The principal causes of liver failure in an AIDS patient are: infections (tuberculosis, atypical mycobacteria, CMV, hepatitis B and C), septicaemia, cryptosporidia cholangitis, extrapulmonary pneumocystosis), drugs (anti-TB medication, paracetamol overdose, antiviral medication), alcohol. Pancreatitis can be induced by medication, such as Hivid® and Videx®.
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Fever can, among other things, be due to tuberculosis or opportunistic infections. Investigations in an AIDS patient with fever should be aimed at detecting treatable causes. Malaria is not an opportunistic infection, but can also occur in HIV patients. Recurrent Salmonella septicaemia is frequent. The reason is that Salmonella bacteria are facultative intracellular pathogens. They are normally eradicated by T-cell-activated macrophages. This mechanism is deficient in AIDS patients. A “functional hypogammaglobulinaemia” exists despite the polyclonal B-cell stimulation and the accompanying hypergammaglobulinaemia. There is an increased risk of infections with encapsulated bacteria (e.g. pneumococci), but also with Branhamella, Haemophilus and Staphylococcus. Infections with Mycoplasma and Legionella are not more frequent in seropositive persons. “Drug fever” occurs more frequently in seropositive than in seronegative persons.

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In Africa persistent cough lasting more than 1 month occurs in approximately one third of AIDS patients. Bacterial pneumonia (pneumococci, Haemophilus) and tuberculosis are prominent in cases of respiratory problems. Atypical mycobacterioses and Pneumocystis carinii pneumonia are rather infrequent in Africa. Deep fungal infections (histoplasmosis, cryptococcosis, blastomycosis) can likewise cause pulmonary lesions. Pneumocystosis usually develops subacutely, with dyspnoea (shortness of breath) and a dry cough. Recurrent bacterial pneumonia occurs frequently in AIDS patients and is a major cause of death. Vomiting blood (haemoptysis) and pleural effusions are principally caused by TB and Kaposi's sarcoma. Sinusitis is quite frequent in AIDS patients. Lymphoid interstitial pneumonitis occurs especially in children, but can also be found in HIV positive adults. It is characterised by diffuse interstitial infiltrates. The alveolar septa are infiltrated with lymphocytes, plasma cells and immunoblasts.

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Pneumocystis carinii was originally described in 1909 by Carlos Chagas. He thought it was a cystic form of Trypanosoma cruzi. In 1910 Antonio Carini observed similar cysts in rats with experimental trypanosomiasis, but thought that it was a new, unknown organism. He sent material to his colleague Laveran for further investigation. In 1912 Laveran’s student Delanoe described similar cysts in lungs of Trypanosoma-free sewer rats. He gave the organism the name Pneumocystis carinii. The taxonomic classification is debatable, though on the basis of DNA analysis it is at present regarded as an unusual fungus. It is a microscopic organism that frequently causes inflammation of the lungs in severe immunosuppressed individuals. Disseminated infections can occur, e.g. with retinal lesions and foci in spleen and kidneys (frequently calcified). It is not easy to confirm the diagnosis via microscopic investigation, as this has a limited sensitivity. The pathogenic organism is best shown via bronchoscopy and broncho-alveolar lavage, though it can also be found in sputum induced in a non-invasive manner. The latter however requires availability of a special aerosol appliance to create a very fine spray of 3% saline solution. The technique is less sensitive. The organism can be shown with Giemsa staining and is recognizable as small, fine blue spots (the capsule is not stained with Giemsa). Gomori methenamine silver staining, which also stains the capsule, is better.

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Several neurological complications can occur in AIDS patients. These can be subdivided into diseases induced by HIV itself, by opportunistic diseases or by medication.
Acute aseptic HIV-meningitis, chronic HIV-meningitis, HIV encephalopathy (AIDS dementia), vacuolar myelopathy, predominantly sensory neuropathy, inflammatory demyelinising polyneuropathy, mononeuritis multiplex, myopathy.
Cerebral toxoplasmosis, Cryptococcus meningitis, tuberculous meningitis, CMV retinitis-encephalitis-radiculitis, herpes encephalitis, progressive multifocal leukoencephalopathy (JC virus), neurosyphilis, primary cerebral lymphoma, metastatic systemic lymphoma.

