient consume the drugs in irregular dose or take the drugs irregularly
  • In such cases, second-line drugs are used
  • Drugs:
    • PAS (Paraminosalicyclic acid) – 5 g BID orally
    • Ethionamide – 0.75 -1 g/day orally
    • Capromycin – 0.75-1 g IM daily
    • Cycloserine – 0.75-1 g/ day orally
    • Ciprofloxacin – 500-750 mg BID orally
    • Ofloxacin – 400 mg BID

Diseases Of The Respiratory System Treatment Of Pulmonary Tuberculosis

Question 3. Four causes of clubbing

Answer:

Clubbing:

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

Clubbing Causes:

  1. Disorders of heart
    • Cyanotic heart disease
    • Subacute bacterial endocarditis
  2. Disorders of lung
    • Suppuration of lung
      • Bronchiectasis
      • Lung abscess
      • Suppurative pneumonia
    • Tumours of lung
      • Mesothelioma
      • Primary lung cancer
      • Metastatic lung cancer
  3. Disorder of GI tract and liver
    • Inflammatory bowel disease
      • Regional ileitis
      • Ulcerative colitis
      • Malabsorption syndrome
    • Cirrhosis of liver
    • Malignancy of liver
  4. Hereditary or idiopathic

Read And Learn More: General Medicine Question and Answers

Question 4. Mantouxtest
(or)
Tuberculin test

Answer:

Mantouxtest

  • It is routinely used method for tuberculin testing

Method:

  • 0.1 ml of purified protein derivative, PPD containing 5 TU( tuberculin unit) is injected intradermally into flexor ascept of forearm
  • It is given between layers of the skin
  • The site is examined after 48-72 hours for induration

Result:

Diseases Of The Respiratory System Mantoux Test Or Tubercullin Test Result

Significance:

Diseases Of The Respiratory System Mantoux Test Or Tubercullin Test Significance

Question 5. Lung abscess

Answer:

Lung abscess

  • It is collection of purulent material in a localised necrotic area of lung parenchyma

Etiopathogenesis:

  1. Infection without obstruction
    • Aspiration of nasopharyngeal contents
    • Involvement of various organisms like staphylococcus, Kleibsella, gram negative and anaerobic organisms
    • Formation of abscess
    • Metastatic spread of infection
  2. Obstruction with or without infection
    • Bronchus obstruction due to tumor, foreign body, lymph node
    • Bronchial collapse
    • Abscess formation

Lung Abscess Clinical Features:

  • High-grade fever with chills and rigors
  • Pleuritic chest pain
  • Dry cough
  • Presence of copious purulent discharge
  • Haemoptysis
  • Weight loss, anorexia
  • Empysema

Question 6. Dyspnoea

Answer:

Definition:

  • It is abnormal and uncomfortable breathing which makes the patient aware of it

Etiology:

  1. Cardiac causes
    • Cyanotic congenital heart disease
    • Left ventricular failure
    • Systemic hypertension
    • Chronic thromboembolism
  2. Pulmonary
    • Obstructive diseases
      • Bronchial asthma
      • Bronchiectasis
      • COPD
    • Parenchymal lung diseases
      • Acute pneumonia
    • Pulmonary vascular diseases
      • Thromboembolism
    • Respiratory muscle diseases
      • Severe kyphoscoliosis
  3. Cardiopulmonary’causes
    • Corpulmonale
  4. Others
    • Metabolic acidosis
    • Carbon monoxide poisoning
    • Severe anaemia

Dyspnoea Types:

Diseases Of The Respiratory System Dyspnoea Types

Question 7. Bronchodilators

Answer:

Bronchodilators:

  • Various bronchodilators are
  1. Sympathomimetics
    • Adrenaline
    • Ephedrine
    • lsoprenaline
    • Salbutamol
    • Terbutaline
  2. Methylxanthines
    • Theophylline
    • Aminophylline
  3. Anticholinergics
    • Atropine
    • Methonitrate
    • Ipratropium bromide

Bronchodilators Actions:

  • Improves effectiveness of cough in clearing secretions by increasing surface velocity of airflow during cough

Question 8. Clinical signs of emphysema

Answer:

Clinical signs of emphysema

  • Emphysema means inflation or distension with air

EmphysemaTypes:

Diseases Of The Respiratory System Clinical Sign Of Emphysema

Question 10. Haematemesis- causes and investigations

Answer:

Haematemesis Definition:

  • It is vomiting of blood

Haematemesis Causes:

  • Prolonged and vigorous retching
  • Irritation or erosion of the lining of the esophagus or stomach
  • Bleeding ulcer located in the stomach, duodenum, or oesophagus
  • Vomiting of ingested blood
  • Vascular malfunctions of the gastrointestinal tract
  • Tumours of the stomach or oesophagus
  • Radiation poisoning
  • Gastroenteritis
  • Gastritis
  • Peptic ulcer

Haematemesis Management:

  1. Minimal blood loss
    • Administration of proton pump inhibitors like omeprazole
    • Blood transfusion
  2. Significant blood loss
    • Resuscitation
    • Fluid and/or blood administration
    • Use of a cuffed endotracheal tube

Question 11. Aspiration pneumonia

Answer:

  • It is the consolidation of the lung in which there is the continued destruction of parenchyma by the inflammatory cells leading to the formation of microabscesses

Aspiration Pneumonia Clinical Features:

  • High intermittent fever
  • Cough
  • Dyspnoea
  • Tachycardia
  • Restlessness
  • Perspiration
  • Weight loss
  • Digital clubbing

Aspiration Pneumonia Compiicatons:

  • Empyema
  • Bronchiectasis
  • Amyloidosis
  • Pulmonary fibrosis
  • Septicaemia

Aspiration Pneumonia Treatment:

  • Oral amoxicillin 500 mg 8 hourly or
  • Cotrimoxazole 9960 mg 12 hourly or
  • Oral metronidazole 400 mg 8 hourly
  • Analgesic for pleuritic pain
  • Physiotherapy
  • Postural drainage for lung abscess

Respiratory Diseases The Breakdown Of Number Of Problems

Question 12. BCG vaccination

Answer:

BCG vaccination

  • BCG vaccine was prepared by Calmette and Guerin
  • It is a live attenuated and freeze-dried vaccine

BCG vaccination Dose and Administration:

  • It is available as a fresh liquid vaccine or in the form of freeze-dried vaccine
  • It is given intradermally in a dose of 0.1 ml soon after birth

BCG vaccination Immune Response:

  • Induces a self-limited infection with multiplication and dissemination of the bacillus in different organs and production of small tubercles
  • It gives rise to delayed hypersensitivity

BCG vaccination Complications:

  • Local abscess, indolent ulcer, keloid, confluent lesion, lupoid lesion
  • Regional enlargement and suppuration of draining lymph nodes
  • Systemic fever, mediastinal adenitis
  • Erythema nodosum

BCG vaccination Contraindications:

  • In patients with AIDS, eczema, pertussis, measles, and patient on steroids

Role of BCG:

  • Makes the disease milder
  • Prevents serious forms of disease

Disturbances In Water Electrolyte And Acid Base Balance Short Essays

Disturbances In Water Electrolyte And Acid Base Balance Important Notes

  1. Metabolic acidosis and alkalosisDisturbances In Water Electrolyte And Acid Base Balance Metabolic Acidosis And Alkalosis
  2. Dehydration
    • It is the loss of water from the body
    • Clinical features
      • Thirst
      • Dry mouth
      • Dizziness
      • Dysphagia
      • Muscular weakness
      • Oliguria
      • Mental confusion
  3. Hypokalaemia
    • Depletion of potassium from the body
    • Clinical features
      • Generalized muscular weakness
      • Depression of tendon reflexes
      • Confusion
      • Coma
      • Paraesthesia
      • Muscle stiffness
      • Polyuria
      • Nocturia
  4. Hyperkalaemia
    • A marked increase in potassium content
    • Clinical features
      • Cardiac arrest
      • Irregular pulse
      • Flaccid paralysis
      • Abdominal distension
  5. Hyponatraemia
    • It is the loss of sodium from the body
    • Clinical features
      • Lassitude
      • Hypotension
      • Tachycardia
      • Reduced skin elasticity
      • Apathy
      • Weakness
      • Coma
      • Oliguria

Disturbances In Water Electrolyte And Acid Base Balance Short Essays

Question 1. Dehydration

Answer:

Dehydration

  • Dehydration is the primary water depletion

Aetiology:

  • Decreased intake of water
  • Increased loss from the skin
  • Increased respiratory loss
  • Increased loss in urine

Clinical Features:

  • Marked thirst
  • Muscle weakness
  • Dry mouth
  • Mental confusion
  • Coma
  • Intracranial haemorrhage
  • Tachycardia

Investigations:

  • Increased blood urea level
  • Raised plasma sodium
  • Urine specific gravity of more than 1.010
  • Polyuria

Treatment:

  • Administration of isotonic saline

Question 2. Hypokalaemia

Answer:

Hypokalaemia

  • A decrease in the concentration of serum potassium is called hypokalaemia

Causes:

  • Overactivity of the adrenal cortex
  • Prolonged cortisone therapy
  • Intravenous administration of potassium-free fluids
  • Treatment of diabetic coma with insulin
  • Prolonged diarrhoea and vomiting

Read And Learn More: General Medicine Question and Answers

Symptoms:

  • Irritability
  • Muscular weakness
  • Tachycardia
  • Cardiomegaly
  • Cardiac arrest

ECG Changes:

  • Flattening of waves
  • Inverted T wave

Question 3. Respiratory alkalosis

Answer:

Respiratory alkalosis

  • Excessive loss of carbon dioxide leads to respiratory alkalosis

Aetiology:

  • Hysterical over breathing
  • Lobar pneumonia
  • Pulmonary embolism
  • Meningitis
  • Salicylate poisoning
  • Hepatic failure

Features:

  • Fall in partial pressure of carbon dioxide and hydrogen ion concentration
  • Decreased plasma bicarbonate level
  • Paraesthesia
  • Numbness
  • Tingling sensation

Treatment:

  • Elimination of underlying disorder
  • Sedation.

