4th year

Cortisol
Adrenal Suppression
 When corticosteroids are administered for more than 2 weeks, adrenal suppression may
occur.
 If treatment extends over weeks to months, the patient should be given appropriate
supplementary therapy at times of minor stress (twofold dose increases for 24-48 hours) or
severe stress (up to tenfold dose increases for 48-72 hours) such as accidental trauma or
major surgery.
 If corticosteroid dosage is to be reduced, it should be tapered slowly.
 If therapy is to be stopped, the reduction process should be quite slow when the dose
reaches replacement levels.
 It may take 2-12 months for the hypothalamic-pituitary-adrenal axis to function properly, and
cortisol levels may not return to normal for another 6-9 months.
 The glucocorticoid-induced suppression is a suprapituitary problem, and treatment with
ACTH does not reduce the time required for the return of normal function.
 If the dose is reduced too rapidly in such patients, the symptoms of the disorder may
reappear or increase in intensity.

Pyrazinamide
 Major adverse effects of pyrazinamide include hepatotoxicity (in 1-5% of patients), nausea,
vomiting, drug fever, and hyperuricemia.

Nevirapine
 Nevirapine levels may increase during coadministration with inhibitors of CYP3A metabolism,
such as cimetidine and the macrolide agents, and decrease in the presence of CYP3A
inducers such as rifabutin and rifampin.

Serum-ascites albumin gradient (SAAG)

 The serum-ascites albumin gradient (SAAG) has supplanted the transudate-exudate model
for categorizing ascites.
 The serum and ascites albumin should be obtained on the same day
 The gradient is calculated by subtracting the ascites albumin from the serum albumin (eg, 3.5
g/dL - 2.5 g/dL = 1 g/dL).
 A calculated SAAG >1.1 g/dL suggests with 97% accuracy that portal hypertension is the
cause of the ascites (for which there are multiple etiologies).
 A calculated SAAG <1.1 g/dL suggests that the pathophysiology of the ascites is not due to
portal hypertension.

Scaphoid
 Boat-shaped; hollowed

Hypoxia
 Hypoxia is O2 deficiency at the tissue level.
 In hypoxic hypoxia and the other generalized forms of hypoxia, the brain is affected first.
 A sudden drop in the inspired PO2 to less than 20 mm Hg, which occurs, for example, when
cabin pressure is suddenly lost in a plane flying above 16,000 m, causes loss of
consciousness in 10-20 seconds and death in 4-5 minutes.
 Less severe hypoxia causes a variety of mental aberrations not unlike those produced by
alcohol: impaired judgment, drowsiness, dulled pain sensibility, excitement, disorientation,
loss of time sense, and headache.
 Other symptoms include anorexia, nausea, vomiting, tachycardia, and, when the hypoxia is
severe, hypertension.
Hypercapnia
 Retention of CO2 in the body (hypercapnia) initially stimulates respiration.
 Retention of larger amounts produces symptoms due to depression of the central nervous
system: confusion, diminished sensory acuity, and, eventually, coma with respiratory
depression and death. In patients with these symptoms, the PCO2 is markedly elevated,
there is severe respiratory acidosis, and the plasma HCO - may exceed 40meq/L.
3

Aura

 Epileptic ictal (Relating to or caused by a stroke or seizure) phenomenon/phenomena

perceived only by the patient

PLEURAL EFFUSION

 It is Excess fluid in the pleural space

 Normally, 10 to 20 mL of fluid is spread thinly over the visceral and parietal pleurae.
 The fluid is similar in composition to plasma except that it is lower in protein ( 1.5 g/dL).
 Pleural fluid enters from the pleural capillaries and exits via parietal pleural stomas and the
lymphatics.
 Pleural effusions are classified as transudates or exudates.
 Transudates are due to elevations in microvascular pressure or to decreases in oncotic
pressure; exudates are due to pleural inflammation (pleurisy), with an increased permeability
of the pleural surface to proteinaceous fluid.
 Lymphatic obstruction may also contribute to accumulation of pleural fluid.
 Many conditions can produce either transudates or exudates
 Hemothorax (blood in the pleural space) occurs most often from trauma and rarely after
rupture of a vessel in a parietopleural adhesion associated with spontaneous pneumothorax
 Chylothorax (a milky or chylous pleural effusion) is caused by traumatic or neoplastic (most
often lymphomatous) injury to the thoracic duct.
 Cholesterol effusion (chyliform or pseudochylous effusion) is rare