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HIV itself affects the brain. Glia cells are infected. HIV causes progressive behavioural, short-term memory and concentration disorders. These develop over the course of several months into presenile dementia with retention of consciousness. Aphasia, alexia and agraphia are usually absent (in contrast to Alzheimer’s disease), though motor abnormalities frequently occur, with unstable gait and a feeling of weakness in the legs. The tendon reflexes are increased. The patient becomes forgetful, can concentrate only with difficulty, quickly loses the thread of a conversation or has to read a text repeatedly in order to understand it. He/she becomes clumsy, suffers from tremor, his/her handwriting becomes blurred (coordination problems) and the sense of balance can become somewhat disturbed, especially when the patient quickly turns his/her head. Awareness of the disease is retained for quite a long time and the patient can describe the symptoms well. Apathy occurs later and the patient becomes mentally retarded. The cerebrospinal fluid often contains a large number of cells, an increased protein level and a discretely reduced glucose level. Agitation, confusion, hallucinations and psychosis can occur. Pyramidal symptoms such as spasticity, hyperreflexia, clonus and the presence of Babinski's sign can occur late. Incontinence also occurs late.

Not only the brain, but also the spinal cord can be affected by HIV (in approximately 20% of cases) resulting in loss of strength in the legs, ataxia and incontinence (vacuolar myelopathy).
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Toxoplasma gondii was first described by Nicolle in 1909 in a North African rodent, Ctenodactylus gondii. The pathogen derives its species name from this. It is a unicellular parasite that is very widespread in nature and can infect many animal species. It is localised and replicates in practically all nucleated cells. The parasite has 3 principal forms: (1) banana-shaped trophozoites (hence the generic name “toxon” = bow) which reproduce asexually in nucleated cells, (2) intracellular dormant cysts with bradyzoites. In the cells the parasite forms cysts that are held in check by the immune system. The parasite thus remains present in the body, especially in muscle cells and in the brain, throughout the animal’s life. (3) oocysts that are the result of the parasite’s sexual cycle in the intestine of the cat. These oocysts can survive in the outside world for several months. If tissue cysts are present the parasite can become active again due to diminished activity of the immune system.

Toxoplasmosis: by far the most frequent
Primary CNS lymphoma
Mycobacterium tuberculosis
Mycobacterium avium complex
Progressive multifocal leukoencephalopathy
Cryptococcus neoformans
Candida sp.
Listeria monocytogenes
Nocardia asteroides
Salmonella group B
Aspergillus sp.
Rhodococcus sp.
Acanthamoeba sp.
Syphilitic gumma (syphilis, Treponema pallidum)
“Classical” bacterial cerebral abscess, e.g. otogenic, from sinus, secondarily to endocarditis.
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Temporal lobe abscess: ipsilateral headache, aphasia, upper homonymic quadrant anopsia.
Frontal lobe abscess: headache, dizziness, confusion, diminished mental capacity, hemiparesis, motoric speech disorders.
Parietal lobe abscess: headache, visual disturbances.
Cerebellar abscess: nystagmus, ataxia, dysmetria, vomiting.
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Various abnormalities are of course possible, but these can be roughly divided schematically into:
Ring-enhanced single lesion: abscess, with frequency toxoplasmosis > TB > cryptococcosis. The peripheral staining by the contrast medium shows the oedema zone around the abscess. On this basis a test therapy will often be started without having formal proof of toxoplasmosis. If there is no improvement within two weeks or if deterioration occurs, a stereotactic brain biopsy should be performed. In addition to these three etiologies, there can be other causes of an intracranial mass: herpes, Histoplasma, Nocardia, Candida, Kaposi, metastasis. In 10% of cases no specific cause is found.

