In systemic sclerosis, fibrosis causes massive dermal expansion and obliteration of hair follicles, sweat glands, and other

appendages (Smooth, shiny, pigmented and indurated skin). Collagen fibre accumulation is prominent in reticular dermis, and the fibrotic process invades the subjacent adipose layer with entrapment of fat cells. The epidermis is atrophic, and the rete pegs are effaced. Euthyroid sick syndrome can be detected as early as 2 hours after the onset of stress. The initial value that most commonly leads to further work-up is an elevated TSH (but, occasionally TSH can be low as well). The most commonly identified abnormality is low serum total T3. D-xylose absorption assay assesses the duodenum/jejunum. The only clinical conditions in which absorption is increased are hemochromatosis and Wilsons disease. Steatorrhea is excretion of >6% of dietary fat intake. Pneumonia is the most common opportunistic infection and clinical presentation of AIDS. Pneumocystis pneumonia constitutes 40% of all AIDS-defining illness. HIV patients are predisposed to Tuberculosis at any stage (no relationship with CD4 Count). It is not an AIDS defining illness (as far as I remember!!). While atypical mycobacterial infections occur at a CD4 count <50/mm3. 90% of AIDS patients will develop an oral/oesophageal condition. In pancreatitis during AIDS, suspect antiretroviral drugs {DDI (didanosine), or DDC (zalcitabine) which are both reverse transcriptase inhibitors}. Pentamidine which is used as a prophylaxis against PCP can also cause pancreatitis. Acute self-limiting lymphocytic meningitis may occur at the time of seroconversion. Chronic neurological syndromes or opportunistic infections occur later in the course of HIV infection. Diseases of hepatobiliary system are a major problem in HIV patients. HIV is associated with approximately a threefold increase in the development of persistent HepB surface antigenemia. Patients infected with both HBV and HIV have decreased evidence of inflammatory liver disease. Therefore, one may see a development of severe hepatitis following the initiation of effective anti-HIV therapy. IFN-alpha is less successful in the treatment of HBV in patients with HIV co-infection. Lamivudine, emtricitabine, or adefovir/tenofovir and entecavir alone or in combination are useful in the treatment of hepatitis B in patients with HIV infection. It is important to remember that all the above-mentioned drugs also have activity against HIV and should not be used as single agents in patients with HIV infection, in order to avoid the rapid development of resistant quasispecies of HIV. Didanosine can cause neuropathy and zidovudine can cause myopathy. AIDS dementia complex is the most frequent neurological condition of HIV infection, and is directly caused by the virus. Primary processes related to HIV infection of the nervous system are reminiscent of those seen with other lentiviruses, such as the Visna-Maedi virus of sheep. Cerebral toxoplasmosis is the most common CNS infection (90% of focal lesions) in AIDS patients. It occurs in 10% of AIDS patients. Retinitis can also be caused directly by the HIV itself. 30% of patients with cutaneous Kaposis sarcoma also have gastrointestinal involvement. Marked seborrhoeic dermatitis can occur during seroconversion of HIV illness. Atazanavir is a new protease inhibitor which has no effect on lipids. All protease inhibitors can cause diabetes, hypertriglyceridemia and hypercholesterolemia (except atazanavir), central adiposity, buffalo hump, peripheral fat loss (lipodystrophy syndrome).

