Explanation:

Serum sickness is due to circulating antibody-antigen complexes (type III). Graves´ disease is due to stimulating antibody (type V). The most severe variety of type I reaction is anaphylaxis, with angio- oedema an intermediate reaction associated with wheeze and swelling of the lips and severe urticaria. These reactions are mediated by histamine 1 receptor stimulation. Congenital C1 inhibitor deficiency is also caused by hereditary angio- oedema. Deficiencies in Clr, s, and 2-4 result in vasculitides; while deficiencies in C2, 3 and 5-8 are associated with an increased risk of septicaemia.

Explanation:

Liver enzymes are elevated in most patients.
Visual disturbances are suggestive of temporal arteritis not PMR, and are due to ischaemic changes in ciliary arteries (optic neuritis/infarction) and less commonly due to central artery occlusion. Raised CK occurs in polymyositis. PMR is rare before the age of 50 years.

Explanation:

Explanation:

Kawasaki´s disease, or mucocutaneous lymph node syndrome, most often involves the coronary vessels when vasculitis is present.

Explanation:

Fibrocystic changes usually come to clinical attention by causing pain (often cyclical, in premenstrual phase), palpable lumps, or mammographic densities and calcifications. The diffuse, small irregularities (“lumpy bumpy” texture) are caused by cysts and fibrosis. Fibrocystic changes do not increase the risk of developing breast cancer, unless there are associated proliferative changes. Epithelial hyperplasia is defined as an Increase in the number of epithelial cell layers in the ductal epithelium. Florid epithelial hyperplasia leads to an increased risk of developing carcinoma, especially if there is associated cellular atypia (atypical ductal hyperplasia). There is a continuum of florid epithelial hyperplasia to atypical ductal hyperplasia to ductal carcinoma in situ with an increasing risk of progression to invasive ductal carcinoma. Adenosis refers to an increase in the number of acini and can be observed in fibrocystic changes as well as in other breast conditions, such as sclerosing adenosis. Physiologic adenosis is part of the changes that occur during pregnancy. Adenosis is not associated with increased risk of breast cancer, except as a component of sclerosing adenosis, where the real risk is if epithelial changes (hyperplasia, atypical lobular hyperplasia, or atypical ductal hyperplasia) have occurred. Apocrine metaplasia describes a benign change of breast epithelial cells that come to resemble the apocrine epithelium of sweat glands. Apocrine cells have abundant granular eosinophilic cytoplasm. Apocrine metaplasia is seen frequently in fibrocystic changes, as well as in normal breast.
Calcium deposition is a nonspecific finding that may occur in a number of both benign and malignant breast changes, including fibrocystic changes, ductal carcinoma in situ, and invasive carcinoma. Calcification is not clinically significant except for its diagnostic value. Mammographic detection of calcium may serve to guide biopsy procedures. Cysts are frequent in fibrocystic changes and result from dilatation of ducts. The nodularity of breasts with fibrocystic changes is due in part to the presence of cysts of various sizes. A classic gross description is that of blue dome cysts which appear brown to blue because of their turbid fluid content. The epithelial lining may undergo apocrine metaplasia or produce papilla projections. There is no direct link between cyst formation and breast cancer.

Explanation:

α2 macroglobulin inhibits the cysteine proteinase family of enzymes, while the other molecules do not. Tissue inhibitor of metalloproteinases (TIMP) is a specific inhibitor for the metalloproteinase enzymes. Aprotinin inhibits mast cell tryptase. αl proteinase inhibitor inhibits elastase. αl chymotrypsin inhibits cathepsin G.

Explanation:

Although air pollution is associated with a number of pulmonary diseases, it has not been definitively linked to carcinoma of the lung. By far, the majority of lung carcinomas result from cigarette smoking, with a dose dependent relationship between the duration and intensity of smoking and mortality from lung cancer. Passive cigarette smoke exposure is also associated with a one and a half to two fold increase in risk, depending on the duration of exposure. Asbestosis increases the risk of all histologic types of lung cancer. There is a synergistic effect with cigarettes, with the risk being increased fivefold in nonsmokers to 50 to 100 times in smokers. Epidemiologic studies have demonstrated an increased risk of lung cancer in persons with dietary deficiencies of vitamin A and beta carotene. Kindred´s with germ line abnormalities of either the p53 or RB tumor suppressor genes have a higher incidence of lung cancer.