Conditions Causing Transudates

1. Heart failure, which increases systemic venous and pulmonary capillary pressures, is the
most common cause of transudative pleural effusions. Usually bilateral, such effusions tend
to be larger on the right side and, if unilateral, are generally right-sided.
2. Hypoalbuminemia may cause pleural effusions, which are usually bilateral and associated
with fluid accumulation elsewhere in the body.
3. Ascites may be associated with pleural effusion because fluid can move from the peritoneal
space into the pleural space through diaphragmatic defects or lymphatic channels
4. In myxedema, pleural effusions are usually transudates but may be exudates.
5. After parturition, small effusions, which clear rapidly, may be seen during the first 24 h.
6. Iatrogenic pleural effusions result when fluid infused through a catheter meant for a
subclavian vein enters the pleural space

Conditions Causing Exudates

1. Mycotic pleurisy produces an exudate, and pleural biopsy may show granulomas
2. In parapneumonic effusions, the visceral pleura overlying pneumonia becomes inflamed;
often, an outpouring of serous exudative fluid accompanies acute pleurisy.
3. Pulmonary embolism produces pleural effusions in 30 to 50% of patients
4. Metastatic neoplasms are the most common cause of exudates in persons > 60 yr. The
most common primary site is the lung, followed by the breast, but carcinomas from any site
can metastasize to the pleura
5. In Hodgkin's disease and non-Hodgkin's lymphoma, pleural effusion is common
6. Malignant mesothelioma (a malignant tumor arising from the pleural mesothelium) is
strongly linked to asbestos exposure
7. Benign fibrous mesothelioma is a rare solid tumor of the pleura that produces chest pain,
dyspnea, fever, and hypertrophic osteoarthropathy in 50% of patients.
8. SLE or drug-induced lupus like syndromes (most often with hydralazine, procainamide,
isoniazid, phenytoin, and chlorpromazine) produces pleural effusions in up to 40% of
patients.
9. Drug-induced pleural effusions are uncommon. Nitrofurantoin is occasionally associated
with an acute febrile illness with pulmonary infiltrates, pleural effusion, and peripheral blood
eosinophilia.
10. Rheumatoid disease causes pleural effusion more often in males even though the disease
is more common in females.
11. Subdiaphragmatic abscess most often produces a sympathetic pleural effusion, a sterile
exudate with neutrophils predominating.
12. Acute pancreatitis is complicated by para-ascitic pleural effusion in about 10% of cases.
13. Pancreatic pseudocysts may burrow into the mediastinum through the aortic or esophageal
hiatus and rupture into one or both pleural spaces.
14. Postcardiac injury syndrome is characterized by fever, pleuropericarditis, and parenchymal
infiltrates beginning weeks after injury to the pericardium or myocardium.
15. Uremia is often complicated by a generalized serositis, and an exudative pleural effusion
may occur with fibrinous pleurisy.
16. Asbestos exposure produces benign pleural effusion in about 3% of asbestos workers after
a latent period ranging from 5 yr to > 30 yr.
17. AIDS causes pleural effusion (usually an exudate) in < 2% of patients.

Bell palsy

DESCRIPTION:
 Paralysis or weakness of the muscles supplied by the facial nerve, typically unilaterally, due
to inflammation and swelling of the facial nerve within the facial canal
 Bell's palsy is an idiopathic facial paresis of lower motor neuron type that has been attributed
to an inflammatory reaction involving the facial nerve near the stylomastoid foramen or in the
bony facial canal.
a) Bell palsy: Idiopathic
b) Ramsay Hunt syndrome: Bell palsy associated with vesicles within the outer ear canal
or behind the ear, due to herpes zoster infection
c) Facial diplegia: The simultaneous development of bilateral Bell palsy is highly unusual
and conditions such as Guillain-Barre syndrome and chronic meningitis should be
considered as possible explanations.