Disturbances In Water Electrolyte And Acid Base Balance Nervous System

Question 4. Hyperkalaemia

Answer:

Hyperkalaemia

  • An increase in the concentration of serum potassium is called hyperkalaemia

Causes:

  • Impaired excretion
  • Excessive intake
  • Tissue breakdown
  • The shift of potassium ions out of the cell

Clinical Features:

  • Cardiac arrhythmia
  • Muscular weakness
  • Respiratory depression

Investigations:

  • ECG Changes:
  • Tall T waves
  • Prolongation of PR interval
  • Reduced height of P wave
  • Prolongation of QRS complex

Treatment:

  • Elimination of the underlying cause
  • 10 ml of 10% calcium gluconate solution is given intravenously slowly over 5-10 min
  • Intravenous administration of glucose along with insulin
  • Intravenous administration of 50-100 ml of 8.4% sodium bicarbonate
  • Nebulization of beta-agonists

Disturbances In Water Electrolyte And Acid Base Balance Short Answers

Question 1. Hyponatraemia

Answer:

Hyponatraemia

  • It indicates the dilution of body fluids by excess water relative to total solute

Aetiology:

  • Increased ECF volume- congestive cardiac failure, nephrotic syndrome, cirrhosis of the liver
  • Reduced ECF volume- sweating, vomiting, diarrhoea
  • Hyperglycaemia
  • Mannitol administration

Clinical Features:

  • Muscle cramps
  • Weakness
  • Fatigue
  • Mental confusion
  • Disorientation
  • Coma
  • Convulsions

Treatment:

  • Administration of loop diuretics and hypertonic saline

Question 2. Metabolic acidosis

Answer:

Metabolic acidosis

  • It is a reduction in bicarbonate concentration which leads to a fall in blood pH

Metabolic acidosis Causes:

  • Diabetes mellitus
  • Renal failure
  • Lactic acidosis
  • Severe diarrhoea
  • Renal tubular acidosis

Metabolic acidosis Treatment:

  • Hyperventilation of lungs
  • This decreases the partial pressure of carbon dioxide

Question 3. Oral rehydration

Answer:

Oral rehydration

  • Oral rehydration solution is used in patients with diarrhoea to replenish the lost water

Oral rehydration Composition:

  • NaCl -3.5 g
  • KCl -1.5 g
  • Trisodium citrate -2.9 g
  • Glucose -20 2
  • Water -1 litre

Oral rehydration Uses:

  • To replace fluids and salts lost from the body during diarrhoea
  • To restore and maintain hydration
  • Maintain electrolyte and pH balance
  • Maintain hydration in patients postsurgically after burns, trauma, and heat stroke

VIVA VOCE

Oral rehydration salts are – sodium chloride, bicarbonate, and glucose

Diseases Of Blood And Lymphoreticular System Long Essays

Diseases Of Blood And Lymphoreticular System Long Essays

Question 1. Classify anemia and its diagnostic approach. 

Answer:

Anaemia  Classification

  1. Pathophysiologic:
    • Anaemia due to increased blood loss
      • Acute posthaemorrhagic anaemia
      • Chronic blood loss
    • Anemias due to impaired red cell production
      • Cytoplasmic maturation defects
        • Deficient haem synthesis: Iron deficiency anemia
        • Deficient globin synthesis: Thalassaemic syndromes
      • Nuclear maturation defects
        • Vitamin B12 and/or folic acid deficiency: Megaloblastic anemia
      • Defects in stem cell proliferation and differentiation
        • Aplastic anemia
        • Pure red cell aplasia
      • Anemia of chronic disorders
      • Bone marrow infiltration
      • Congenital anaemia
    • Anemias due to increased red cell destruction (Haemolytic anemias).
      • Extrinsic (Extracorpuscular) red cell abnormalities
      • Intrinsic (Intracorpuscular) red cell abnormalities
  2. Morphologic:
    • Microcytic, hypochromic
    • Normocytic, normochromic
    • Macrocytic, normochromic
  3. Diagnosis:
    • Laboratory diagnosis of anemia includes
      • Peripheral blood smear
        • It shows
          • Variations in the size of RBCs-microcytic or macrocytic
          • Variations in the shape of RBCs poikilocytosis
          • Spherocytosisspindle shaped RBCs
          • Nucleated RBCs
          • Inadequate hemoglobin formation
          • Presence of HowellJolly bodies
          • Irregularly contracted red cells
    • Hemoglobin content
      • Hemoglobin content decreases in anemia
    • Red cell indices are used like MCV, MCH, MCHC
    • ESR estimation
    • Bone marrow aspiration
    • Leucocyte and platelet count
    • Reticulocyte count

Question 2. Describe the etiological factors, clinical features, and management of iron deficiency anemia,
(or)
Outline the causes of iron deficiency anemia and how to manage such a case
(or)
Classify anemia. Describe clinical features, diagnosis, and management of iron deficiency anemia
(or)
Enumerate causes of iron deficiency anemia. Describe its clinical features and findings in the peripheral blood smear of this condition and treatment

Answer:

Iron Deficiency Anaemia:

  • It is a chronic, microcytic, hypochromic anemia that occurs either due to inadequate absorption or excessive loss of iron from the body

Iron Deficiency Anaemia Causes:

  • Inadequate intake of iron in the diet
  • Malabsorption of iron due to diarrhea
  • Increased requirements in a growing child and pregnancy
  • Increased loss of iron due to injury, epistaxis, and peptic ulcer
  • Gastrotomy

Iron Deficiency Anaemia Clinical Features:

Diseases Of Blood And Lymphoreticular System Iron Deficiency Anaemia Diagnosis

Iron Deficiency Anaemia Diagnosis:

  • Serum iron and ferritin are low.
  • Total iron binding capacity is increased n Transferrin saturation is below 16%.
  • Stool examination for parasites and occult blood is useful.
  • Endoscopic and radiographic examination of the GI tract is needed to detect the source of bleeding.
  • Hematological findings: Examination of peripheral blood picture.
  • Size: Microcytic anisocytosis
  • Chromicity: Anisochromia is present.
  • Shape: Poikilocytosis is often present, a pear-shaped tailed variety of RBC, elliptical form common.
  • Reticulocytes: Present, either normal/reduced
  • Osmotic fragility: slightly decreased
  • ESR: Seldom elevated
  • Absolute value: MCV, MCH, and MCHC are reduced.

Read And Learn More: General Medicine Question and Answers

Bone Marrow Findings:

  • Marrow cellularity increased due to erythroid hypoplasia micronormoblast.
  • Marrow iron reduces reticuloendothelial iron stores and the absence of siderotic iron granules from developing normoblasts.

Bone Marrow Findings Management:

  • Iron supplement
  • Ferrous sulfate 300 mg 34 times/day for 6 months only
  • Iron sorbitol 1.5 mg/kg body weight given parentally

Question 3. Describe etiological factors, clinical features, and management of megaloblastic anemia

Answer:

Megaloblastic Anaemia:

  • It is macrocytic anemia with megaloblasts in the bone marrow

Etiology:

  1. Inadequate dietary intake
  2. Malabsorption
    • Intrinsic factor deficiency
      • Pernicious anemia
      • Gastrectomy
      • Congenital lack of factor
    • Intestinal causes
      • Tropical sprue
      • Ileal resection
      • Crohn’s disease
    • Removal of B12 from the intestines
      • Bacterial proliferation in intestinal blind loop syndrome
      • Fish tapeworm infestation
    • Drugs, for example, PAS, neomycin

Megaloblastic Anaemia Clinical Features:

  • Anemia,
  • Glossitis,
  • Neurological manifestations numbness, paraesthesia, weakness, ataxia, and diminished reflexes.
  • Others mild jaundice, angular stomatitis, purpura, malabsorption, and anorexia.

Megaloblastic Anaemia Diagnosis:

  1. Blood picture:
    • Hemoglobin concentration falls.
    • MCV and MCH increases
    • MCHC decreases/remains normal.
    • Reticulocyte count is low
    • Red blood cell blood smear demonstrates anisocytosis, poikilocytes, and the presence of macroovalocytes
    • Leucocytes’ total WBC count is less
    • Thrombocytes giant platelets are present.
  2. Bone marrow findings:
    • Marrow cellularity hypercellular bone marrow with decreased myeloid: erythroid ratio.
    • Erythropoiesis erythroid hyperplasia is due to characteristic megaloblastic erythropoiesis.
    • Megaloblasts are abnormal, large, nucleated erythroid precursors, having nuclear-cytoplasmic asynchrony. Nuclei are large, having fine reticular and open chromatin,
    • Abnormal mitosis may be seen in megaloblasts.
    • Marrow iron increases in the number and size of the iron granules in erythroid precursors. Iron in reticulum cells is increased.

Megaloblastic Anaemia Management:

  1. Vitamin B12 deficiency
    • Parenteral administration of hydroxocobalamin 1000 microgram twice a week during the first week
    • Followed by 1000 micrograms weekly for 6 weeks
    • Maintenance therapy includes hydroxocobalamin 1000 microgram intramuscular every 3 months for the rest of life
  2. Folate deficiency
    • A daily dose of 5 mg of folic acid as an initial dose
    • A dose of 5 mg of folic acid once a week as a maintenance dose

Question 4. Describe the differential diagnosis of megaloblastic anemia. Add a note on the treatment of pernicious anemia

Answer:

Differential Diagnosis of Megaloblastic Anaemia:

  1. Iron deficiency anemia
    • Clinical Features:
      • Anaemia:
        • Usual symptoms are weakness, fatigue, dyspnoea on exertion, palpitations, pallor of skin, mucous membranes, and sclera.
        • Older patients may develop angina and congestive cardiac failure.
        • Womenmenorrhagia is a common symptom.
      • Epithelial tissue changes:
        • Nails (koilonychia or spoon-shaped nails)
        • Tongue (Atrophic glossitis)
        • Mouth (angular stomatitis)
  2. Thrombocytopenia
  3. Gastritis
  4. Peripheral neuropathy
    • Numbness, paraesthesia, weakness, ataxia, diminished reflexes.