Direct investigation: amoebae, trypanosomes, filaria
Cell counts: type and number (nl < 3/mm3)
Biochemistry: protein content (nl 25-40 mg%), glycorrhachia (nl 40-90 mg%, nl 50-80% of the glycaemia)
Serology: Syphilis, intrathecal production of various antibodies (compare with titre in serum sample)
Antigen-detection: Cryptococcus
PCR: Mycobacteria, JC virus, herpes, toxoplasmosis
Stains: Gram, Indian ink, Ziehl
Culture: virus, bacteria, mycobacteria, fungi
Cytology: only in case of suspected carcinomatous meningitis

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Cryptococcosis is a cosmopolitan infectious disease caused by a yeast, Cryptococcus neoformans. There are two varieties: C. neoformans var. neoformans and C. neoformans var. gattii. These differ in their geographical distribution, ecology and biochemical characteristics. The antigenic specificity of the polysaccharide capsule determines four serotypes: A, B, C and D. Serotypes A and D are found worldwide in bird droppings (avian excreta), especially of pigeons. Serotypes B and C are geographically associated with certain Eucalyptus trees. C. n. neoformans occurs worldwide, whereas C. n. gattii is restricted to the tropics and subtropics. In Australia Eucalyptus camadulensis trees form the natural habitat for the var. gattii. The typical vegetative form of C. neoformans is a yeast with a diameter of 2.5 to 10 µm. The organism can also reproduce sexually. As it is a basidiomycete (Filobasidiella neoformans) it forms sexual spores: “basidiospores”. [Basidiospore: Gr: “basidon”: small base and “sporon”: seed. This indicates the morphology: a club-shaped cell with the haploid spores at the far end.] Infection can probably occur as a result of inhalation of either dehydrated yeast form or basidiospores. Cryptococcus neoformans primarily causes a chronic meningitis. Systemic infections, inflammation of the lungs and cutaneous lesions also occur as a result of these yeasts. The demonstration of cryptococcal meningitis in a patient is at present considered proof of HIV infection and AIDS.

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Tuberculous meningitis usually presents with a non-specific clinical picture. The cranial nerves are frequently affected. Tuberculous meningitis induces an increase in the number of lymphocytes in the cerebrospinal fluid and a decrease in glycorrhachia. Acid-fast bacilli can sometimes be shown by direct examination, but in view of the low sensitivity of direct examination, a culture (Löwenstein-Jenssen) may be necessary. Nodular thickenings, i.e. tuberculomas of the meninges can be observed on CT scan or MRI.

