Drug Information

Drug Interaction:

FACTS ON FINGER TIPS (MIMS)

1.. HODGKIN’S DISEASE

Salient Features

Epidemiology

Relatively an uncommon disorder
The common form of affects more than women, but nodular sclerosing lymphoma affects more women.
Age at presentation is usually 15-35 years

Pathogenesis

A neoplastic disorder of unknown aetiology that usually involves the reticuloendothelial and lymphatic systems

Clinical features

Painless lymphadenopathy, mostly cervical and mediastinal
It can be localised or disseminated
Weight loss
Night sweats ior unexplained fevers
Pruritus
Splenomegaly
Horner’ syndrome may be present

Investigations

FBC, ESR,LFTs
Reed -Stemberg cells in lymph nodes or other sites
Lymph nodes biopsy is diagnostic

Differential management

Non-Hodgkin’s lymphoma
Acute leukaemia
Epstein- Bar virus Infection/Infectious mononucleosis
Tuberculosis
Lung Cancer
Other infections

Management

Urgent haematological assessment
Radiotherapy and/or chemotherapy

Key Points

Emergency presentation include superior vena cva blockage and bone marrow failure
Staging determines the most appropriate treatment and likelihood of positive results

Indication:

14. DISORDERS AND /OR ADVERSE REACTIONS - METABOLISM SYSTEM -SUMMARY

Refer - Other information

Contents

1. Evidence Based Medicine

2.Facts on Finger Tips i. Hodgkin's Disease ii. Prostrate Cancer iii. Raised Cholesterol Levels iv. Mesothelioma

3.Disorders and/or Adverse Reactions Items 1 to 13

FACT ON FINGER TIPS (MIMS)

2. PROSTRATE CANCER

Salient points

Epidemology

1. Prostrate cancer is second to only to lung cancer in terms of male cancer deaths

2.Men with no family history have a one-in-12 lifetime risk. The incidence is increasing,

probably because of an aging population and the increasing use of prostrate specific

antigen (PSA) screening.

Risk factors

1.Age

2.Family history

Clinical features

1.It is slowly progressive, so the cancer may remain symptomatiic

2.Symptoms include hesistency and post -micuration dribbing

3.Haematuria

4.Rectal examination shows a firm irregularly enlarged prostrate

5.Co-exising bone pain may indicate metastatic disease

Investigations

1. Elevated Prostrate-Specific Antigen(PSA) levels

2.Prostrate cancer produces osteoblastic bony metastatis. Detecting these

on bone scan or X-ray is usually diagnostic

3.Diagnosis is confirmed by trans-rectal utltrasound

Management and prevention

1.In elderly patients with local disease, a policy of watchful waiting with serial

PSA measurements may be adopted

2.The three main treatments are radical prostrectomy, radical radiotherapy and

bracytherapy with less ercetile dysfunction. In younger patients , treatment

involves radical prostatecomy

3.Treatment with androgen ablation is usual. Quarterly injections of LHRH are

preferred to bilateral orchidectomy

4.The largest urological study to date investigated finasteride to see if it would

prevent prosrate cancer. The trial was stopped prematurely when it was shown

that finasteride acheived a reduction of 24% in the prevalence of prostrate cancer.

A worrying finding was that a greater proportion of poorly differentiated cancers

occured among the finasteride group.

Key points

1.50 percent of men aged 80 have prostrate cancer at autopsy, but only 4% die of it.

2.Most men have modrately well differiatiated tumors and should benefit from

radical treatment if life expectantcy is more than 10 years

3.Only a minority of cancers detected on screening spread beyond the gland

to cause disease and shorten life expectancy. Many men die with prostrate

cancer rather than because of it.