 Coronary artery disease, end-stage liver failure (due to co-infection with hepatitis B and C) and malignancy (lymphoma) are now common causes of death in patients with HIV/AIDS. Serum ferritin is one the acute phase proteins, so like CRP, fibrinogen and immunoglobulins it is increased in inflammatory illness. If the ESR is increased then the serum ferritin may not be an accurate reflection of iron stores. It is also released from damaged hepatocytes, so it is falsely elevated in transaminits. Iron staining of bone marrow aspirate is the gold standard to diagnose iron deficiency state. It is usually not done because of its invasive nature (but gold standard!!) Hemolytic anemias usually cause macrocytic picture. HUS usually occurs in children while TTP occurs in adults. Polychromasia refers to variation in erythrocyte coloration. This variation is usually due to variation in RBC maturation as the younger forms will appear bluer. Increases in polychromasia suggests an increased bone-marrow response. Most cases of TTP arise from inhibition of the enzyme ADAMTS13, a metalloprotease responsible for cleaving large multimers of von Willebrand factor (vWF) into smaller units. Current therapy is based on support and plasmapheresis to reduce circulating antibodies against ADAMTS13 and replenish blood levels of the enzyme. Unlike in DIC, TTP/HUS has normal tests of coagulation (but not the platelet count). Gauchers (pronounced as Goshez!!) disease is the most common lysosomal storage disease. Neutropenia for more than 3 months is known as chronic neutropenia. In Blacks and Arabs, mild neutropenia is a normal feature. A promyelocyte is a granulocytic precursor, developing from the myeloblast and developing into myelocyte. Unlike the myeloblast, the promyelocytes cytoplasm contains large black or purple granules. Nucleoli may be present. A myelocyte is smaller than the myeloblast or the promyelocyte. Unlike the myeloblast and promyelocyte, the myelocytes cytoplasm contains specific granules, i.e., brick red (eosinophils), large, blue-black granules (basophils), and lilac granules (neutrophils). Nucleus still has a round or oval shape and no nucleoli are present. Band cells (may be neutophilic, eosinophilic or basophilic) account for 0 to 5% of the total leucocytes count in circulating blood of an adult. Auer Rods are classically seen in myeloid blasts of M1, M2, M3, and M4 acute leukaemia. Early CLL is usually not treated and the patients usually live in peace for many years and usually die of some other unrelated conditions. Late CLL may be treated with chemotherapy (oral chlorambucil or fludarabine) and immunotherapy. Only mantle cell lymphoma and typical B cell CLL are usually CD5 positive. Cryoglobulins may be present in Mycoplasma pneumonia, multiple myeloma, MGUS, certain leukaemia, some autoimmune diseases, such as SLE and RA. They are found in 35% of Hepatitis C infections. Although polycythemia refers to increased in all types of cells in the blood (see poly cellemia, i.e., RBC, WBC and platelets), yet most of the time, it is used in place of erythrocythemia. Similarly in polycythemia vera, all types of cells are increased. Thrombophilia testing in case of arterial thrombosis is usually unrewarding, unless done in very young patients. Thrombophilia screening is recommended in patients <40 years of age (for venous thrombosis) and <30 years of age (for arterial thrombosis). Recurrent thrombosis, familial tendency and unusual site of thrombosis also warrant thrombophilia testing.

 Monoclonal cryglobulins are usually associated with haematological conditions, whereas mixed cryoglobulins are found in many infectious and systemic disorders. Rheumatoid arthritis without rheumatoid factor is known as seronegative rheumatoid arthritis. Rheumatoid factor may also be a cryoglobulin; it can either be type 2 (monoclonal IgM to polyclonal IgG) or type 3 (polyclonal IgM to polyclonal IgG) cryoglobulin. Negative acute phase reactants are the proteins whose concentrations decrease during inflammation. The examples are albumin, pre-albumin, transferrin, etc. CRP (C-reactive protein) was so named because it reacted with the C polysaccharide of Pneumococcus. CRP binds to phosphocholine on microbes. It is thought to assist in complement binding to foreign and damaged cells and enhances phagocytosis by macrophages, which express a receptor for CRP. It is also believed to play another important role in innate immunity, as an early defence system against infections. The life time risk of schizophrenia is almost equal in women and men (around 1%), but men consistently have an earlier age of onset. In clinical practice, Schneiders First Rank Symptoms occur in 70% of Schizophrenic (NOT 100%) patients. These symptoms can also occur in almost 10% manic patients. Tardive dyskinesia occurs in >30% patients on traditional antipsychotics for long. Positive symptoms respond better than negative symptoms to antipsychotic therapy; the atypical antipsychotics are probably better for negative symptoms (IT STILL MEANS THAT POSTIVE SYMPTOMS ARE BETTER CONTROLLED!!). The genetic