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Progressive multifocal leukoencephalopathy (PML) is a demyelinising disease caused by infection with a papova virus, the JC virus. The family of the Papovaviridae is divided into two genera: Papilloma virus (e.g. wart virus) and Polyoma virus (including JC virus, BK virus and the SV40 virus). The name papova is derived from papilloma, polyoma and vacuolating agent. They are small double-stranded DNA viruses that are potentially oncogenic. The infection preferentially destroys the oligodendrocytes, leading to demyelinisation since the myelin sheath around axons in the central nervous system is formed by concentric folds of the cytoplasma membrane of the oligodendrocytes (analogous to the Schwann cells in the peripheral nervous system). The disease was first described in 1958 by Aström. By injection into experimental animals the virus can induce a number of brain tumours (gliomas, meningomas, neuroblastomas, medulloblastomas). JC virus undergoes intranuclear replication in the astrocytes and oligodendrocytes, as well as in other cells (the virus can be found in epithelial cells in urine, liver, spleen, lymph nodes and lungs). Infections with this virus are frequent but nearly always remain without further consequences. However, in severe immunosuppresion (CLL, Hodgkin’s disease, sarcoidosis, SLE, AIDS) a neurological syndrome can occur. Selective destruction of myelin takes place, but the axons are spared. There is little inflammation (in contrast to multiple sclerosis, where there is an inflammatory lymphocytic infiltrate). Multiple distinct foci of myelin destruction are observed in brain tissue obtained via stereotactic biopsy. The foci become confluent after a while. The lesions are asymmetrical without any preferred localisation, although lesions rarely occur in the spinal cord. The oligodendrocytes exhibit intranuclear viral inclusions. Giant astrocytes with pleomorphic, hyperchromatic nuclei strongly reminiscent of glioblastomas also occur. The clinical evolution is rapid, with an average course of disease of 2 to 4 months. Remission seldom occurs. Mono- or hemiparesis, speech disorders, mental deterioration with progression to dementia and death are the rule. Transverse myelopathy is rare. There is no fever. Headache and fits or convulsions are exceptional. The differential diagnosis includes other opportunistic infections (mycobacteria, fungi, Toxoplasma, cytomegalovirus), syphilis, cerebral lymphoma, endocarditis with embolism, HIV encephalopathy and multiple sclerosis. The EEG is usually diffusely disturbed and aspecifically slow. The cerebrospinal fluid is normal, though the virus can be detected in the fluid by PCR. CT brain scans and, even better, MRI scans show the subcortical lesions in the white matter. There is no mass effect and no staining of the lesions with contrast medium. As regards treatment, the results with various medications have hitherto been disappointing. Regression of the lesions has sometimes been seen under treatment with “HAART”.

Mononeuritis (for example, facial paralysis) can occur at any stage of the HIV infection. Polyneuritis (often with severe pain and sensory disorders) in persons who are not taking any medication occurs almost exclusively in an advanced stage of the disease. Severe radiculitis with nerve pain can be caused by cytomegalovirus infection. Antiretroviral therapy, in particular Hivid®, Zerit® and Videx®, can cause neuritis. Neuritis can also be provoked by nicotibine (INH) and by alcohol, as well as vitamin B deficiency and diabetes. Neurosyphilis should be excluded in neurological problems.

Dark brown (on black skin) or purplish plaques and nodules (on white skin) on the skin or reddish-purple elevations in the mouth indicate Kaposi's sarcoma. This is a cancer that can affect any part of the body (lung, intestine, eye etc.) in AIDS patients, in contrast to the so called endemic Kaposi in Africa, which develops slowly and usually causes lesions only on the feet and legs. [Note: The disease was first described in 1872 by Moritz Kaposi, a Hungarian dermatologist. The disease is encountered principally in persons from Eastern Europe and the Mediterranean basin]. Kaposi's sarcoma thus occurs less frequently in Southeast Asia than in Africa. Since Kaposi's sarcoma occurs much more frequently in homosexual men than in patients infected with HIV via blood, an infectious cause was suspected. Kaposi's sarcoma also occurs more frequently in HIV-negative transplant patients. Immunosuppression appears to be needed for expression of the agent. A new herpes virus genome (KSHV [Kaposi's Sarcoma Herpes-like Virus] or HHV-8 [human herpes virus 8]) was found in the DNA of Kaposi's sarcoma cells and certain lymphomas. This virus apparently has a causal role in these cancers (and also in a variant of Castleman’s disease, a lymphoproliferative disease of B-cells). The virus is found in sperm, though much higher concentrations occur in saliva. This virus is also suspected of playing a role in pulmonary hypertension, but more research is needed.

Herpes genitalis is a sexually transmissible disease caused by herpes simplex virus type 2, sometimes by type 1. Primo-infection with HSV-2 is symptomatic in only 37% of cases. Transmission of the virus by asymptomatic carriers is possible, even after many years. A first acute episode is either a primo-infection in a person who has never been infected with HSV-1 of HSV-2 before, or a first clinical manifestation of herpes genitalis in a patient who has been carrying the virus for some time. This first episode is classically expressed as blisters followed by ulcerations accompanied by a burning sensation, discomfort and sometimes intense pain. Some patients also report headache and symptoms indicating a neurological disorder: neuralgia, sensory disorders in the calves and urine retention. Recurrences are generally less serious than the first episode. Recurrences are more frequent with HSV-2 infection than with HSV-1 infection. With time, however, the frequency of relapses decreases. Application of steroid-containing crèmes should be avoided, especially with eye lesions.