Explanation:

In this condition, the levels of parathyroid hormone are elevated but there is relative resistance to the effects of PTH by the kidney, resulting in osteopenia. Postmenopausal osteoporosis, disuse osteoporosis, phosphorus deficiency, and hypocalcitoninemia do not manifest with elevated PTH.

Explanation:

Cryptococcus spp. is a major cause of AIDS related meningitis. Listeria monocytogenes is seen in neoplastic meningitis, while Streptococcus pneumoniae is observed as the cause of meningitis in all age groups of immunocompetent individuals. Haemophilus influenzae type b meningitis is important in neonates and young children, and Staphylococcus aureus is important in hospital-acquired and parenteral drug abuse-associated meningitis.

Explanation:

The lung, followed by breast, stomach, and contralateral kidney, are the most common. Prostate metastases to the kidney are very uncommon.

Explanation:

Plasmodium vivax is a subtype of malaria that is associated with abnormal liver function tests. Malaria is diagnosed in a suspected individual from an endemic area by looking at the peripheral blood smear and finding the organism within red blood cells. Babesiosis is associated with tick bites and is endemic in Long Island, New York, and certain New England states. Thrombocytopenia is common. Salmonella is usually associated with diarrhea, which this patient does not have. It is also occasionally associated with “rose spot” rashes. Ehrlichiosis is occasionally associated with a dog tick and is not common in India. Listeriosis is associated with meningitis and mental status changes in immunocompromised individuals.

Explanation:

Known as disease producing agents only since the 1950s, Mycobacterium avium infection is diagnosed in up to 30% of AIDS patients. Compared to Mycobacterium tuberculosis, it is less virulent. The organism frequently colonizes body surfaces or secretions without causing disease. The organism is ubiquitous in nature and has been isolated from tap water, domestic and wild animals, soil, house dust, and birds. Infection most often results from inhalation or direct inoculation from environmental sources. Person to person transmission is rare.

Explanation:

Hemochromatosis is a disorder of iron storage in parenchymal cells, which is either genetically based or acquired. Clinical manifestations include cardiomyopathy and cirrhosis of the liver. Hypogonadotropic hypogonadism results from iron deposition in the pituitary. Diabetes mellitus, resulting from iron deposition in the pancreas, is particularly common in persons with a family history of diabetes. Hypothyroidism is not characteristic of hemochromatosis, although affected persons frequently complain of weakness and lassitude.

Explanation:

This patient has mumps, which is caused by a negative sense RNA virus in the Paramyxovirus family. Since the advent of the live attenuated MMR vaccine virus has become rare, but the mention of a poor rural family suggests that the child may not have received adequate pediatric vaccinations or medical care. Bilateral parotitis and inflammation of the pancreas or testes are hallmarks of the infection in this age group. Within the Paramyxoviridae, parainfluenza virus and mumps virus attach to host cells using a hemagglutinin neuraminidase glycoprotein. F glycoprotein is the molecule responsible for formation of syncytia or multinucleated giant cells in infections with respiratory syncytial virus and measles virus. It is responsible for the destabilization of the cellular membrane that allows the virus to move from cell to cell. G glycoprotein is the cellular attachment glycoprotein used by respiratory syncytial virus, which belongs to the Pneumovirus genus of the Paramyxoviridae. H glycoprotein is the hemagglutinin molecule used as the cellular attachment molecule of the measles virus, which is a Morbillivirus within the Paramyxovirus family. N glycoprotein is the neuraminidase molecule, which in some viruses, mediates virus maturation by clipping off sialic acid residues as the virus leaves the cell. There is no member of the Paramyxoviridae that has a separate neuraminidase molecule.

Explanation:

Explanation:

One of the most efficient mechanisms for eliminating extracellular pathogenic bacteria is by opsonization and phagocytosis by macrophages. The IgG and IgM antibody produced in response to the organism reacts with the capsular structure, stimulating the activation of the classical pathway of the complement system. This pathway produces large amounts of C3b that coat the organism, preparing it for phagocytosis. ADCC cells are actually natural killer (NK) cells that find virally infected cells and tumor cells that have been coated with antibody and react with and destroy them. These cells do not destroy antibody-coated bacteria, only body cells that are coated with antibody. Cytotoxic T lymphocytes react only with cells that have antigen epitopes presented in association with class I MHC molecules. An example would be a virus epitope from a virally infected cell presented by class I molecules on the surface of the cell. LAK cells are NK cells that have been activated by IL-2. They are considered to be super activated NK cells. The NK cells are cells of the innate immune system that destroy virally infected cells or tumor cells. This does not involve antibody and it does not involve extracellular pathogens.