Treatment of Pernicious Anaemia:

  • Parenteral administration of vitamin B12
  • Physiotherapy for neurologic deficits B Blood transfusion
  • Follow-up visits for early detection of cancer of the stomach
  • Corticosteroid therapy to improve gastric lesions

Question 5. Mention causes of aplastic anemia. Describe its clinical features, diagnosis, complications, and management.

Answer:

Aplastic anemia

  • Aplastic anemia is characterized by
    • Anaemia
    • Leukopenia
    • Thrombocytopenia
    • Hypocellular bone marrow

Etiology:

  • Idiopathic
  • Secondary to drugs, viruses, pregnancy
  • Hereditary

Aplastic Anaemia Clinical Features:

  • Anaemia
  • Excessive tendency to bleed
  • Easy bruising
  • Epistaxis
  • Gum bleeding
  • Heavy menstrual flow
  • Petechiae
  • Predisposition to infections

Aplastic Anaemia  Investigations:

  • Blood smear shows normocytic, microcytic anemia, decreased granulocytes, and platelet count
  • Chromosomal studies for inherited disorders

Aplastic Anaemia  Complications:

  • Bleeding
  • Infection
  • Death within 6-12 months

Aplastic Anaemia  Treatment:

  • Bone marrow transplantation
  • Immunosuppressive therapy
  • Packed red cell transfusions
  • Granulocytes transfusions

Question 6. Describe etiological factors, clinical features, and management of polycythemia vera

Answer:

Polycythaemia Vera:

  • It is a clonal disorder characterized by increased production of all myeloid elements resulting in pinocytosis

Etiology:

  • Chromosomal abnormalities like 20q, trisomy 8 and 9p

Polycythaemia Vera Clinical Features:

  • Headache
  • Vertigo
  • Tinnitus
  • Visual disturbances
  • Increased risk of thrombosis
  • Increased risk of hemorrhages
  • Splenomegaly
  • Pruritis
  • Increased risk of urate stones and gout

Polycythaemia Vera Management:

  • Phlebotomyto reduce total blood cell count
  • Anticoagulant therapy to treat thrombosis
  • Chemotherapy to induce myelosuppression
  • Use of uricosuric drugs to treat hyperuricemia
  • Interferon-alpha

Question 7. Classify leukemias. Describe the clinical features and management of one of them
(or)
Classify leukemias. Outline clinical features and diagnosis of chronic myeloid leukemia
(or)
Describe etiology, clinical features, and management of chronic myeloid leukemia

Answer:

Leukaemias Classification:

  1. Based on cell types predominantly involved.
    • Myeloid
    • Lymphoid.
  2. Based on the natural history of the disease:
    • Acute
    • Chronic.

WHO classification of myeloid neoplasm:

  1. Myeloproliferative Diseases:
    • Chronic myeloid leukaemia (CML), {Ph chromosome t(9;22) (q34;2), BCR/ABLpositive}
    • Chronic neutrophilic leukemia
    • Chronic eosinophilic leukemia/ hypereosinophilic syndrome
    • Chronic idiopathic myelofibrosis
    • Polycythaemia vera (PV)
    • Essential thrombocythaemia (ET)
    • Chronic myeloproliferative disease, unclassifiable
  2. Myelodysplastic/Myeloproliferative Diseases:
    • Chronic myelomonocytic leukemia (CMML)
  3. Myelodysplastic Syndrome (MDS):
    • Refractory anemia (RA)
    • Refractory anemia with ring sideroblasts (RARS)
    • Refractory cytopenia with multilineage dysplasia (RCMD)
    • RCMD with ringed sideroblasts (RCMDRS)
    • Refractory anemia with excess blasts (RAEB1)
    • RAEB2
    • Myelodysplastic syndrome unclassified (MDSU)
    • MDS with isolated del 5q
  4. Acute Myeloid Leukaemia (AML):
    • AML with recurrent cytogenetic abnormalities
      • AML with t(8;21) (q22;q22)
      • AML with abnormal bone marrow eosinophils {inv (16) (p13q22)}
      • Acute promyelocytic leukaemia {t(15;17) (q22;q12)}
      • AML with 11q23 abnormalities (MLL)
    • AML with multilineage dysplasia
      • With prior MDS
      • Without prior MDS
      • AML and MDS, therapy-related
      • Alkylating agent related
      • Topoisomerase type 2 inhibitor-related
      • Other types
    • AML, not otherwise categorized
      • AML, minimally differentiated
      • AML without maturation
      • AML with maturation
      • Acute myelomonocytic leukemia (AMML)
      • Acute monoblastic and monocytic leukemia
      • Acute erythroid leukemia
      • Acute megakaryocytic leukemia
      • Acute basophilic leukemia
      • Acute panmyelosis with myelofibrosis
      • Myeloid sarcoma
  5. Acute Biphenotypic Leukaemia

Chronic Myeloid Leukemia:

  • Etiology:
    • It is a myeloproliferative disorder.
    • Occurs as a result of the malignant transformation of pluripotent stem cells leading to the accumulation of a large number of immature leukocytes in the blood.
    • Radiation exposure and genetic factors have been implicated in the development of CML

Chronic Myeloid Leukemia Clinical Features:

  • Onset is usually slow, initial symptoms are often nonspecific. g: weakness, pallor, dyspnoea, and tachycardia.
  • Symptoms due to hypermetabolism such as weight loss, anorexia, and night sweats.
  • Splenomegaly is almost always present and is frequently massive. In some patients, it may be associated with acute pain due to splenic infarction.
  • Bleeding tendencies such as bruising, epistaxis, menorrhagia, and hematomas may occur.
  • Visual disturbance, neurologic manifestations.
  • Juvenile CML is more often associated with lymph node enlargement than splenomegaly.

Peripheral Blood Picture:

  1. Leucocyte count is elevated often > 1,00,000 cells/1.
  2. Circulating cells are predominantly neutrophils, metamyelocytes, and myelocytes but basophils and eosinophils are also prominent.
  3. The typical finding is an increased number of platelets (thrombocytosis).
  4. Anaemia is usually of moderate degree and is normocytic, normochromic in type. Normoblasts may be present occasionally.
  5. A small portion of myeloblasts usually <5% are seen.

Bone marrow examination:

  1. Cellularity Hyper is cellular with total/partial replacement of fat spaces by proliferating myeloid cells.
  2. Myeloid cells Myeloblasts are only slightly increased.
  3. Erythropoiesis Normoblasts but there is a reduction in erythropoietic cells.
  4. Megakaryocytes are Conspicuous but are usually smaller in size than normal.
  5. Increase in number of phagocytes.

Chronic Myeloid Leukemia Management:

  • Imatinib oral therapy
  • Allogenic bone marrow transplantation
  • Interferon-alpha
  • Chemotherapy drugs used are busulfan, cyclophosphamide, and hydroxyurea

Question 8. Mention various types of diagnostic criteria and complications of leukemia, outline the significance of the system disorder in dental practice

Answer:

Complications of Leukemia:

  • Infections
  • Clogging in blood vessels
  • Stroke
  • Impaired bodily functions
  • Development of other cancers like
    • Kaposi sarcoma
    • Melanoma
    • Lung cancer
    • Stomach cancer
    • Throat cancer
  • Death

Dental Significance:

Question 9. Describe etiological factors, clinical features, and management of eosinophilia

Answer:

Eosinophilia

An increase in the number of eosinophilic leukocytes is referred to as eosinophilia.

The causes of eosinophilia are as follows:

  1. Allergic disorders: Bronchial asthma, urticaria, drug hypersensitivity
  2. Parasitic infestations: Trichinosis, echinococcosis, intestinal parasitism.
  3. Skin diseases: Pemphigus, dermatitis herpetiformis, erythema parasitism.
  4. Certain malignancies: Hodgkin’s disease and some non-Hodgkin’s lymphomas.
  5. pulmonary infiltration which is eosinophilia syndrome
  6. Irradiation.
  7. Miscellaneous disorders: Sarcoidosis, rheumatoid arthritis, polyarteritis nodosa.

Eosinophilia Clinical Features:

  • Dyspnoea
  • Orthopnoea
  • Wheezing
  • Cough with mucoid expectoration
  • Chest pain

Eosinophilia Management:

  • Diethvlcarbamazine 2 mg/kg three times a day for 2 weeks
  • Antihistamines are given to treat allergic reactions

Question 10. Describe oral manifestations of hematological disorders. How would you treat a case of agranulocytosis

Answer:

Hematological Disorders:

  1. Disorders due to vascular disorders:
    • OslerWeberRendu disease
    • Inherited disorders of the connective tissue matrix
    • Acquired vascular bleeding disorders
  2. Disorders due to platelet disorders:
    • Thrombocytopenia
    • Thrombocytosis
    • Disorders of platelet functions
  3. Coagulation disorders:
    • Hemophilia A
    • Hemophilia B
    • Von Willebrand disease
  4. Disorders due to Fibrinolytic defects
  5. Disseminated intravascular coagulation, DIC

Hematological Disorders Oral Manifestations:

  • Gingivasevere hemorrhage
  • Soft tissue hematoma formation
  • Jaw recurrent subperiosteal hematoma
  • Tumourlike malformation
  • Teethhigh caries index
  • Severe periodontal disease
  • Oropharyngeal bleeding
  • Severe bleeding at the injection site

Treatment of Agranulocytosis:

  • Removal of the offending agent
  • Transfusion of red cell constituent when hemoglobin is less than 10 gm/dl
  • Antibiotics to control septicemia
  • Combination of drugs
  • Administration of granulocyte-macrophage colony-stimulating factors
  • Dental management for ulcers5% dyclonine and 5% Benadryl mixed with magnesium hydroxide or Kaolin with pectin

Question 11. How will you investigate a case of bleeding diathesis? Mention some of the dental considerations

Answer:

Bleeding Diathesis Investigations:

  1. Investigations of disordered vascular hemostasis
    • Bleeding time
      • It is based on the principle of formation of a hemostatic plug following a standard incision on the ulnar aspect of the forearm and the time from incision to when bleeding stops is measured
      • Normal 3-8 minutes
    • Hess capillary resistance test
      • This test is done by tying the sphygmomanometer cuff to the upper arm and raising the pressure in it between diastolic and systolic for 5 minutes
      • After deflation, the number of petechiae appearing in the next 5 minutes in a 3 cm2 area over the cubital fossa is counted
      • The presence of more than 20 petechiae is considered a positive test
  2. Investigation of blood coagulation
    • Screening test
      • Whole blood coagulation time
        • The estimation of whole blood coagulation time done by various capillary and tube methods
        • Normal value 49 minutes
      • Activated partial thromboplastin time (PTTK)
        • This test is used to measure the intrinsic system factors as well as factors common to both intrinsic and extrinsic factors
        • One stage of prothrombin time measures the extrinsic system factor VTT as well as factors in the common pathway
    • Special tests
      • Coagulation factor assays
        • These are based on the results of PTTK or prothrombin time tests
      • Quantitative assays
        • Done by immunological and other chemical methods

Bleeding Diathesis Dental Considerations:

  • It is essential to prevent accidental damage to the oral mucosa when carrying out any procedure in the mouth
  • Blood loss can be controlled locally with direct pressure or periodontal dressings with or without topical antifibrinolytic agents
  • Patients with bleeding disorders can be given dentures as long as they are comfortable
  • Fixed and removable orthodontic appliances may be used along with regular preventive advice and hygiene therapy
  • Endodontic treatment is generally low risk for patients with bleeding disorders
  • Aspirin should not be used.