Herpes zoster, zona or shingles results from reactivation of latent varicella zoster virus. The initial infection with this virus will result in chickenpox. Afterwards, the virus will stay dormant in the dorsal root ganglia and cranial nerve ganglia. The reactivation will result in a totally different clinical picture. There will inflammation of the posterior and anterior horns of the gray matter, the meninges, and the dorsal and ventral roots. This can proceed subclinical. Skin lesions will appear in a dermatome and sometimes in adjacent dermatomes. The initial symptom is often pain along the site of the future eruption. This pain precedes the rash by 2-3 days. Afterwards, characteristic crops of vesicles will appear. These have an erythematous base. Hyperaesthesia of the affected zone might develop. Dissemination to other parts of the skin and/or to visceral organs can occur, especially in immunodepressed people. Although fewer than 4% of non-immunedepressed people will experience a recurrence, new flare-ups are common in AIDS patients. Postherpetic neuralgia can persist for many months, even years. When herpes zoster affects the otic/geniculate ganglion, geniculate zoster, better known as the Ramsay Hunt syndrome will follow. Pain in the ear and facial paralysis will follow. There will be a vesicular eruption in the external auditory canal. Taste may be lost in the anterior two thirds of the tongue. If the gasserian ganglion in affected, ophthalmic herpes zoster will appear. A vesicular rash in the distribution area of this branch of the fifth cranial nerve is typical. Vesicles on the tip of the nose are a warning sign which indicate involvement of the nasociliary nerve. In this case, corneal lesions are to be expected (75% probability). If there is no lesion on the tip of the nose, the eyeball is involved in 30% of patients. Herpetic keratitis is vision-threatening.

In Southeast Asia infection with Penicillium marneffei should be included in the differential diagnosis of skin lesions. This fungus causes high fever (95%), hepatomegaly (40-90%), lymphadenopathy (50-90%), cough (50%), anaemia (40-80%), emaciation or weight loss (75%), splenomegaly (15-60%) and skin lesions (70%). The skin shows several papules with central umbilication. The chest X-ray can resemble tuberculosis. The organisms can be demonstrated in a smear from the skin, lymph nodes, sputum and/or from the bone marrow (a bone marrow analysis is the most sensitive). The white blood cell count varies greatly. The fungus is sometimes found in neutrophils in peripheral blood. Culture is also possible. The fungus is sensitive to amphotericin B and itraconazole. Do not confuse the yeast cells with other fungi or leishmania amastigotes.

A papulopruriginous to nodular skin rash occurs in about 10 % of the seropositive population in the tropics. The cause of this nodular prurigo is not known. The itching is sometimes intolerable and difficult to treat. The differential diagnosis includes scabies (also frequent and sometimes very severe) and onchocerciasis. One gets the impression that HIV positive persons react more violently and with more itching (pruritus) to various insect bites. Cutaneous rash - not necessarily with itching – can occur as a result of side-effects of medication (sulphamethoxazole, thiosemicarbazone). Symptomatic treatment is often the only treatment for itch. Seborrheic dermatitis is very frequent (3% in the general population, but up to 50% in AIDS patients). This seems to be connected with a reaction to the skin yeast Pityrosporon ovale. Immunodeficient persons often develop a chronic, refractory, extensive but quite benign skin infection with a pox virus: molluscum contagiosum. This results in numerous small umbilicated papules. Psoriatic skin lesions are frequently activated during HIV infection.