4.Surgery can lead to erectile dysfunction and incontinence

Adverse Reaction:

FACTS ON FINGER TIPS (MIMS)

3. RAISED CHOLESTEROL LEVELS

Salient Features

Definition

1.Serum cholesterol is defined as high if above 200mg/dL

Aetiology

1.Related to a diet rich in saturated fats and refined carbohydrates

2.Can be familial

Associated problems

1.Increased risk of CHD and cerebrovascular disease

2.increased risk of peripheral vascular disease

Who to screen

1.Patients with a family history of either dyslipidaemia or CHD before

the age of 65

2.Patients who have other risk factors for CHD, inculding hypertension, diabetes

and smoking

3.Patients who present with xanthomata or xanthelesmata or those who have

a corneal arcus before the age of 50

Management

1.Advice patients about a healthy lifestyle, encourage increased excercise

and weight loss if the patient is overweight.

2.Reduce intake of saturated fats to less than 10 percent of calorie intake

3.Modify other risk factors, such as giving up smoking

4.Treat patients with known CHD

5.For patients without established CHD, use risk tables to guide treatment

decisions

6.Active treatment for primary prevention should be considered when MI risk

exceeds 3 percent per year

7.Statins are first- line treatment

8.Fibrates and anion exchange resins, such as cholestryramine, are second -line

agents

9.Refer patients with varying high triglycerides levels or resistent high cholesterol

as this may indicate a familial hyperlipedaemia

Key points

1.Take a holistic look at reducing the risk of CHD by attempting to modify all relevant

risk factors

2.Primary prevention can substantially reduce the risk of coronary events but does not

use a lot of resources

Contra-Indications:

FACTS ON FINGER TIPS (MIMS)

3. RAISED CHOLESTEROL LEVELS

Salient Features

Definition

1.Serum cholesterol is defined as high if above 200mg/dL

Aetiology

1.Related to a diet rich in saturated fats and refined carbohydrates

2.Can be familial

Associated problems

1.Increased risk of CHD and cerebrovascular disease

2.increased risk of peripheral vascular disease

Who to screen

1.Patients with a family history of either dyslipidaemia or CHD before

the age of 65

2.Patients who have other risk factors for CHD, inculding hypertension, diabetes

and smoking

3.Patients who present with xanthomata or xanthelesmata or those who have

a corneal arcus before the age of 50

Management

1.Advice patients about a healthy lifestyle, encourage increased excercise

and weight loss if the patient is overweight.

2.Reduce intake of saturated fats to less than 10 percent of calorie intake

3.Modify other risk factors, such as giving up smoking

4.Treat patients with known CHD

5.For patients without established CHD, use risk tables to guide treatment

decisions

6.Active treatment for primary prevention should be considered when MI risk

exceeds 3 percent per year

7.Statins are first- line treatment

8.Fibrates and anion exchange resins, such as cholestryramine, are second -line

agents

9.Refer patients with varying high triglycerides levels or resistent high cholesterol

as this may indicate a familial hyperlipedaemia

Key points

1.Take a holistic look at reducing the risk of CHD by attempting to modify all relevant

risk factors

2.Primary prevention can substantially reduce the risk of coronary events but does not

use a lot of resources

Dosages/ Overdosage Etc:

42. MESOTHELIOMA

Salient Features

Epidemiology

The incidence will rise for the next 10-15 years until asbestos regulations are put into practice

Aetiology

The primary aetiological factor is asbestos exposure
Other aetiological factors include chronic intrathoracic infection, TB pleuritis and other fibre exposures

Clinical features

Upto 90 percent of cases present with dyspnoea and chest pain
Symptoms include sweats, fevers, cough, malaise and weight loss

Investigations

Chest X-ray and CT scanning of the thorax and abdomen
Biopsy isneeded for diagnosis
Distinction from adenocarcinoma is often difficult
In stage I, the disease is limited to the thorax
In Stage Ii, the thorax and local nodes are affected
Stage III is locally extensive disease
In Stage Iv, there is distant spread

Management

Surgery: in rare cases a pleuro-pneumonectomy may be performed
Palliative radiotherapy can help chest pain
Chemotherapy : the drug response is less than 20 per cent

Prognosis

Median survival is 22 months for stage I, 17 mnths for Stage II, and 11 months Stage III

Other Information:

14.DISORDERS AND /OR ADVERSE REACTIONS - METABOLISM - SUMMARY

( Ref- Harrisons - Priniciples of Internal Medicine Ninth Edition )