contribution to mood disorder is strongest for bipolar disorders. An expansive mood is a lack of restraint in expressing ones feelings, frequently with an overvaluation of ones significance or importance (easily irritated and annoyed). Biological symptoms in depression (e.g., diurnal variation, insomnia, weight loss, etc) are especially important because their presence predicts response to physical treatments. They are also known as somatic, endogenous or melancholic symptoms. If physical symptoms of depression are present then physical treatment is indicated, whatever the apparent pschosocial precipitant. In generalized anxiety disorder, patient never returns to a baseline level of zero anxiety. There is a large overlap in Obsessive Compulsive Disorder with depressive disorder, and the two conditions often coexist: 30% of patients with OCD have associated depression while 25% of patients with depression have obsessions. Anorexia nervosa is a deadly disease (Jaanlewa patloo panaa!!). The long term outcome is poor, with only 20% making a full recovery (means that 80% will remain thin!!). The long-term mortality is around 15-20% (Jaanlewaa hai!!). Bulimia nervosa is not unrelated to anorexia nervosa. About one-third of bulimia nervosa patients have a previous history of anorexia nervosa and in this category the outcome is worse. Bulimia nervosa patients are not low weight (i.e., loss of >15% average body weight) as compared to anorexia nervosa. Just behaviour of self-vomiting is not a characteristic of bulimia; it may be present in anorexia nervosa (bulimic type). Therefore, if a girl induces vomiting and has lost >15% of average body weight; she is having anorexia nervosa bulimic type (not bulimia nervosa!!). Bulimia nervosa patients dont hate food. They actually have persistent preoccupation with eating and an irresistible craving for food. But they are preoccupied with fattening effects of the food and therefore vomit out their food (not only vomiting!! They can also practise the

following: periods of starvation, purgative/diuretic abuse, appetite suppressants, thyroid hormone abuse, neglect to use insulin, etc). They want to enjoy the food but hate foods calorific values. Although anorexia nervosa patients are thin but they are usually prone to get hypercholesterolemia and carotinemia. Non-fatal deliberate self-harm is a strong risk factor for eventual completed suicide (10-20% will eventually commit suicide). Actually 20% of these persons will repeat within one year. Features that raise the possibility of an organic disorder in psychiatric presentations include visual perceptual abnormalities (illusions or hallucinations), cognitive deficit clearly preceding other symptoms, neurological symptoms and fluctuating symptoms. EEG tests for delirium are sensitive but not specific; results may be abnormal (slowing of rhythm, low voltage trace) in the absence of clear cognitive abnormalities. Abulia is a lack of desire to carry out an action, while apraxia is a lack of ability to carry it out. Alzheimers disease is more common in females. But multi-infarct dementia is more common in males. Presenting symptoms in multi-infarct dementia are more likely emotional (NOT COGNITIVE!!). Virtually 100% of patients with Addisons disease have psychiatric features. Narcolepsy onset is typically between the age of 10 and 20 years. First degree relatives of narcolepsy have 40 times increased risk of getting it. In narcolepsy, REM sleep occurs at the onset of nocturnal sleep. Daytime attacks also consist of periods of REM sleep occurring out of context. Antipsychotics have immediate sedative action but the antipsychotic action may be delayed for three weeks. Atypical antipsychotics (clozapine, olanzapine and, to a lesser extent, risperidone) are linked to hyperglycaemia, impaired glucose tolerance and occasionally to fatal diabetic ketoacidosis. Typical antipsychotics can lower seizure threshold and can prolong QTc. Abrupt cessation of paroxetine is infamous to cause a discontinuation syndrome with flu-like symptoms, dizziness and insomnia. The British National Formulary (BNF) recommends use of benzodiazepines for only 2-4 weeks. PEFR (Peak Expiratory Flow Rate) reflects central airway obstruction and therefore, is most useful in asthma. This is also why it may underestimate disease severity in COPD (more distal obstruction!!). Less than 50% of the usual or normal PEFR indicates medical emergency (severe airway narrowing). Normal Flow-Volume loop is triangle sitting on a semicircle. The p50 (the partial pressure of oxygen, pO2, at which haemoglobin is 50% saturated) is 26 mmHg. In chronic asthma structural changes (including thickening of the basement membrane, goblet cell hyperplasia and hypertrophy of smooth muscle) develop and ultimately lead to irreversible fibrosis of the airways. Leukotriene receptor antagonists may be particularly useful in Exercise-induced asthma, and in patients with Aspirin sensitivity. Long-term prognosis in COPD is determined by post-bronchodilator FEV1. Low birth weight and low socioeconomic status also predispose to development of COPD.