Anterior segmentKeratitis can be caused by various organisms ranging from herpes viruses to microsporidia.
Posterior segment Minor infarctions in the retinal nerve layer (“cotton-wool spots”) are very frequent. They are transient and are of no further significance. In Europe before the era of antiviral combination therapy approximately 20% of AIDS patients developed ocular lesions due to infection with the cytomegalovirus. CMV retinitis is rare in developing countries as most patients do not survive a very severe immunodeficiency condition for a sufficiently long period of time (they die earlier of something else). CMV spreads from cell to cell in the retina and causes a peripheral or paracentral scotoma (retinal necrosis) that gradually becomes larger. Tunnel vision is one consequence of the destruction of the peripheral retina. Multiple minor haemorrhages and perivascular sheathing is characteristic of this infection. Retinal detachment can follow focal atrophy of the retina. If left untreated it can lead to blindness. Blindness is caused less frequently (3%) by toxoplasmosis retinitis. In cases of toxoplasmosis of the retina there is also a high risk (30%) of toxoplasmosis of the brain. Pneumocystis carinii choroiditis is very rare. Retinal necrosis can be caused by herpes simplex or herpes zoster virus.

Weight loss is very frequent. It occurs in more than 90% of patients and can be very substantial ("slim disease"). It is probably multifactorial: hypermetabolic patients with various infections, cytokine mediated effects, direct effects of HIV itself, malabsorption, anorexia, etc. Many patients die of extreme cachexia. In many cases tuberculosis is found in unusual sites upon autopsy. Many patients develop lymphadenopathy in the course of their illness. Tuberculosis should be excluded in cases of seriously enlarged (> 4 cm) or asymmetrically enlarged lymph nodes (lymph node aspirate with Ziehl staining). Syphilis, toxoplasmosis and non-Hodgkin’s lymphoma can also cause lymph node swelling.

1. Where do the multiple, firm, mottled blood clots come from?
Answer: The multiple firm mottled blood clots are probably emboli. The most common site of origin is from deep venous thrombi in ilieac, femoral, popliteal veins or in the inferior vena cava.
2. The lung has a dual circulation, i.e. pulmonary and bronchial arteries only the pulmonary vessels were obstructed. Why did the parenchyma undergo necrosis?
Answer: In the presence ofcongestive heart failure the poor cardiac output reduces the blood supply to the entire arterial system including the bronchial arteries. This additional impairment of blood flow to the lungs, added to the obstruction of pulmonary vessels, may be sufficient to reduce tissue oxygenation below the level of a critical deficiency resulting in tissue necrosis.

1. On the basis of the histopathology, could the infarct have been present seven days before the death of the patient? Why or why not?
Answer: The infact could not have been present seven days before the death of the patient. The changes of neutrophilic infiltrate and coagulative necrosis are compatible with an acute myocardial infarction. At seven days, the infarction should show early fibrovascular changes and the presence of macrophages.

1. Using the histopathological changes as a guide, estimate when the infarct and its possible extension(s) occurred.
Answer: The histopathologic changes are compatible with an older myocardial infarction, though various stages are seen. The organization (fibrovascular proliferation, chronic inflammation) and fibrosis and suggestive of an infarct ranging from 2-6 weeks.
2. Explain the development of heart failure on the basis of the appearance of this infarct?
Answer: The heart failure in this case is a result of a decrease in functioning myocardial cells. This has arisen from myocardial cells having become necrotic in the past and having been replaced by organizing tissue and fibrous connective tissue..