Diseases Of Blood And Lymphoreticular System Reduced inflammation

Question 12. Classify bleeding and coagulation disorders. Write clinical features, diagnosis, complications, and management of hemophilia.

Answer:

Bleeding and Coagulation Disorders Classification:

  1. Disorders due to vascular disorders
    • OslerWeberRendu disease
    • Inherited disorders of the connective tissue matrix
    • Acquired vascular bleeding disorders
  2. Disorders due to platelet disorders
    • Thrombocytopenia
    • Thrombocytosis
    • Disorders of platelet functions
  3. Coagulation disorders
    • Hemophilia A
    • Hemophilia B
    • Von Willebrand disease
  4. Disorders due to fibrinolytic defects
  5. Disseminated intravascular coagulation, DIC

Hemophilia A:

  • It is an inherited disorder of factor 8 deficiency

Hemophilia A Clinical Features:

  • Initially diagnosed in infancy Males are commonly affected
  • Characterized by easy bruising
  • Prolonged bleeding after trauma
  • Bleeding into subcutaneous tissue
  • Hematoma formation
  • Epistaxis
  • Gastric hemorrhage
  • Recurrent hemarthrosis
  • Osteoporosis
  • Intracranial hemorrhage
  • Hematuria

Hemophilia A Oral Manifestations:

  • Gingivasevere hemorrhage
  • Soft tissue hematoma formation
  • Jawrecurrent subperiosteal hematoma
  • Tumourlike malformation
  • Teethhigh caries index
  • Severe periodontal disease
  • Oropharyngeal bleeding
  • Severe bleeding at the injection site

Hemophilia A Diagnosis:

  • Bleeding time normal
  • Prothrombin time normal
  • Platelet count normal
  • Activated partial thromboplastin time prolonged
  • Specific factor 8 assay

Complications:

  • Excessive blood loss
  • Bleeding in brain
  • Long-term joint problems
  • Abnormal thrombosis and clot formation

Management:

  • Replacement therapy by the use of fresh frozen plasma
  • Administration of factor 8
  • Prevention of complications by the use of a synthetic analog of antidiuretic ldeamino8darginine vasopressin
  • Genetic counseling to prevent inheritance

Question 13. Describe etiopathogenesis, clinical features, investigations, and management of hemophilia B

Answer:

Hemophilia B

Etiology:

  • It is an inherited 10linked disease due to a reduction in plasma factor 9 level
  • It is due to aberration in the factor 9 gene

Hemophilia B Clinical Features:

  • Prolonged bleeding during circumcision
  • Prolonged bleeding after surgical procedures
  • Prolonged bleeding from cuts
  • Excessive bruising
  • Excessive and prolonged epistaxis
  • Blood in urine and feces
  • Internal bleeding causing pain and swelling
  • Bleeding in the skull after childbirth
  • Spontaneous bleeding

Hemophilia B Investigations:

  • Factor 9 test
  • Activated partial thromboplastin time
  • Prothrombin time
  • Fibrinogen test

Hemophilia B Management:

  • Factor 9 injections
  • Application of desmopressin acetate to small wounds

General Medicine Question and Answers

General Medicine Question and Answers

 

Immunological Factors In Disease Short And Long Essay Question And Answers

Immunological Factors In Disease Important Notes

  1. Hypersensitivity reactionsImmunological Factors In Disease Hypersensitivity Reactions
  2. Anaphylactic reaction
    • It is a state of rapid developing immune response to an antigen mediated by IgE antibodies
    • Clinical features:
      • Systemic anaphylaxis
      • Pruritus
      • Wheel and flare lesions
      • Bronchospasm
      • Tightness of chest
      • Wheezing
      • Laryngeal edema
      • Dyspnea
      • Cyanosis
      • Shock
      • Diarrhea
      • Pulmonary edema
      • If not treated death occurs Local anaphylaxis
      • Hay fever
      • Bronchial asthma
      • Food allergies
      • Contact dermatitis
      • Angioedema

Immunological Factors In Disease Long Essays

Question 1. Classify allergic reactions. Describe clinical features and management of generalised anaphylaxis.

Answer:

Allergic reactions

  • Hyperscusillvity/allergy In defined an an exaggerated/inappropriate state of normal Immune response with the onset of adverse effects on the body.
  • Lesions of hypersensitivity are a form of antigen-antibody reaction
  • Hypersensllivlly reactions are classified into 4 types,
    • Type 1: Anaphylactic (atopic) reaction
    • Type 2: Cyloxlc (cytolytic) reaction
    • Type 3: Immune complex-mediated (arthus) reaction,
    • Type 4: Delayed hypersensitivity (cell-mediated) reaction.
  • Depending, upon the rapidity, duration, and type of immune response, they are classified into immediate type and delayed type.
    • Immediate type: On administration of antigen, reaction occurs immediately, This includes types 1, 2, and 3.
    • Delayed type: Reaction is slower in onset, develop within 24-48 hours and the effects is prolonged. Includes type 4 reaction.

Anaphylaxis:

  • Anaphylaxis or type 1 hypersensitivity is defined as a state of rapidly developing immune responses to an antigen (i.e., allergen) to which the individual is previously sensitised.
  • The reaction appears within 15 – 30 min of exposure to antigen.

Read And Learn More: General Medicine Question and Answers

Etiology:

  • Type 1 reaction is mediated by humeral antibodies of IgE type or regain antibodies in response to antigen.
  • The definite cause is not known, but the following may be responsible.
  • Environmental pollutants
  • Genetic basis
  • Concomitant factors Allergic response may be linked to the occurrence of certain viral infections of upper respiratory tract.

Anaphylaxis Effects:

  • Increased vascular permeability
  • Smooth muscle contraction
  • Vaaocontriction followed by vasodilation
  • Shock
  • Increased gastric secretion
  • Increased nasal and lacrimal secretions
  • Eosinophils and neutrophilia.

Anaphylaxis Examples:

  1. Reactions against mycobacterial infection.
    • Tuberculin reaction, the granulomatous reaction in tuberculosis, leprosy.
  2. Reaction against virally infected cells
  3. Reaction against malignant cells in the body.
  4. Reaction against organ transplantation, for example, transplant rejection, graft versus host reaction.

 

Immunological Factors In Disease Short Essays

Question 1. Anaphylaxis

Answer:

Anaphylaxis

  • Anaphylaxis or type 1 hypersensitivity is defined as a stale of rapidly developing immune response to an antigen (i.e., allergen) to which the individual is previously sensitised.
  • The reaction appears within 15 – 30 min of exposure to antigen.

Etiology:

  • Type 1 reaction is mediated by humoral antibodies of IgE type or regain antibodies in response to antigen.
  • The definite cause is not known, but the following may be responsible.
  • Environmental pollutants
  • Genetic basis
  • Concomitant factors – Allergic response may be linked to occurrence of certain viral infections of upper respiratory tract.

Anaphylaxis Effects:

  • Increased vascular permeability
  • Smooth muscle contraction
  • Vasoconstriction followed by vasodilation
  • Shock
  • Increased gastric secretion
  • Increased nasal and lacrimal secretions
  • Eosinophia and neutrophilia.

Anaphylaxis Examples:

  1. Reactions against mycobacterial infection.
    • Examples: Tuberculin reaction, granulomatous reaction in tuberculosis, leprosy.
  2. Reaction against virally infected cells
  3. Reaction against malignant cells in the body.
  4. Reaction against organ transplantation for example, transplant rejection, graft versus host reaction.