 Alpha1-antitrypsin deficiency causes panacinar emphysema which is more marked in the bases. Doxapram is a stimulant of chemoreceptors in the carotid bodies, which in turn stimulates the respiratory centre in the brainstem. Administered intravenously, doxapram stimulates an increase in tidal volume, and respiratory rate. It is sometimes used in type II respiratory failure (especially in patients who have taken excessive doses of drugs such as buprenorphine which may fail to respond adequately to treatment with naloxone). CURB-65 score of three or more is regarded as severe community acquired pneumonia and it indicates high mortality. Treatment for up to 21 days is recommended for Legionella pneumonia. Hospital-acquired pneumonia (HAP) or Nosocomial pneumonia refers to any pneumonia contracted after at least 48-72 hours of being admitted to a hospital. This is the second most common nosocomial infection (after Urinary Tract Infection). Lung abscesses are usually suspected when patient is slow to recover from pneumonia. Bronchiectasis is more commonly seen in upper lobes in patients affected with ABPA, Cystic Fibrosis, Sarcoidosis and Tuberculosis. HRCT is diagnostic in >90% of patients with bronchiectasis (not 100%!!). Inflammatory Bowel Diseases (Ulcerative colitis) is associated with bronchiectasis. Cystic Fibrosis: In the sweat glands there is a failure to reabsorb chloride and in the airway there is failure of chloride secretion. Bronchiectasis is predominantly in the upper lobes in Cystic Fibrosis (see point no. 89). Asbestos pleural plaques usually occur 20 or more years after low-density exposure. Patients with all of the asbestos-related diseases (except the presence of only pleural plaques) are entitles to state compensation and a disability pension (in the UK). Silicosis causes eggshell calcification around enlarged hilar lymph nodes. Byssinosis symptoms are worse on the first day back after a break from work, and include chest tightness, cough, dyspnea, and wheeze. There is a progressive decline in the FEV1 during the working shift, most marked on the first day of the week. The most common occupational lung disease nowadays is Occupational Asthma. This type of asthmas symptoms may even persist despite termination of exposure. Once occupational asthma has developed, bronchospasm may be precipitated by other non-specific triggers such as cold air, exercise, etc. Reactive Airway Dysfunction Syndrome (RADS): This denotes the development of a persistent asthma-like condition with airway hyperresponsiveness developing in a previously healthy, asymptomatic individual within 24 hours of a single exposure to concentrated respiratory irritants. It is a chronic asthma-like syndrome resulting from a single, acute exposure to a respiratory irritant (e.g., high concentration of irritant gas, aerosols or particles). RADS is new-onset (within 24 hours!!), irritant-induced, non-allergic asthma. The patient has a documented absence of preceding respiratory complaints. Consider this -- > A non-smoker, healthy adult male develops asthma-like symptoms after few hours of being rescued from a house-fire where he got exposed to heavy smoke and (mind you!!) these symptoms persist even later on. A similar entity called Irritant Induced Asthma (IIA) occurs following multiple exposures to lower concentrations of irritants.