1. Hyponatremia ( 417 )
2. Hyperkalemia ( 442 )
3. Hypokalemia ( 441 )
4. Metabolic acidosis ( 446 )
5. Hypercalcemia ( 1835 )
6. Hyperuricemia ( 483 )
7. Hyperglycemia ( 386 )
8. Porphyria exacerbation ( 494 )
9. Hyperbilirubinemia ( 1454 )
10. Leukemias (1620)
11. Chronic Granulocytic leukema (1630)
12.Hodgkins Disease (1635)
13. Squamous -cell carcinoma ( 1653)

1. Hyponatremia ( 417 )

Hyponatremia indicates that the body fluids are diluted by an excess of water relative to total solute.Hyponaremia is not equivalent to sodium depletion, which is only one of a number of clinical states in which it may occur . Most types of hyponaremia can be considered to result from defective urinary dilution

Adverse reaction- drugs ( 386 )
   a. Dilutional
    1. Vincristine
    2. Cyclophosphamide
    3. Chlorpropamide
    4. Diuretics

    b. salt wasting
    1. Diuretics
    2. Corticosteroids ( withdrawal )
    3. Enemias
    4. Mannitol

2. Hyperkalemia ( 442 )

Hyperkalemia are caused by renal failure, adrenal insufficiency, diuretics which inhibit potassium secretion etc. Inadequate renal excretion is the most frequent cause.

   Adverse reaction- drugs ( 386 )
    1. Spironolcatone
    2. Triamterene
    3. Amiroride
    4. Cyctotoxics
    5. Corticosteroids ( withdrawal )
    6. Succinyl chloride
    7. Digitalis overdose
    8. Potassium salts of drugs
    9. Potassium preparations including salt substitute
    10. Lithium

3. Hypokalemia ( 441 )

The principal cause of potassium depletion are, gastrointestinal , renal, osmotic diuretics, excessive minerlocorticoid effects, renal tubular diseases etc. The most frequent cause of potassium depletion is probably administration of diuretics without adequate potassium supplementation. Potassium excretion is increased during osmotic diuretics.

    Adverse reaction- drugs ( 386 )
     1. Diuretics
     2. Laxative abuse
     3. Corticosteroids
     4. Amphotericin B
     5. Alkali -induced alkalosis
     6. Insulin
     7. Osmotic diuretics
     8. Carbenoxolone
     9. Gentamicin
     10. Degraded tetracycline
     11. Vitamin B12

4. Metabolic acidosis ( 446 )

Metabolic acidosis is caused by one of three mechanisms. 1. increased production of nonvolatile acids, 2. decreased acid excretion by the kidney, 3. loss of alkali.

    Adverse reaction- drugs ( 386 )
     1. Paraldehyde ( degraded )
     2. Phenformin
     3. Acetazolamide
     4. Spironlocatone
     5. Salicylates

5. Hypercalcemia ( 1835 )

Hypercalcemia is the most common manifestation of hyperparathyroidism. Careful consideration must be given to the justification of surgical exploration in the absence of definite hypercalcemia.

There are numerous reports of so-called - normocalcemic hyperparathyroidism- with normal calcium but elevated values of immunoactive PTH (iPTH) . However, careful scrutiny of the reports reveal that in those with adenomas, the patients were ,in fact, hypercalcemic at some time in their course, they could be more correctly described , therefore as having intermittant hypercalcemia, perhaps an early feature of hyperparathyroidism

   Adverse reaction- drugs ( 386 )
     1. Antacids with absorbale alkali
     2. Vitamin D
     3. Thiazides

6. Hyperuricemia ( 483 )

The biochemical hallmark and prerequite of gout is hyperuricemia. The concentration of uric acid in body fluids is determined by the balance between rates of production and eliminatiion . Uric acid formed by oxidation of purine bases , which may be exogenous or endogenous in origin

   Adverse reaction- drugs ( 386 )
     1. Thiazides
     2. Chlorthalidone
     3. Ethacrynic acid
     4. Furosemide
     5. Aspirin
     6. Cytotoxics
     7. Hyperalimentation
     8. Fructose ( IV )