Genetics: There is a familial tendency toward Bell palsy

SIGNS AND SYMPTOMS:

 Sudden onset or onset over days
 Unilateral total or partial paralysis of the facial muscles
 Mild "numbness" on the affected side
 Ipsilateral inadequate tear production; ipsilateral tearing
 Ipsilateral loss of taste
 Ipsilateral ear ache
 Ipsilateral exaggerated sound
 Ipsilateral loss of corneal reflex

CAUSES:
Bell palsy
 Inflammation of the facial nerve within the facial canal
 Exposure to cold
 Probably viral
Ramsay Hunt syndrome
 Herpes zoster
 Rarely Herpes simplex
Diabetes mellitus

RISK FACTORS:
 Age over 30
 Exposure to cold
 Diabetes
 Pregnancy
 Upper respiratory infection (coryza, influenza)

Respiratory acidosis

 Respiratory acidosis results from decreased alveolar ventilation and subsequent

hypercapnia. Pulmonary as well as nonpulmonary disorders can cause hypoventilation.

Symptoms and Signs

 With acute onset, there is somnolence and confusion, and myoclonus with asterixis may be
seen.
 Coma from CO2 narcosis ensues.
 Severe hypercapnia increases cerebral blood flow and cerebrospinal fluid pressure.
 Signs of increased intracranial pressure (papilledema, pseudotumor cerebri) may be seen.

Widal test

 The Widal test is problematic.

 It measures the titer of agglutinating serum antibodies against the O and H antigens of S.
typhi.
 In untreated disease, only one-half to two-thirds of patients have a four-fold or greater
increase in titer of agglutinins against typhoid O antigen.
 Antimicrobial therapy interferes with immunologic response.
 Moreover, the Widal test is not specific.
 Serologic tests (Widal reaction) are not as useful as cultures because both false-positive and
false-negative results occur.
 A fourfold rise in titer of O (somatic) agglutinins is suggestive but not diagnostic of infection.

Aspirin

 Aspirin (the prototype of the salicylates) is a nonsteroidal anti-inflammatory agent (NSAIA)

and also exhibits antithrombotic, analgesic; and antipyretic activity.
 Aspirin is used extensively in the treatment of mild to moderate pain, fever, and inflammatory
diseases.
 Aspirin is also used in the prevention of arterial and possibly venous thrombosis.
 Aspirin affects hemostasis. Single low doses of aspirin (about 80 mg daily) produce a slightly
prolonged bleeding time, which doubles if administration is continued for a week
 The antiplatelet action of aspirin contraindicates its use by patients with hemophilia.

Pleurodesis

 The creation of a fibrous adhesion between the visceral and parietal layers of the pleura, thus
obliterating the pleural cavity; it is performed surgically by abrading the pleura or by inserting
 a sterile irritant into the pleural space, and applied as treatment in cases of malignant pleural
effusion, recurrent spontaneous pneumothorax, and chylothorax.
 Bleomycin is used by intracavitary injection as a sclerosing agent for the management of
pleural effusions and for prevention of recurrent pleural effusions caused by metastatic
tumors
 surgical insertion of a thoracostomy tube with subsequent intrapleural instillation of a
sclerosing agent generally is considered the treatment of choice for such effusions
 When instilled into the pleural space, sclerosing agents cause inflammation that results in
fibrosis and adherence of serosal surfaces (pleurodesis), thereby obliterating the pleural
space and reducing the chance of fluid reaccumulation
 Bleomycin appears to be at least as effective as and possibly better tolerated than
tetracycline in the treatment of these effusions.

Tube thoracostomy

 Insertion of a tube into the pleural space through a small incision.

 Chest tube insertion and drainage is commonly used for spontaneous or traumatic
pneumothorax involving > 25%collapse or enlargement, especially if it causes respiratory
distress or a serious gas exchange abnormality; for massive or recurrent benign pleural
effusions not responding to thoracentesis; for empyema; for hemothorax; and for malignant
effusions
 Complications include hemorrhage from intercostal vessel injury, subcutaneous emphysema,
injury due to a malpositioned tube (e.g. into the major fissure, and occasionally into the lung),
and local infection or pain.
 Reexpansion pulmonary edema due to increased capillary permeability may occur in the
reexpanded lung, especially after prolonged lung collapse and rapid reinflation.
 Tube insertion may be difficult because of adhesions or a very thick pleura. .
 Other problems include inadequate drainage of the pleural space due to clots or gelatinous
inflammatory material and plugging or kinking of the tube.