Apomorphine (and Bromocriptide) A D2 agonist used in the treatment of parkinsons It acts on the D2 receptor in the CTZ to cause vomiting Morphine In excess amounts, also acts on D2 receptors Syrup of Ibericat Irritates the gut, causing activation of 5HT3 receptors Cisplatin Anti cancer drug which causes release of serotonin in the gut, which then acts on 5HT3 receptors

The main area in the brain responsible for vomiting is the vomiting center This area is located in the lateral reticular formation of the medulla It receives input from many areas: Chemoreceptor trigger zone Located in the floor of the 4th ventricle in the area postrema It picks up circulating chemical in the blood It is important because it lies outside the BBB, therefore, circulating toxins (e.g.bacterial food poisoning toxins, chemotherapy) can cause vomiting, even though they do not pass through the BBB Vestibular apparatus Tractus solitarius vagal afferents from the gut, heart and testes Direct input from gut (reflex)

• For motion sickness
• Promethazine
• H1 antagonist (classical)
• Used as a sedative in children (it is a very safe sedative)
• Also has antimuscarinic actions
• It is very effective at preventing motion sickness (since the vestibular afferents input in the vomiting center which has H1 and Muscarinic receptors
• Not used for the driver because is makes them drowsy
• Hyocine (scopolamine)

1. Following rheumatic fever, what causes the mitral valve to become insufficient?
Answer: As a result of the inflammatory process involving the mitral valve with possible development of vegetations, there is damage to the valve resulting in eventual scarring and deformity of the valve. This causes the cardiac valve to become incompetent and results in mitral insufficiency (regurgitation).
2. What is the most common disease process causing constrictive pericarditis?
Answer: Constrictive pericarditis can be caused by acute rheumatic heart disease. The most common cause of pericarditis is idiopathic and may be secondary to an inflammatory process such as viral disease.

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1. Which organism is most frequently found in drug addicts with infective endocarditis?
Answer: Staphyloccus aureus is the most frequent organism found in drug addicts along with other skin contaminants.
2. What is the most frequent final outcome of this disease in drug addicts with antibiotic treatment and valve replacement?
Answer: There is a very high mortality rate in drug addicts that develop acute bacterial endocarditis despite antibiotic treatment and valve replacement.

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1. Although the pathogenesis ofatherosclerosis is unclear, name the lesion that may represent the earliest morphologic stage of a plaque.
Answer; The earliest morphologic stage of an atherosclerotic plaque is most likely the fatty streak.
2. Describe the "complicated" plaque found in atherosclerosis.
Answer: The complicated plaque found in atherosclerosis may be characterized by ulceration, calcification, hemorrhage, thrombosis, and the development of an aneurysm.

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-Hematopoesis is known to be guided by more than 20 genes. There are a bunch of mutations that create impairment because of this. Certain mutations will arrest differentiation in different stages and you won’t have an effective population of certain cells to carry out a specific function. This commonly leads to lethality of the cell line since critical cells are not produced.
-Significant subset of genes relative to hematopoesis and to functioning of the differentiated cells are a set of growth factors and their receptors. They function to regulate replication of the hematopoetic cells and transcription of these genes. There are two broad categories of these receptors/growth factors

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-spherocytosisà spheroid looking cells instead of the concave shape
-ovalocyte shapes- oval shaped
-spiculated red cells- looking like spiny protrusion
-sickled shape
-all of these abnormal shapes will shorten the survival of the RBC and lead to anemias.
There is a class of cytosekeletal proteins beneath the cytoplasmic membrane of the RBC
-function to contribute to the appropriate shape of the cell, when one is structurally modified or absent because of mutation there will be an aberrant shape that will lead to anemia due to premature lysis. The lysis comes about to them being trapped in the spleen because of their aberrant shape, they will then be phagocytosed.

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-remember that they are non nucleated vesicles that arise from megakaryocytes.
-mutation in many genes can interfere with the function of the platelets
-there have been more than 50 platelet plasma membrane proteins that have been recognized. And there are this many genes in which mutations can interrupt function. These 50 have been assigned into 5 gene families.
-Integrin family

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-Diverse Immunoglobulin gene deficiencies exist.
-complete deficiency in immunoglobulins X-Linked agammaglobulinemia. Absence of gamma-globulins
-specific Ig chain deficiencies, you will see a selective set of susceptibility to a certain set of microorganisms.
-X-linked-hyperimmunoglibulin M, an excess of IgM production. Seen mostly in males.