 Hypersensitivity pneumonitis are usually IgG mediated (not IgE!!). Actually, the demonstration of specific IgG antibodies in the serum against the identified antigen is usually required for concrete diagnosis. Corticosteroids may be helpful in acute cases of hypersensitivity pneumonitis but once established fibrosis develops, steroids may not be useful. Hypersensitivity pneumonitis is usually due to type III hypersensitivity reaction (sometimes type IV reaction). Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it isn't restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi. Hypersensitivity pneumonitis may manifest, histologically, as usual interstitial pneumonia, i.e. it looks like idiopathic pulmonary fibrosis under the microscope; however, certain features may suggest it is a hypersensitivity pneumonitis. UIP does not typically have multinucleated giant cells, nor does it typically have a centrilobular distribution; the presence of these features suggest the diagnosis of hypersensitivity pneumonitis. The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help. This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated. Thus, a lung biopsy, in some cases, may make a decisive difference. Wheezing may not be a feature of hypersensitivity pneumonitis (remember it is basically a restrictive disorder). One more thing -- > no eosinophilia is observed (it is not a type I allergic reaction, actually it is type III or IV). 20% of smokers will develop lung cancers (in the UK). If we look from other side - -> Over 90% of the lung cancer patients have history of smoking. Lung cancer is seen more frequently with: Cryptogenic Fibrosing Alveolitis and Systemic Sclerosis. C-ANCA is present in 90% of cases with Wegeners granulomatosis. Chronic Eosinophilic pneumonia: Reverse Bat-Wing appearance (photonegative of pulmonary edema). In general, the pleural line is convex towards the lateral chest wall in pneumothorax, whereas a large bulla tends to be concave towards the lateral chest wall. Histiocytosis is frequently associated with Diabetes Insipidus, even after several years of diagnosis and successful therapy. About 80% of people with rheumatoid arthritis have detectable Rheumatoid Factor. Those who dont are called as Seronegative. The higher the levels of RF the more destructive articular disease. Rheumatoid Factors are present in almost 100% of patients with Sjogrens syndrome. It is also found in almost 100% of patients with Rheumatoid Arthritis who have extra-articular features. 4% of normal population and almost 25% of the elderly have positive RF. In rheumatoid arthritis, RF is an assessment of prognosis rather than a diagnostic test. Cervical spine is involved in around 30% of cases with RA. In rheumatoid arthritis, there is an association with HLA-DR4 and patients with DR4 tend to have more severe disease.

 Extensors tendon rupture is more common than flexure tendon rupture in rheumatoid arthritis. True extra-articular activity is present in almost 30% of patients with rheumatoid arthritis and in this arthritis tends to be more severe. The rheumatoid factor is always positive. The most characteristic extra-articular features of RA are rheumatoid nodules. These rheumatoid nodules may mimic lung malignancy and may present as lung cavitations and of course, like any other extra-articular feature the rheumatoid nodules are also associated with more severe arthritis (and 100% RF positivity!!). These nodules are quite firm to touch (like an unripe fruit!!). Gouty nodules are softer (pilpilaa aaloo aur sakht aaloo!!). Methotrexate (used as DMARDS for rheumatoid arthritis) may induce development of rheumatoid nodules. Therefore, practice caution while prescribing Methotrexate in RA if these nodules are present (bhai worse ho saktey hain). Iritis is not a feature of Rheumatoid Arthritis, unlike spondyloarthropaties. Synovial fluid examination cant diagnose Rheumatoid Arthritis but is helpful sometimes to rule out other forms of arthritis (gout, septic, etc). Biologic disease-modifying agents (e.g., infliximab, adalimumab, etanercept, anakinra, etc) are reserved for more severe active rheumatoid arthritis when standard DMARDs have failed. Failure means that Methotrexate and one other DMARD have failed. These drugs onset of clinical effects is rapid. These biological agents may cause immunosuppression, injection site reactions and worsening of heart failure. Because of this low specificity of rheumatoid factor (RF), new serological test have been developed, which tests for the presence of so called anti-citrullinated protein antibodies (ACPAs). Like RF, these tests are positive in only a proportion (67%) of all RA cases, but are rarely positive if RA is not present, giving it a specificity of around 95%. As with RF, there is evidence for ACPAs being present in many cases even before onset of clinical disease. The most common tests for ACPAs are the anti-CCP (cyclic citrullinated peptide) test and the Anti-MCV assay (antibodies against mutated citrullinated Vimentin). Recently a serological point-of-care test (POCT) for the early detection of RA has been developed. This assay combines the detection of rheumatoid factor and anti-MCV for diagnosis of rheumatoid arthritis and shows a sensitivity of 72% and specificity of 99.7%.