Kaposi sarcoma

 Kaposi's sarcoma (KS) is a malignant, vascular tumor characterized by purple macules,

papules, or nodule, usually on the lower legs
 A neoplasm characterized by vascular tumors of skin and viscera
 The etiology of Kaposi's sarcoma is likely related to the human herpesvirus-8, which is found
in most cases of KS.KS has also been reported in all organs of the body except the brain.
 The lesions typically appear as violaceous or erythematous macules with associated
cutaneous edema.
 KS cannot now be cured, so it is a lifelong problem.
 Its primary treatment is antiviral therapy of the HIV infection itself.
 Kaposi associated with HIV infection (epidemic): Skin lesions widely disseminated, on the
face, arms and trunk, Lesions on mucous membranes, Lesions in lymph nodes, Lesions in
viscera and Immunosuppression of host is important co-factor in development of KS

Herpes Zoster

 Herpes zoster is a neurocutaneous disease caused by the reactivation of varicella-zoster

virus (VZV) from a clinically latent state in dorsal sensory or cranial ganglia.
 VZV reactivation preferentially affects elderly persons and usually results in dermatomal pain
and a vesicular skin eruption.
 The other strong risk factor for zoster is cellular immune dysfunction.
 Other potentially important but less well-established risk factors include physical trauma,
radiation therapy, psychologic stress, and white race
 VZV causes primary infection when it invades the respiratory tract of a VZV-naive individual.
From the respiratory tract, VZV disseminates in the blood and infects the skin, causing the
rash of chickenpox. During this time, VZV also infects dorsal sensory and cranial nerve
ganglia where it establishes a latent, lifelong infection.

Cerebrospinal fluid

 In humans, the volume of CSF is about 120-150mL and the rate of CSF production is about
550mL/d.
 Thus the CSF turns over about 3.7 times a day.
 The meninges and the CSF protect the brain
 When the head receives a blow, the arachnoid slides on the dura and the brain moves, but
its motion is gently checked by the CSF cushion and by the arachnoid trabeculae.
 Diagnosis of meningitis.
 The CSF must he examined as soon as possible whenever meningitis is suspected, even if
there is some clinical evidence of increased in tracranial pressure, for this is the only
means by which the diagnosis can be established and the causal agent identified. The CSF
is usually turbid and may be distinctly purulent.
 Microscopic examination shows it to contain numerous neutrophil leucocytes.
 The protein content is raised and the sugar reduced or absent
 The causal organisms are often apparent, although in some cases they can be detected
only by culture.

Splenomegaly

 Participation of the spleen in immune responses involves hyperplasia of the Malpighian

bodies, often with formation of germinal centres and also accumulation of plasma cells
throughout the red pulp.
 These changes alone are, however, seldom sufficient to cause significant splenic
enlargement and, apart from the lymphoid neoplasias, splenomegaly is usually due to
enlargement of the red pulp.
 The major categories of splenomegaly are as follows.
1. Infections and granulomatous conditions.
2. Congestive splenomegaly.
3. Diseases of the blood and bone marrow.
4. Lipid storage diseases.
5. Amyloid disease.
6. The lymphomas.

Infections
 Because of its vascular nature and phagocytic role, the spleen is exposed to blood-borne
infection: it has, however, strong defences against pyogenic bacteria, and abscess formation
is uncommon except for septic infarcts in pyaemia
 However, bacteria are commonly arrested in the spleen and may be recovered from it in non
pyogenic generalised infections, as in typhoid fever, brucellosis and generalised tuberculosis.
 Significant splenomegaly is not usual in acute viral infections, but an exception is infectious
mononucleosis, in which it is often palpable.
 Colonisation of the spleen with enlargement is brought about also by trypanosomes, and by
micro-organisms which are capable of survival and multiplication within macrophages, as in
leishmaniasis, histoplasmosis and brucellosis.
 The spleen is also enlarged in malaria, in which it is an important site of destruction of the
infected red cells.
 Acute pyogenic infections
 Non-pyogenic bacterial infections
 In typhoid fever, splenic enlargement is an important feature, the weight sometimes reaching
500 g; the spleen is deep red from congestion and firm
 Undulant fever is due to infection with small Gram-ve bacilli, the Brucellae.
 Tuberculosis. In acute miliary tuberculosis the tubercles are especially numerous in the
spleen. They generally appear as minute grey points about the size of Malpighian bodies,
 Sarcoidosis. The spleen is commonly involved in sarcoidosis,
 Protozoal infections- In malaria the spleen swells acutely during each attack of pyrexia, due
to the accumulation of red cells containing the parasites.
 The spleen is greatly enlarged in the tropical splenomegaly syndrome which appears to be
caused mainly by chronic falciparum malaria.
 Kala-azar is the generalised (visceral) type of leishmaniasis, in which there is widespread
colonisation of macrophages by the leishmanial form of the protozoon, Leishmania donovani
Splenomegaly occurs also in early trvpanosomiasis and in disseminated histoplasmosis, but
is not an important feature of these conditions.