Question 2. Oedema- causes

Answer: Oedema

Oedema Causes:

  • Congestive heart failure
  • Nephrotic syndrome
  • Severe malnutrition
  • Hepatic cirrhosis
  • Acute or chronic renal failure
  • Hypothyroidism

Question 3. Diagnostic procedures for hypersensitive reactions

Answer:

Hypersensitive Reactions Diagnostic Tests:

  1. Precipitation test
    • When a soluble antigen reacts with its antibody in the presence of electrolytes at optimal temperature and pH, the antigen-antibody complex forms an insoluble precipitate called precipitation
    • Tests:
      • Ring test
        • Ring is formed at the junction of antigen and antibody
      • Flocculation test
        • When instead of sedimenting, the precipitate is suspended as floccules, the reaction is called flocculation
      • Immunodiffusion test
        • Gel is used in it
        • Types
          • Single diffusion in one dimension
          • Double diffusion in one dimension
          • Single diffusion in two dimension
          • Double diffusion in two dimension
          • Immunoelectrophoresis
          • Electroimmunodiffusion
    • Counter immune electrophoresis
    • Rocket electrophoresis
  2. Agglutination:
    • In it antigen combines with its antibody in presence of an electrolyte to form clumps of particles
    • Types:
      • Slide agglutination test
      • Tube agglutination test
      • Coombs test
      • Heterophile agglutination test
        • Weil Felix reaction
        • Paul-Bunnel test
        • Streptococcus MG agglutination test
      • Passive agglutination test
        • Latex agglutination test
        • Haemagglutination test
        • Coagglutination
  3. Complement fixation test:
    • Antigen-antibody complex formed fixes complement
  4. Neutralisation test
    • Bacterial exotoxins neutralises antibody
  5. Immunofluorescence:
    • Antigen-antibody complexes produce fluorescence

Immunological Factors In Disease Short Answers

Question 1. T cells

Answer:

T cells

  • T cells are lymphocytes
  • They are thymus-dependent

T cells Types:

  1. Regulatory T cells
    • T helper cells
      • Facilitates B cell response to produce immunglobulin
      • Balance between T helper cell and T suppressor cells produces optimum immune response
      • Overactivity of helper cells leads to autoimmunity
      • Decreased activity of helper cells causes an immunodeficiency state
    • T suppressor cells
      • They block immune reaction
      • Overactivity of suppressor cells leads to an immunodeficiency state
      • Decreased activity of suppressor cells causes an autoimmunity state
    • Effector cells
      • Cytotoxic T cells
        • It can lyse specific target cells
      • Delayed-type hypersensitivity cells
        • Responsible for delayed hypersensitivity reaction

Question 2. Penicillin anaphylaxis

Answer:

Penicillin anaphylaxis

  • Penicillin allergy develops within minutes and is called an immediate hypersensitivity reaction
  • It can induce both type of reactions
  1. Humoral-mediated immunity- causes
    • Type 1- Anaphylaxis
    • Type 2-Cytolytic reaction
    • Type 3- Arthus reaction
  2. Cell-mediated immunity- causes
    • Delayed hypersensitivity reaction
    • Induces synthesis of IgE antibodies
    • Formation of antigen-antibody complexes
    • Degranulation of mast cells
    • Release of inflammatory mediators
    • Bronchospasm
    • Laryngeal edema
    • Hypotension

Question 3. Serum sickness

Answer:

Serum sickness Causes:

  • After the administration of foreign serum
  • Tetanus antitoxin
  • Rabies antiserum

Serum sickness Mechanism:

  • Antibodies form immune complexes in blood vessels with administered antigens
  • These complexes fix complement which attract the leukocytes to the area causing direct tissue injury

Serum sickness Features:

  • Fever
  • Swelling
  • Lymphadenopathy
  • Joint and muscle pain
  • Rash
  • Peripheral neuritis
  • Kidney disease
  • Myocardial ischemia

Question 4. Pemphigus Vulgaris

Answer:

Pemphigus Vulgaris

  • It is the most common type of pemphigus

Pemphigus Vulgaris Features:

  • Age: 40-70 years
  • Sex: Common in females

Pemphigus Vulgaris Presentation:

  • Development of vesicles and bullae over skin and mucous membrane
  • Rupture of vesicles or bullae
  • Formation of painful ulcers that bleed profusely
  • Oblique pressure on the unaffected aeas around the lesion causes the stripping of the normal skin or mucous membrane called “Nikolsky’s sign”
  • Areas affected:
    • Skin lesions- over scalp, trunk, and umbilical areas
    • Orallesions- cheek, palate, and gingiva
      • Leads to excessive pain, excessive salivation, difficulty in intake of food, halitosis

Question 5. Allergy

Answer:

Allergy

  • Allergy is a state of hypersensitivity induced by exposure to a particular antigen
  • This antigenic substance capable of inducing type 1 IgE-mediated immune response
  • The first dose of allergenic exposure sensitizes B lymphocytes
  • The subsequent exposure results in harmful immunologic activation resulting in expression of an allergic reaction

Question 6. Urticaria

Answer:

Urticaria Types:

  • IgE dependent urticaria
  • Complement mediated urticaria
  • Nonimmunologic urticaria
  • Idiopathic urticaria

Urticaria Features:

  • Formation of wheal and flare cutaneous lesions involving only superficial portions of the dermis
  • This results in circumscribed wheals with erythematous raised borders with blanched centers

Question 7. Angioedema

Answer:

Etiology:

  • Food or drug allergy
  • Biochemical abnormality
  • Absence of inhibitor of Cl esterase enzyme from serum
  • Formation of kinin-like substances

Angioedema Clinical Features:

  • Exhibits as smooth, diffused, edematous swelling involving face, lips, chin, eyes, tongue, and extremities
  • Leads to edema of glottis resulting in suffocation

Angioedema Treatment:

Immunological Factors In Disease Angioedema

Question 8. Steven Johnson syndrome

Answer:

Steven Johnson syndrome

  • It is a severe form of erythema multiforme with widespread involvement, typically involving the skin, oral cavity, eyes, and genitalia

Steven Johnson syndrome Clinical Features:

  1. Symptoms:
    • Fever
    • Malaysia
    • Photophobia
    • Eruptions on oral mucosa, genital mucosa, and skin
  2. Skin Lesions:
    • Flemorrhagic
    • Vesicle and bullae are present
  3. Eye Lesions:
    • Photophobia
    • Conjunctivitis
    • Corneal ulceration
    • Keratoconjunctivitis
  4. Genital Lesions:
    • Non-specific urethritis
    • Balanitis
    • Vaginal ulcers
  5. Complications:
    • Trachea-bronchial ulceration
    • Pneumonia

Steven Johnson syndrome Treatment:

  • ACTH
  • Cortisone
  • Chlortetracycline

VIVA VOCE

  1. Adrenaline is drug of choice in anaphylaxis

Acute Poisoning Question And Answers

Acute Poisoning And Environmental Emergencies Important Notes

  1. Different poisoningAcute Poisoning And Environmental Emergencies Different Poisoning
  2. Fluorosis
    • Dental fluorosis is caused by excessive intake of fluoride during tooth development
    • Features:
    • Dental fluorosis
      • Mottled enamel
      • Presence of hypoplastic areas
      • Mottled areas may stain yellow/ brown
      • Fluoride occurs symmetrically within dental areas, commonly affecting premolars
    • Skeletal Fluorosis
      • Severe pain in
        • Backbones
        • Joints
        • Hips
    • Stiffness in joints and spine
    • Knock-knee syndrome
      • Outward bending of legs and hands
      • Damage to fetus
      • Blocking and calcification of blood vessels
      • Cripping fluorosis
  3. Effect On Kidney
    • May aggravate renal disease

Acute Poisoning And Environmental Emergencies Long Essays

Question 1. Describe the management of acute poisoning.

Answer:

Steps Of Management:

  1. Resuscitation and initial stabilization
    • Maintain airway, breathing, and circulation
    • Blood sample collection for examination
    • Rectal temperature is obtained
    • Treatment of hypotension with crystalloids
    • Administration of a cocktail of 50% dextrose, naloxone, and thiamine
  2. Diagnosis of various types of toxins
    • History
      • Reveals type of poison and amount of overdose taken
    • Examination
      • Helps to detect a syndrome associated with certain poisons
    • Investigations
      • Colour of urine
      • Colour of blood
      • Crystals in urine
      • Ketonuria
      • Anion gap
  3. Nonspecific treatment
    • Reduces levels of toxin in the body
    • Gastric decontamination- includes
      • Removal of unabsorbed poison from the gut
      • Induction of emesis
      • Gastric lavage
      • Cathartics
      • Use of activated charcoal
      • Whole bowel irrigation
    • Enhancement of excretion of absorbed toxins from the body
      • Forced diuresis- alkaline diuresis
      • Use of multiple doses of activated charcoal
      • Peritoneal and hemodialysis
    • Dialysis
  4. Specific therapy
    • A specific antidote is administered

Question 2. Describe the signs, symptoms, and management of fluorosis.

Answer:

Fluorosis

  • Excessive intake of fluoride causes fluorosis

Fluorosis Types:

  1. Dental Fluorosis
    • Caused by fluoride intake above 2 ppm
    • Its symptoms are:
    • Mottling of enamel
    • Discoloration of teeth
    • Teeth become weak and rough
    • Brown or yellow patches appear on their surfaces
  2. Skeletal Fluorosis
    • Caused by fluoride intake above 20 ppm
    • It causes:
    • Pathological changes in the bone
    • Hypercalcification
    • Bone density of limbs, pelvis, and spine increases
    • Ligaments of the spine and collagen of bones get calcified
    • Neurological disturbances may also occur
  3. Genu valgum
    • It is an advanced stage of Fluorosis
    • In it, individuals are unable to perform their routine work
    • Joints become stiff
    • Individuals are crippled

Read And Learn More: General Medicine Question and Answers

Fluorosis Management:

  • Vomiting is induced wi a syrup of ipecac or digital or mechanical stimulation the of tongue or throat
  • Decrease the absorption of fluoride by administering fluoride-binding liquids like warm water, calcium hydroxide, antacids containing aluminum or magnesium hydroxide, or milk
  • The stomach should be thoroughly washed with additional lime water
  • Calcium gluconate should be administered intravenously along with lime to prevent shock

Acute Poisoning And Environmental Emergencies Short Essays

Question 1. Atropine

Answer:

Atropine

  • Atropine is a natural anticholinergic drug

Atropine Mechanism of Action:

  • Bind to muscarinic receptors
  • Blocks the effects of acetylcholine

Atropine Actions:

  • Increases heart rate
  • Vasodilation
  • hypotension
  • Reduces all secretions
  • Muscle relaxation
  • Bronchodilation
  • Relaxes ureter
  • Produces mydriasis
  • CNS stimulant

Atropine Uses:

  • Anti-spasmodic
  • Mydriatric and cycloplegic
  • Preanaesthetic medication
  • Organophosphorous poisoning
  • Bronchial asthma
  • Peptic ulcer
  • Parkinsonism
  • Motion sickness
  • During labor

Atropine Adverse Reactions:

  • Blurring vision
  • Dry mouth
  • Dysphagia
  • Dry skin
  • Fever
  • Constipation
  • Urinary retention
  • Skin rashes
  • Palpitation
  • Flushing
  • Restlessness
  • Delirium
  • Hallucination
  • Psychosis
  • Convulsion
  • Coma