7. Hyperglycemia (1749)

   Adverse reaction- drugs
    1. Corticosteroids
    2. Oral contraceptives
    3. Chlorthalidone
    4. Ethacrynic acid
    5. Thiazides
    6. Furosemide
    7. Diazoxide
    8. Growth Hormone

8. Porphyria exacerbation ( 494 )

   The porphyrias are a group of clinically hetrogenous diseases associated with inherited or
   acquired disturbances in heme biosynthesis. Porphyrins are tetrapyrrole pigments that serve as intermediates in this pathway. They are formed from precursors delta- aminolevulinic  acid ( ALA ) and porphobilinogen Heme, the ferrous iron complex of protoporphyrin IX , functions   as prostatic group of hemoproteins such as haemboglobin.

   Adverse reaction- drugs ( 386 )
    1. Barbiturates
    2. Chlordiazepoxide
    3. Meprobamate
    4. Sulfonamides
    5. Estrogens
    6. Oral contraceptives
    7. Chlorpropamide
    8. Phenytoin
    9. Glutethimide
    10. Grisefluvin
    11. Rifampicin

9. Hyperbilirubinemia ( 1454 )

In disorders associated with hemolysis, most commonly hemolytic anemias, the rate of bilirubin productoin is increased and may even exceed the amount that can be removed by normal liver. This resulting in jaundice is prinarily an uncogugated hyperbilirubinemia

   Adverse reaction- drugs ( 386 )
     1. Rifampicin
     2. Novobiocin

10. Leukemias (1620)

Leukemia is a disease characterized by neoplastic proliferation of one of the blood-forming cells. The different types of leukemia are classified according to cell type involved, and as acute or chronic, depending on the state of maturity of the neoplatic cells and the expected duration of the disease. If left unattended all forms of ledukema are fatal, death is usually due to complications resulting from infiltration of the bone marrow by leukemic cells and replacement of normal hematopietic cells. The average survivial of untreated patients with acute leukemia is about 3 months, but the course of the disease may vary considerably

11. Chronic Granulocytic leukema (1630)

Chronic granulocytic leukemia (CGL) can occur at any age, but majority of the patients are
between 30 and 50 yeas old. Although there is no well-defined etiologic factor, an increase
in both acute and chronic granulocytic leukemia was noted 5 to 8 years following atomic bomb explosion in Japan

The chronic phase of CGL begins as a myeloproliferative disorder in which there is an excessive proliferation and accumulation and accumulation of granulocytic cells of intermediative maturity as well as ploymorphoninuclear leukocytes. The median white cell count at the time of diagnosis is about 200,000 per cubic millimeter

12.Hodgkins Disease (1635)

Hodgkins disease usually presents either with asympathomatic discrete, painless, rubbery
enlargement of lymph nodes or with symptoms of liver, night sweats, weight loss, and sometimes pruritus associated with adenopathy. Sympatomatic adenospathy may be noted by the patient or by the doctor on a routine physical examination. Often mediastinal adenopathy is noted on a routine physical examination. Often mediastinal adenopathy is noted on a routine X-ray or film taken because of a persistent , dry, nonproductive cough. The presentations are more common in young people and such patients often have the nodular sclerosing variety of the disease.

13. Squamous -cell carcinoma ( 1653)

Squamous cell carcinoma also arises from the epidermis but shows significant squamous
differentiation and usually keratin production. These tumors have a variable tendency to
metastaize , depending upon their size, extent of invasion, and whether they arise from
a premalignant lesion, a burn scar, a chronic inflammatory condition, or from apparently
normal skin. The typical squamous cell carcinoma is a painless, firm, red nodule or plaque
with visible scales on the surface. Ulceration and crusting may occur

DISORDERS AND/OR ADVERSE REACTIONS - 14. METABOLISM - SUMMARY

Drug Interaction

Indication

Adverse Reaction

Contra-Indications

Dosages/ Overdosage Etc

Other Information

Drug Interaction:

Indication:

Adverse Reaction:

Contra-Indications:

Dosages/ Overdosage Etc:

Other Information:

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