Congestive splenomegaly
 This results from a persistent rise in pressure in the splenic vein.
 The most important causes are systemic venous congestion in right heart failure and portal
hypertension most commonly due to hepatic cirrhosis or the ‘pipestem’ hepatic fibrosis of
schistosomiasis
 Less commonly it results from occlusion of the hepatic or portal veins by thrombosis, tumour,
etc.
 Congestive splenomegaly in portal hypertension is the commonest cause of hyperspplenism

Haematological disorders
 Numerous abnormalities of the red cells, as for example in various types of hemolytic and
rnacrocvtic anemia’s, are accompanied by an increased rate of their destruction in the spleen
and as a consequence there is a great increase in the number of macrophages in the red
pulp.
 The degree of splenomegaly depends on the severity and duration of the process, and is due
mainly to engorgement of the red pulp with red cells.
 Similarly, in idiopathic thrombocytopenic purpura there is increased splenic destruction of the
antibody-coated platelets, although splenomegaly is usually absent or slight.
 The spleen may become greatly enlarged in conditions in which the bone marrow is
extensively replaced, e.g. in myelofibrosis or secondary carcinoma (particularly of the
prostate): the enlargement is due to extramedullary haemopoiesis and the spleen is firm and
red or pink, sometimes with deeper red patches
 Splenomegaly is a feature of leukaemia.
 Great enlargement occurs in chronic granulocytic and sometimes in chronic lymphocytic
leukaemia.
 In acute leukaemia, enlargement is usually moderate.
 In summary the haematological disorders accompanied by great splenomegaly, i.e. to about
2 kg are chronic myeloid leukaemia, myelofibrosis and sometimes chronic lymphocvtic
leukaemia.
 Moderate splenomegaly, up to about 1 kg, occurs in acute leukaemia, various haemolytic
anaemias and polycythaemia rubra vera.

Disorders involving lipid storage

 Storage of lipids in macrophages occurs in human disease in two groups of conditions.
(a) The hyperlipidaemias include the familial forms of hyperchylomicronaemia
(b) Various rare hereditary lipid storage diseases, such as Gaucher’s disease and
Niemann-Pick disease, in which the lipid storage becomes excessive in various tissues
and the enlargement of the spleen is very great.
Amyloid disease
 The spleen is commonly involved in generalised amyloidosis.
 Deposition may be mainly in the Malpighian bodies, which are changed to translucent
rounded patches— sago spleen—or there may be diffuse involvement of the red pulp, in
which case the spleen is most often enlarged, sometimes to over 1 kg.

Tumours
 Malignant lymphomas. As in the lymph nodes, the commonest forms of primary neoplasia in
the spleen are the various malignant lymphomas
 Metastatic tumours. Splenic metastases occur more frequently in sarcoma than in carcinoma,
 Benign tumours of the spleen, including fibroma, myoma, haemangioma and lymphangioma
have been described, but all are rarities.
 Cysts of the spleen are occasionally seen.
 Angio-immunoblastic lymphadenopathy is an uncommon cause of generalised lymph node
enlargement, occurring usually in old people, and accompanied by hepatosplenomegaly,
cutaneous rashes, polyclonal hypergammaglobulinaemia and sometimes auto-immune
haemolytic anaemia.

Warfarin
 Warfarin sodium and other coumarin anticoagulants act by inhibiting the synthesis of vitamin
K dependent clotting factors, which include Factors II, VII, IX and X, and the anticoagulant
proteins C and S
 An anticoagulation effect generally occurs within 24 hours after drug administration.
 However, peak anticoagulant effect may be delayed 72-96 hours.
 The duration of action of a single dose of racemic warfarin is 2-5 days
 Warfarin sodium is used for prophylaxis and treatment of venous thrombosis and its
extension, prophylaxis and treatment of pulmonary embolism, prophylaxis and treatment of
thromboembolic complications associated with atrial fibrillation and/or cardiac valve
replacement, and as an adjunct in the treatment of coronary occlusion.
 The drug also is used to reduce the risk of death, reinfarction, and thromboembolic events
such as stroke or systemic embolization following myocardial infarction.