Acute Poisoning And Environmental Emergencies General Medicine Acute Poisoning

Question 2. Arsenic poisoning

Answer:

Arsenic Poisoning Features:

  • Gingivitis
  • Stomatitis
  • Painful mucosal ulceration
  • Hyperpigmentation and hyperkeratosis
  • Excessive salivation
  • Vomiting
  • Diarrhea
  • Neurological disturbances

Question 3. Symptoms of lead poisoning

Answer:

Symptoms of lead poisoning Features:

  • Excessive salivary secretions
  • Metallic taste in the oral cavity
  • Swelling of the salivary glands
  • Development of the dark lead line along the gingival margin
  • Convulsions
  • GI upset
  • Anaemia
  • Neuritis
  • Basophilic stippling of the RBC cells

Question 4. Fluorides in Health and Disease

Answer:

Importance of Fluoride in Health:

  • The kidney excretes it
  • It passes the placental barrier
  • Fluoride prevents the development of dental caries
  • It converts hydroxyapatite to fluorapatite
  • It is mostly found in bones and teeth
  • It is deposited in other calcified tissues also
  • It is required for the proper development of bones
  • It inhibits the activities of certain enzymes
  • Sodium fluoride inhibits enolase in glycolysis
  • Fluoroacetate inhibits aconitase in TCA cycle

Fluoride in Disease:

  • Excess of fluoride causes fluorosis
  • Drinking water containing less than 0.5 ppm of fluoride causes development of caries in children

Question 5. Dental care in mental retardation

Answer:

Dental care in mental retardation

  • Familiarise the patient with the office and dental personnel to reduce his/her fear of the unknown before undertaking any treatment
  • Speech must be slow and simple
  • Only one instruction at a time should be given
  • Tell, show, and do technique is used in mild cases and sedation in moderate cases
  • Carefully listen to the patient
  • Appointments should be short and scheduled during the early part of the day
  • Children should be managed with a blend of kindness and firmness
  • Generalanesthesiaa may be indicated in cases where adequate levels of cooperation cannot be achieved

VIVA VOCE

  1. Atropine is used in organophosphorus poisoning
  2. BAL is used for heavy metal poisoning
  3. EDTA is used for metal poisoning
  4. Dimercapto succinate is used for lead poisoning
  5. Penicillamine is used for copper poisoning
  6. Desferrioxamine is used for iron poisoning
  7. Premolars are the most commonly affected teeth in fluorosis

 

Acute Poisoning And Environmental Emergencies Question and Answers

Acute Poisoning And Environmental Emergencies Short Answers

Question 1. Fluorosis

Answer:

Fluorosis

Dental fluorosis is caused by excessive intake of fluoride during tooth development

Fluorosis Clinical Features

  • Lustreless, opaque white patches in the enamel which may become mottled, striated, or pitted
  • Mottled areas may become stained yellow or brown
  • Hypoplastic areas may also be present to such an extent in severe cases that normal tooth form is lost
  • Enamel fluorosis is a developmental phenomenon due to excessive fluoride ingestion during amelogenesis
  • Once crowns are formed no further fluorosis occurs
  • The hypocalcified areas of the mottled enamel are less soluble in acids
  • They have a greater permeability to dyes
  • They emit fluorescence of higher intensity then normal enamel
  • Fluorosis occurs symmetrically within arches
  • The premolars is usually first affected followed by second molar, maxillary incisor, canine, first molar, and mandibular incisors

Question 2. Food poisoning

Answer:

Food poisoning Management:

  1. Resuscitation and initial stabilization
  2. Diagnosis of type of poison by
    • History
    • Examination
    • Laboratory investigations
    • Nonspecific therapy- to reduce the levels of toxin
  3. Specific therapy- to reduce toxic effects on the body
  4. Supportive care- to support functions of vital organs

Question 3. Arsenic poisoning

Answer:

Arsenic poisoning Features:

  • Gingivitis
  • Stomatitis
  • Painful mucosal ulceration
  • Hyperpigmentation and hyperkeratosis
  • Excessive salivation
  • Vomiting
  • Diarrhea
  • Neurological disturbances

Read And Learn More: General Medicine Question and Answers

Question 4. Barbiturate poisoning

Answer:

Barbiturate poisoning

  • Fatal dose of phenobarbitone is 6-10 gram

Barbiturate poisoning Symptoms:

  • Respiratory depression with slow and shallow breathing
  • Hypotension
  • Skin eruptions
  • Cardiovascular collapse
  • Renal failure

Barbiturate poisoning Treatment:

  • Gastric lavage followed by administration of activated charcoal
  • Maintain BP
  • Airway maintenance
  • Adequate ventilation
  • Oxygen administration
  • Forced alkaline diuresis with sodium bicarbonate, a diuretic and 4 fluids
  • Hemodialysis

Question 5. Scorpion bite

Answer:

Types of Scorpion Venom:

  1. Venom of the genera Hadrurus, Vejovis, and Uroctonus
    • Effects:
      • Sharp burning
      • Swelling
      • Discoloration at the bite site
      • Rarely anaphylaxis
  2. Venom produced by genera of the poisonous varieties of centuries
    • Effects
      • Block sodium channels
      • Spontaneous depolarization of parasympathetic and sympathetic nerves
      • Tachycardia
      • Hypertension
      • Sweating
      • Piloerection
      • Hyperglycemia
      • Pulmonary edema
      • Seizures
  3. Treatment:
    • Patient is hospitalised for at least 12 hours
    • Maintain airway maintenance
    • Administration of 1-2 vials of intravenous anti-venin

Question 6. Lead poisoning

Answer:

Lead poisoning Features:

  • Excessive salivary secretions
  • Metallic taste in the oral cavity
  • Swelling of the salivary glands
  • Development of the dark lead line along the gingival margin
  • Convulsions
  • GI upset
  • Anaemia
  • Neuritis
  • Basophilic stippling of the RBC cells

Question 7. Adverse drug reactions

Answer:

Adverse drug reactions Definition:

  • It is defined as any response to a drug that is noxious and unintended and that occurs at the dose used in man for prevention, diagnosis, or therapy

Adverse drug reactions Types:

  1. Side effects
    • They are unwanted effects of a drug
  2. Toxic effects
    • They are seen with higher doses of the drug
  3. Intolerance
    • A person cannot tolerate a drug
  4. Idiosyncrasy
    • It is a genetically determined abnormal reaction to a drug
  5. Allergic reactions
    • They are immunologically mediated reactions
  6. Iatrogenic diseases
    • These are drug-induced diseases
  7. Drug dependence
    • It is a state of compulsive use of drugs despite the knowledge of the risks associated with its use
  8. Teratogenicity
    • A drug can cause fetal abnormalities when administered to a pregnant woman
  9. Teratogenicity and mutagenicity
    • Drugs causing cancers and genetic abnormalities

Acute Poisoning And Environmental Emergencies Medcial interview

Question 8. Organophosphorous poisoning

Answer:

Organophosphorous poisoning

Acute Poisoning And Environmental Emergencies Organophosphorous Poisoning

Question 9. Thrush

Answer:

Thrush

  • Acute pseudomembranous oral candidiasis is also known as thrush

Common Sites Involved:

  • Buccal mucosa
  • Tongue
  • Palate

Etiology:

  • Causative organism- Candida albicans
  • Prolonged antibiotic therapy
  • Immuno-suppression

Predisposing Factors:

  • Infancy
  • Debilitating illness
  • Metabolic diseases
  • Diabetes
  • Hypothyroidism

Thrush Features:

  • Foul taste
  • Leads to inflammation, erythema, and eroded areas
  • Presence of adherent white plaques
  • It can be removed by scraping
  • It is more common in women

Thrush Treatment:

  1. Anti-fungal antibiotics
    • Nystatin
    • Amphotericin suspension or lozenges
  2. For AIDS patient
    • Oral fluconazole is used

Question 10. Halitosis

Answer:

Halitosis Definition:

  • Unpleasant odor exhaled in breathing is called halitosis

Halitosis Classification:

  1. Physiologic
  2. Pathologic
    • Oral
    • Extraoral

Halitosis Causes:

  1. Physiologic
    • Mouth breathing
    • Medication
    • Fasting
    • Aging
    • Tobacco
    • Food
  2. Pathologic
    • Periodontal infection
    • Tongue coating
    • Stomatitis
    • Xerostomia
    • Faulty restoration
    • Unclean denture
    • Ulcers
    • Abscess
    • Systemic diseases

Halitosis Treatment:

  • Scaling
  • Irrigation
  • Burning sensation
  • Tongue brushing
  • Use of moouth rinse
  • Use of Halita

Question 11. Macroglossia

Answer:

Macroglossia

  • Macroglossia is a relatively common condition characterised by an increase in the size of the tongue

Types And Causes

  1. Congenital macroglossia
    • Overdevelopment of the tongue musculature
    • Lysosomal storage diseases
    • Down’s syndrome
    • Multiple endocrine neoplasia syndrome
  2. Acquired macroglossia
    • Tumours in the tongue
    • Amyloidosis
    • Endocrine disorders
    • Lymphatic obstruction in the tongue
    • Cystic lesions in the tongue

Macroglossia Clinical Features:

  • Causes displacement of teeth and malocclusion
  • Disturbances in speech and feeding
  • Cosmetic deformity
  • Indentation or scalloping on the lateral margins of the tongue
  • Development of tongue-thrusting habits
  • Airway obstruction

Macroglossia Treatment:

  • Removal of the primary cause
  • Surgical reduction or trimming

Question 12. Ciprofloxacin

Answer:

Ciprofloxacin

  • Ciprofloxacin is the first generation of fluoroquinolone

Ciprofloxacin Uses:

  • Urinary tract infection
  • Typhoid
  • Diarrhea
  • Gonorrhea
  • Chancroid
  • Respiratory tract infection
  • Bone, joint, soft tissue, and intra-abdominal infections
  • Tuberculosis
  • Bacterial prostatitis and cervicitis
  • Eye infections
  • Anthrax
  • Orodental infections

Ciprofloxacin Adverse Reactions:

  • Nausea, vomiting, abdominal discomfort, diarrhea
  • Rashes
  • Tendinitis
  • Damages growing cartilage

Question 12. Phenobarbitone

Answer:

Phenobarbitone

  • Phenobarbitone is an anti-epileptic drug

Mechanism of Action:

  • Enhances inhibitory neurotransmission in the CNS
  • Enhances activation of GABA receptors
  • Facilitates GABA-mediated opening of chloride ion channels

Phenobarbitone Uses:

  • Generalized tonic-clonic seizures
  • Partial seizures

Phenobarbitone Adverse Reactions:

  • Sedation
  • Tolerance
  • Nystagmus
  • Ataxia
  • Megaloblastic anemia
  • Osteomalacia
  • Skin rashes
  • Hypersensitivity reactions

Disease Of Connective Tissues Bones And Joints Short Essays

Disease Of Connective Tissues Bones And Joints Short Essays

Question 1. Osteoporosis-clinical features and treatment

Answer:

Osteoporosis

  • Osteoporosis is a disease characterised by increased porosity of the skeleton resulting from reduced bone mass

Osteoporosis Types:

  1. Localized
  2. Generalized
    • Primary
      • Postmenopausal
      • Senile
  3. Secondary
    • Endocrine disorders
    • Neoplasia
    • Gastrointestinal disorders

Question 2. Rheumatoid arthritis

Answer:

Rheumatoid arthritis

  • Rheumatoid arthritis is a systemic disease that usually affects many joints
  • It is characterised by the progressive destruction of the joint structures

Etiology:

  • Increased serum IgG
  • Increased rheumatoid factor
  • Presence of antinuclear antibodies

Rheumatoid Arthritis Clinical Features:

  • Age- third and fourth decade of life
  • Sex- females are more affected
  • fever
  • Malaise
  • Weight loss
  • Anaemia
  • Raised ESR
  • Joint becomes swollen and stiff
  • Presence of pain
  • Restricted jaw movements
  • Tenderness in joints
  • Malocclusion

Rheumatoid Arthritis Treatment:

  • Systemic steroid therapy
  • Antibiotics

Question 3. Gout

Answer:

Gout

  • Gout occurs due to increased production of uric acid or decreased renal excretion of uric acid

Gout Clinical Features:

  • It comprises of four stages
  • Onset may be insidious or sudden
  • Recurrent attacks
  • Aggregate deposits of monosodium urate monohydrate in and around the joints
  • Renal diseases
  • Uric acid nephrolithiasis

Gout Diagnosis:

  • Elevation of serum uric acid levels
  • Presence of urate crystals in synovial fluid

Read And Learn More: General Medicine Question and Answers

Gout Treatment:

  • NSAIDS are used

Question 4. Scleroderma

Answer:

Scleroderma

  • Scleroderma is characterized by progressive fibrosis and calcification of skin and mucosa

Etiology:

  • Endocrinal disturbances
  • Nervous disturbances
  • Vascular disturbances
  • Allergic reactions
  • Infections

Disease Of Connective Tissues Bones And Joints

Scleroderma Clinical Features:

  • Cutaneous changes- indurated edema and erythema of the skin
  • Fixation of epidermis to underlying tissues
  • CVS disturbances
  • CNS disturbances
  • The tongue becomes stiff and broad
  • Difficulty in mouth opening
  • Xerostomia

Scleroderma Treatment:

  • Corticosteroid therapy

Question 5. COX-2 inhibitors

Answer:

COX-2 inhibitors

  • COX-2 inhibitors are advantageous
  • Some of the COX-2 inhibitors are:
    • Meloxicam
    • Coxibs- celecoxib, rofecoxib, parecoxib, etori- coxib, valdecoxib
    • Nimesulide

COX-2 inhibitors Properties:

  • Analgesic
  • Anti-inflammatory
  • Anti-pyretic effect
  • Less gastric ulcerogenic effect
  • Do not inhibit platelet aggregation

COX-2 inhibitors Disadvantages:

  • Increases risk of cardiovascular events
  • Increases cerebrovascular thrombotic events
  • Increases risk of myocardial infarction and stroke

Balanced Diet And Nutritional Disorders Question and Answers

Balanced Diet And Nutritional Disorders Important Notes

  1. Marasmus
    • It is a common form of protein energy malnutrition
    • Mostly occurs 6-12 months postnatally
    • Clinical features
      • Large head
      • Distended abdomen
      • Diarrhea
      • Stick like limbs
      • Reduced body weight
  2. Kwashiorkor
    • It is a disease of protein energy malnutrition occurring in the second year of life
    • Clinical features
      • Generalized edema
      • Change in color of hair
      • Diarrhea
      • Palpable liver
      • Pigmentation of skin and ulceration
  3. Fat-soluble vitamins
    • Vitamin A
    • Vitamin D
    • Vitamin E
    • Vitamin K
  4. Water soluble vitamin
    • Vitamin B complex
    • Vitamin C

Balanced Diet And Nutritional Disorders Long Essays

Question 1. Describe the various manifestations of avitaminosis with particular reference to the oral cavity. How will you treat them?

Answer: 

The various manifestations of avitaminosis with particular reference to the oral cavity

  • Vitamins are essential for growth and normal body functions
  • A deficiency of vitamins causes various clinical manifestations as follows

Balanced Diet And Nutritional Disorders Avitaminosis Treatment

Question 2. Describe the etiology, clinical features, diagnosis, and treatment of scurvy
Answer:

Scurvy Etiology:

  • Vitamin C deficiency results in scurvy.

Scurvy Clinical Features:

  • Lesions and clinical manifestations of Vitamin C deficiency are seen more commonly in two extreme age groups i.e., early childhood and geriatric patients.

The following manifestations are seen in vitamin C deficiency.

  1. Hemorrhage diathesis – A marked tendency to bleed which is the characteristic of scurvy. There may be hemorrhages in the skin, mucous membranes, gums, muscles, joints, and underneath the periosteum.
  2. Skeletal lesions – There is a deranged formation of osteoid matrix but not deranged mineralization. Growing tubular bones as well as flat bones are affected.
  3. Delayed wound healing.
  4. Anaemia Normocytic normochromic type.
  5. Skin rash Hyperkeratotic and follicular rash may occur.
  6. Lesions in teeth and gums – Scurvy may interfere with the development of dentin.
    • The gums are soft and swollen, may bleed easily, and get infected commonly.

Read And Learn More: General Medicine Question and Answers

Scurvy Diagnosis:

  • Through clinical features

Scurvy Treatment:

  • 250 mg of vitamin C orally three times a day
  • Removal of the underlying cause

Question 3. Describe the etiology, clinical features, diagnosis, and treatment of thiamine deficiency

Answer:

Thiamine Deficiency:

  • Occurs due to vitamin B1
  • It leads to beriberi

Thiamine Deficiency Types:

  1. Wet beriberi
    • Characterized by edema of legs, face, trunk, and serous cavities
  2. Dry beriberi
    • Associated with neurological manifestations
  3. Infantile beriberi
    • Seen in infants

Thiamine Deficiency Clinical Features:

  • Loss of appetite
  • Weakness
  • Constipation
  • Nausea
  • Mental depression
  • Peripheral neuropathy
  • Irritability
  • Numbness in tire legs

Thiamine Deficiency Diagnosis:

  • Diagnosis is made from clinical manifestations

Thiamine Deficiency Treatment:

  • The initial dose of 50 mg intramuscularly is given for several days then 2.5-5 mg is given daily by mouth

Balanced Diet And Nutritional Disorders population Of Numbers

Balanced Diet And Nutritional Disorders Short Essays

Question 1. Malnutrition

Answer:

Malnutrition

  • Malnutrition occurs due to absolute or relative deficiency of energy and protein

Malnutrition Clinical Features:

  • Mild growth retardation
  • Loss of weight
  • Thirst
  • Weakness
  • Feeling cold
  • Nocturia
  • Amenorrhoea
  • Pale and dry skin
  • Thinning of hair
  • Cold extremities
  • Muscle wasting
  • Oedema
  • Subnormal body temperature
  • Distended abdomen
  • Diminished tendon jerks
  • Apathy
  • Depression
  • Susceptibility to infections

Malnutrition Management:

  • Extra feeding
  • Repletion of proteins, energy, vitamins, and micronutrients

Question 2. Beriberi-types and clinical features

Answer:

Beriberi Types:

  1. Wet beriberi
    • Characterized by edema of legs, face, trunk, and serous cavities
  2. Dry beriberi
    • Associated with neurological manifestations
  3. Infantile beriberi
    • Seen in infants

Beriberi Clinical Features:

  • Loss of appetite
  • Weakness
  • Constipation
  • Nausea
  • Mental depression
  • Peripheral neuropathy
  • Irritability
  • Numbness in the legs

Question 3. Vitamin A deficiency

Answer:

Lesions in Vitamin A deficiency:

  1. Ocular lesions:
    • Night blindness
    • Xerophthalmia, dry and scaly sclera, conjunctiva
    • Keratomalacia due to infections of corneal ulcers,
    • Pilots spots are focal triangular areas of opacities due to the accumulation of keratinized epithelium.
    • Blindness due to infection, scarring, and opacities.
  2. Cutaneous lesions: Xeroderma/toad-like appearance of skin because of papular lesions due to follicular hyperkeratosis and keratin plugging in the sebaceous glands.
  3. Other lesions:
    • Squamous metaplasia of
    • Respiratory epithelium,
    • Pancreatic ductal epithelium,
    • Urothelium
    • Long-standing metaplasia may progress to anaplasia.
    • Immune dysfunction,
    • Pregnant women may have an increased risk of maternal infection, mortality, and impaired embryonic development.