Heparin
 Heparin, an anionic, sulfated glycosaminoglycan anticoagulant present in mast cells, acts as
a catalyst to markedly accelerate the rate at which antithrombin III (heparin cofactor)
neutralizes thrombin and activated coagulation factor X (Xa).
 Heparin is used for prophylaxis and treatment of venous thrombosis and its extension;
prophylaxis of postoperative deep-vein thrombosis and pulmonary embolism in patients
undergoing major abdominal or thoracic surgery who are at risk for thromboembolism;
prophylaxis and treatment of pulmonary embolism; treatment of embolization associated with
atrial fibrillation and/or prosthetic heart valve replacement; diagnosis and treatment of acute
and chronic consumptive coagulopathies (disseminated intravascular coagulation); and in
prophylaxis and treatment of peripheral arterial embolism.

Ptosis

 Ptosis-a droopy upper lid-may be congenital or acquired but is usually congenital in children
owing to a defective levator muscle.
 Other causes of ptosis are myasthenia gravis, lid injuries, and third nerve palsy.
 Ptosis may be associated with astigmatism and amblyopia.
 Neurologic causes of ptosis include Horner's syndrome, in which the pupil is constricted, and
third nerve palsy, in which there are abnormalities of eye movements and the pupil may be
dilated.
 Myasthenia gravis is always considered; pupils are normal.
D-Xylose test

 A D-xylose absorption test is an indirect but relatively specific measure of proximal small-
bowel absorption.
 Abnormal findings are usual in primary jejunal disease but rare in other causes
 D-Xylose 5 g po is given to the fasting patient, and urine is collected for the next 5 h.
 This dose is slightly less sensitive than a larger (25-g) dose but does not cause nausea or
diarrhea.
 Provided that urine output is adequate and the GFR is normal, < 1.2 g of D-xylose in the 5-h
collection is considered abnormal, and 1.2 to 1.4 g is considered borderline.
 To check the integrity of the small intestinal mucosal, perform a D-xylose test.
 D-xylose is a 5-carbon pentose sugar that is absorbed across the intact intestinal mucosal.
 A 25-g dose is given orally, followed by a 5-hour urine collection, and a 2-hour post ingestion
serum level.
 A normal individual will secrete more than 5 g of D-xylose in the urine, and have D-xylose
present in the serum sample.
 If an abnormally low level of D-xylose is found in the urine or serum, endoscopy of the small
intestine with mucosal biopsies and aspiration for cultures should be performed to exclude
mucosal disease or bacterial overgrowth.
 If the D-xylose test is normal, consider a pancreatic cause for the malabsorption
 A variant of this is the D-xylose test.
 In this test, D-xylose is given orally, usually in a dose of 25 g.
 Blood xylose concentration is measured after 1 and 3 hours and urinary excretion is
measured for 5 hours after ingestion.
 Failure of blood xylose levels to rise above 20 mg/100mL at 1 hour and above 22.5
mg/100mL at 3 hours or failure of urinary output to exceed 5 g/5 h suggests malabsorption.
 For any of these oral tolerance tests a finding of malabsorption suggests mucosal
dysfunction because none of these sugars depends on pancreatic enzymes or bile acids for
absorption.

Nystagmus

 Nystagmus is an involuntary rhythmic to-and-fro movement of the eyes.

 Jerk nystagmus is characterized by a slow-phase eye movement in one direction mediated
by the smooth pursuit system followed by a quick-phase eye movement in the reverse
direction mediated by the saccadic system.
 Pendular nystagmus is characterized by equal-velocity eye movements in both directions.
 The features by which nystagmus is classified include waveform character, direction of the
quick phase, periodicity, and changes in amplitude as a function of gaze direction.
 Some forms of nystagmus are physiologic (optokinetic nystagmus, endpoint nystagmus,
vestibular jerk nystagmus), whereas others are pathologic.

Meningism

 A condition in which the symptoms simulate as meningitis, but in which no actual

inflammation of these membranes is present.