Question 4. Night blindness

Answer:

Night blindness

  • Night blindness is a common symptom of vitamin A deficiency. It is a defective dark adaptation due to defective synthesis of rhodopsin in rods
  • It is supported by low plasma retinol concentration
  • If untreated the condition progresses with loss of the normal mucous cells from the cornea leading to xerophthalmia

Question 5. Pellagra

Answer:

Pellagra

  • Niacin deficiency causes Pellagra i.e., rough skin
  • The cardinal manifestations of pellagra are referred to as the three Ds ie, dermatitis, diarrhea, and dementia and if not treated may lead to 4th D i.e., death.
  • Dermatitis: Sun-exposed areas of skin developed erythemia resembling sunburn which may progress to chrome type with blister formation.
  • Diarrhoea This is seen along with stomatitis, glossitis, enteritis, nausea, and vomiting
  • Dementia: Degeneration of neurons of the brain of the spinal tract results in neurological symptoms such as dementia, peripheral neuritis, ataxia, and visual and auditory disturbances.
  • Oral findings include:
    • Bald tongue of sandwich,
    • Raw beefy tongue
    • Mucosa becomes fiery red and painful
    • Profuse salivation
  • Chronic alcoholics are at high risk of developing pellagra because, in addition to dietary deficiency, niacin absorption is impaired in them.

Question 6. Vitamin B12

Answer:

Vitamin B12

  • It is cyanocobvilamine

Coenzyme Forms:

  • 5 Deoxyadenosyl cobalamin
  • Methylcobalamin

Coenzyme Functions:

  1. Synthesis of methionine from homocysteine
    • Vitamin B12 is used as methylcobalamin in this reaction
  2. Isomerization of methyl malonyl CoA to succinyl CoA
    • It occurs m the presence of vitamin B12 coenzyme, deoxy adenosylcobalamin

Coenzyme Daily Requirements:

  • Adults- 3 micrograms/day
  • Children -0.5-1.5 micrograms/ day
  • During pregnancy and lactation- 4 micrograms/day

Coenzyme Deficiency Manifestation:

  • Cyanocobalamine or vitamin B12 deficiency leads to
  1. Pernicious anemia
    • Characterized by low hemoglobin levels, decreased number of erythrocytes, and neurological manifestations
  2. Neuronal degeneration
  3. Demyelination of the nervous system

Question 7. Riboflavin deficiency

Answer:

Riboflavin deficiency

  • Riboflavin deficiency symptoms include
  1. Cheilosis
    • The presence of fissures at the corner of the mouth
  2. Glossitis
    • The tongue appears smooth and purplish
  3. Dermatitis

Question 1. Balanced diet

Answer:

Balanced diet

  • It is defined as a diet that contains different types of foods possessing the nutrients- carbohydrates, fats, proteins, vitamins, and minerals in a proportion to meet the requirements of the body
  • It supplies a little more of each nutrient than the minimum requirement to keep the body in a state of good health and protect against leanness
  • Its basic composition varies from country to country
  • Indian balanced diet is composed of
    • Cereals
    • Pulses
    • Roots and tubers
    • Fruits
    • Milk and milk products
    • Fats and oils
    • Sugar
    • Groundnuts
  • Meat, fish, and eggs in non-vegetarians
  • Additional amounts of milk and pulses in vegetarians

Question 2. Scurvy

Answer:

Scurvy Etiology:

  • Vitamin C deficiency results in scurvy.

Scurvy Clinical Features:

  • Lesions and clinical manifestations of Vitamin C deficiency are seen more commonly in two extreme age groups i.e., early childhood and geriatric patients.
  • The following manifestations are seen in vitamin C deficiency.
  1. Hemorrhage diathesis – A marked tendency to bleed which is characteristic of scurvy. There may be hemorrhages in the skin, mucous membranes, gums, muscles, joints, and underneath the periosteum.
  2. Skeletal lesions – There is a deranged formation of the osteoid matrix but not deranged mineralization. Growing tubular bones as well as flat bones are affected.
  3. Delayed wound healing.
  4. Anaemia Normocytic normochromic type.
  5. Skin rash Hyperkeratotic and follicular rash may occur.
  6. Lesions in teeth and gums Scurvy may interfere with the development of dentin.
    • The gums are soft and swollen, may bleed easily, and get infected commonly.

Question 3. Rickets

Answer:

Rickets

  • Rickets is a clinical disorder seen in growing children from 6 months to 2 years of age due to a deficiency of Vitamin D.

Rickets Clinical Features:

  • The gross skeletal changes depend on the severity of the rachitic process, its duration, and in particular the stresses to which individual bones are subjected.
  • Craniotabes, are the earliest bony lesions due to small round unossified areas in the membranous bones of the skull.
  • Harrisons sulcus occurs due to in drawing of soft ribs on inspiration.
  • Pigeon chest deformity
  • Bow legs occur In ambulatory children due to weak bones of lower logs.
  • Knocked knees may occur due to enlarged ends of the femur, tibia, and fibula.
  • Lower epiphyses of the radius may be enlarged.
  • Lumbar lordosis due to involvement of the spine and pelvis.

Read And Learn More: General Medicine Question and Answers

Question 4. Niacin

Answer:

Niacin

  • It is vitamin M3
  • It is a pyridine derivative

Coenzyme Forms:

  • Nicotinamide adenine dinucleotide, NAD+
  • Nicotinamide adenine dinucleotide phosphate, NADP+

Niacin Functions:

  • Involved in an oxidation-reduction reaction
  • Participates in almost all the metabolism

Niacin Deficiency Manifestation:

  • Pellagra

Question 5. Vitamin D

Answer:

Vitamin D

  • It is a fat-soluble vitamin
  • It resembles sterols in structure
  • Its best source is sunlight
  • Its active form is calcitriol
  • It is involved in calcium metabolism
  • Required in bone formation
  • Its daily requirement is 400 IU
  • Its deficiency leads to rickets in children and osteomalacia in adults

Question 6. Vitamin C

Answer:

Vitamin C

  • It Is a water-soluble vitamin
  • It plays an important role in human health and disease
  • It is readily absorbed by the intestines and excreted in urine
  • About 60-70 mg of vitamin C is required per day Citrus fruits are the main sources of vitamin C
  • Its deficiency leads to scurvy

Question 7. Vitamin E

Answer:

Vitamin E

  • Vitamin E is a fat-soluble vitamin

Vitamin E Sources:

  • Vegetable oils
  • Meal
  • Milk
  • Butler
  • Eggs

Vitamin E Requirements:

  • Males-10 mg
  • Females- 8

Vitamin E Deficiency Manifestations:

  • Neurological dysfunction

Question 8. Bitot’s spots

Answer:

Bitot’s spots

  • Bitot’s spot may appear as glistening white plaques of desquamated thickened conjunctival epithelium, usually triangular and firmly adherent to the underlying triangular and firmly adherent to the underlying conjunctival.
  • It occurs due to vitamin A deficiency.

Bitot’s Spots Treatment:

  • Oral administration of retinol 30 mg daily for 3 days
  • In advanced cases, vitamin A is given in the dose of 50,000 IU parenterally for three days

Bitot’s Spots Prevention:

  • Good nutrition
  • Intake of fresh leafy green vegetables
  • Intake of vitamin A

Question 9. Vitamin B12

Answer:

Vitamin B12

  • It is cyancvohalamine

Vitamin B12 Coenzyme Forms:

  • 5-Deoxyadenosyl cobalamin
  • Methylcobalamin

Vitamin B12 Functions:

  1. Synthesis of methionine from homocysteine
    • Vitamin B12 is used as methylcobalamin in this reaction
  2. Isomerization of methyl malonyl CoA to succinyl CoA
    • It occurs in the presence of vitamin B12 coenzyme, deoxy adenosylcobalamin

Vitamin B12 Daily Requirements:

  • Adults- 3 micrograms/day
  • Children -0.5-1.5 micrograms/day
  • During pregnancy and lactation- 4 micrograms/day

Question 10. Vitamin A deficiency

Answer:

Vitamin A deficiency

  • Vitamin A deficiency leads to
  1. Night blindness
  2. Xerophthalmia
  3. Keratomalacia
  4. Retarded growth

Question 11. Vitamin K

Answer:

Vitamin K

  • It is fat soluble vitamin

Vitamin K Sources:

  1. Animal sources
    • Egg yolk, meat, liver, cheese, and dairy products
  2. Plant sources
    • Cabbage, cauliflower, tomatoes, alfalfa, spinach

Vitamin K Functions:

  • Helps in coagulation
    • Daily Requirement- 70-140 micrograms/day

Vitamin K Deficiency Symptoms:

  • Diminished blood clotting
  • Increased prothrombin time

Question 12. Vitamin B6

Answer:

Vitamin B6 Sources:

  • Milk
  • Liver
  • Meat
  • Legumes
  • Whole grains
  • Cereals
  • Nuts
  • Vegetables

Vitamin B6 Functions:

  • Acts as a cofactor for several enzymes involved in amino acid metabolism
  • Involved in the metabolism of fat, carbohydrates, and several vitamins
  • Involved in heme synthesis

Question 13. Pyridoxine deficiency

Answer:

Pyridoxine deficiency Symptoms:

  • Glossitis
  • Cheilosis
  • Weakness
  • Peripheral neuropathy
  • Depression
  • Irritability
  • Microcytic, hypochromic anemia
  • Seizures

Pyridoxine deficiency Treatment:

  • Oral administration of vitamin B6 in the dosage of 10-20 mg/day

Question 14. Cyanocobalamine deficiency

Answer:

Cyanocobalamine deficiency

Cyanocobalamine or vitamin B12 deficiency leads to

  1. Pernicious anemia
    • Characterized by low hemoglobin levels, decreased number of erythrocytes, and neurological manifestations
  2. Neuronal degeneration
  3. Demyelination of the nervous system

VIVA VOCE

  1. Scurvy occurs due to vitamin C deficiency.
  2. Vitamin D deficiency leads to rickets and osteomalacia.
  3. Bitot’s spots occur in vitamin A deficiency.
  4. Pernicious anemia occurs due to vitamin B12 deficiency.
  5. Pellagra occurs due to vitamin B6 deficiency.
  6. Thiamine deficiency leads to beriberi.
  7. Vitamin A is an antioxidant.
  8. Warfarin antagonizes vitamin K.
  9. Craniotabes is the earliest bony lesion seen in infants with rickets.
  10. Starvation is severe undernutrition resulting from prolonged inadequacy of food.
  11. Undernutrition is a state of negative energy balance.