Fluoroquinolones

 e.g. ciprofloxacin, levofloxacin, enoxacin, lomefloxacin, ofloxacin, and pefloxacin

 Quinolones block bacterial DNA synthesis by inhibiting bacterial topoisomerase II (DNA
gyrase) and topoisomerase IV.
 Inhibition of DNA gyrase prevents the relaxation of positively supercoiled DNA that is
required for normal transcription and replication.
 Fluoroquinolones may damage growing cartilage and cause an arthropathy.
 Thus, they are not routinely recommended for use in patients under 18 years of age.

Leukodystrophy

 Term for a group of white matter diseases, some familial, characterized by progressive
cerebral deterioration usually in early life, and pathologically by primary absence or
degeneration of the myelin of the central and peripheral nervous systems with glial reaction;
probably related to a defect in lipid metabolism; most leukodystrophies are autosomal
recessive, several X-linked recessive, and a few autosomal dominant

Beta-Adrenoceptor Blockers

 Propranolol and similar drugs have antiarrhythmic properties by virtue of their beta receptor-
blocking action and direct membrane effects.
 Beta-blockers are correctly considered dangerous in patients with severe congestive heart
failure because they may precipitate acute decompensation of cardiac function.
 Evidence for this paradoxic effect began to appear many years ago but was initially
considered to be limited to patients with diastolic dysfunction or cardiomyopathies, in whom
slowing of cardiac rate and contraction velocity could improve cardiac output
 Studies with bisoprolol, carvedilol, and metoprolol have shown a reduction in mortality in
patients with stable class II and class III heart failure

Beck’s triad [acute compression triad]

 The rising venous pressure, falling arterial pressure, and decreased heart sounds of
pericardial tamponade.
Classic presentation of cardiac tamponade
1. Hypotension
2. Jugular venous distention (JVD) -JVD may be absent in hypovolemic patients
(distended neck veins)
3. Muffled heart sounds (distant heart sounds)

Phenobarbital

 Phenobarbital is a barbiturate anxiolytic and sedative

 Phenobarbital should be withdrawn slowly in order to avoid precipitating seizures or status
epilepticus.
 The drug is also used in the prophylactic management of epilepsy.

Nocturnal dyspnea

 It is a dyspnea occurring at night, several hours after assuming recumbent position.

 Occurs in heart failure and results from reabsorption of water from dependent areas after
removal of effect of gravity, causing hypervolemia, aggravating left-ventricular failure.

Paroxysmal nocturnal dyspnea

 It is an acute dyspnea appearing suddenly at night, usually waking the patient from sleep;
caused by pulmonary congestion with or without pulmonary edema those results from left-
sided heart failure following mobilization of fluid from dependent areas after lying down.

Pitting edema
 It is an edema that retains for a time the indentation produced by pressure.

Rale

 Ambiguous term for an added sound heard on auscultation of breath sounds; used by some
to denote rhonchus and by others for crepitation. SYN: crackle.
 Bubbling rale is a moist sound heard through the stethoscope as a result of air entering
portions of lung tissue containing exudate and thus creating bubbles; sometimes associated
with resolving pneumonia or small lung cavities.
 Crackling rale are very fine sounds produced by fluid in very small airways in pneumonia or
congestive heart failure.

Bonnier syndrome

 It is a syndrome due to a lesion of Deiters nucleus and its connection; the symptoms include
ocular disturbances (e.g., paralysis of accommodation, nystagmus, diplopia), as well as
deafness, nausea, thirst, anorexia, and symptoms referable to the involvement of the vagus
centers.

Niacin

 Niacin (nicotinic acid) is a water-soluble, B complex vitamin that is used as an antilipemic

agent.
 Niacin deficiency (prophylaxis and treatment)-Niacin and niacinamide are indicated for
prevention and treatment of vitamin B 3 deficiency states.
 Vitamin B 3 deficiency may occur as a result of inadequate nutrition or intestinal
malabsorption but does not occur in healthy individuals receiving an adequate balanced diet.
 Deficiency of niacin may lead to pellagra
 Hyperlipidemia (treatment)-Niacin (but not niacinamide) is also indicated in the treatment of
hyperlipidemia.
 Niacin is recommended for use only in patients with primary hyperlipidemia (type IIa, IIb, III,
IV, or V hyperlipoproteinemia) and a significant risk of coronary artery disease who have not
responded to other measures alone.
 It is one of the drugs of first choice for initiating therapy to reduce low density lipoprotein
(LDL) - cholesterol concentrations and triglycerides, and to increase high density lipoprotein
(HDL) - cholesterol concentrations