Explanation:

Mycobacterium tuberculosis is an intracellular pathogen that lives inside macrophages. The protective immune response to this organism depend son the stimulation of more efficient intracellular killing in phagocytic cells by the cytokines of TH1 cells. Interferon-gamma (IFN-γ) is a product of TH1 cells that acts on macrophages to enhance their microbicidal activities. Interferon-alpha is a product of leukocytes that inhibits viral replication. It is unlikely to have an effect on an intracellular bacterial infection. Interferon-beta is a product of fibroblasts that inhibits viral replication. It is unlikely to have an effect on an intracellular bacterial infection. Interleukin-2 is a product of TH cells that causes proliferation (cloning) of other lymphocytes. Because the macrophage is an end cell, incapable of further replication, it would not be affected by IL-2 administration. Tumor necrosis factor-alpha, a product of macrophages and NK cells, is cytotoxic for tumor cells, induces cytokine production, and causes the cachexia of chronic inflammation. It is unlikely to have a beneficial result on a bacterial infection of macrophages.

Explanation:

The suspected disease is temporal arteritis, also known as giant cell arteritis because of the focal granulomatous inflammation (with giant cells) that characterizes the process. The cranial arteries (branches of the carotid system) are most often involved vigorous attempts at diagnosis, which may require biopsying 2 cm lengths of each temporal artery, are indicated because the process can be patchy. Correct diagnosis is essential because untreated temporal arteritis can involve the ophthalmic artery, leading to irreversible blindness.
Atherosclerosis is almost never seen in the distal (lower blood pressure) part of the temporal artery. Leukocytoclastic vasculitis is a feature of hypersensitivity angiitis. Widespread neuronal necrosis with Negri bodies (intracytoplasmic eosinophilic inclusions) are pathognomic of rabies. Symptoms usually start in the peripheral nervous system after bacteria from a bite travel to the central nervous system, causing myelitis and encephalitis and resulting in hallucinations, aggression, confusion, agitation, paralysis, salivation, and hydrophobia. Normal tissue may be found in cluster headache, which may be episodic or chronic and is typically unilateral temporal/periorbital. Attacks are sudden, with extreme pain, tearing of the eye, and nasal stiffness and rhinorrhea. Cluster headache is not associated with any consistent pathologic findings.

Explanation:

The clinical scenario describes a patient with type 2 diabetes mellitus (DM). The diagnosis is strongly suggested by the clinical presentation and the presence of glucosuria, but confirmed with an abnormal 2 hour postprandial serum glucose (upper limit of normal is 200 mg/dL). In type 2 DM, there is hyperglycemia because of insulin resistance, and therefore hyperinsulinemia in this case, there is activation of pyruvate dehydrogenase in the liver. Pyruvate is converted to acetyl CoA. Therefore, one would expect increased levels of acetyl CoA. Fatty acid synthase is rapidly induced in the liver by high glucose and insulin levels. The carbons from acetyl CoA are incorporated into the fatty acid produced. The citrate shuttle transports acetyl CoA from the mitochondria to the cytoplasm for laity acid synthesis. Acetyl CoA combines with oxaloacetic acid in the mitochondria to form citrate and then is transported into the cytoplasm, instead of going into the citric acid cycle. Insulin promotes this process.
Triglycerides are converted to glycerol and fatty acids in the presence of low insulin levels, and therefore increased levels of cortisol and epinephrine. The glycerol enters the liver where it is converted to glucose by gluconeogenesis. The fatty acids also enter the liver, where they undergo beta-oxidation to yield acetyl CoA. The reactions in the liver are supported by glucagon and cortisol.

Explanation:

Rubella, also called German measles or 3 day measles, is a disease caused by a Togavirus, which is a small, enveloped, single-stranded, (+) linear RNA virus. Approximately 40% of patients are asymptomatic or have mild symptoms. In symptomatic patients, the clinical presentation typically consists of an erythematous rash that begins on the head and spreads downward to involve the trunk, and lasts for approximately 3 days. In addition to a transient rash, symptoms include fever, posterior cervical lymphadenopathy, and arthralgias. The greatest danger from rubella is to the fetus. If clinical rubella develops or seroconversion is demonstrated, there is a high risk of congenital abnormalities or spontaneous abortion. The risk varies from 40% to 60% if infection occurs during the first 2 months of gestation to 10% by the 4th month. Women of childbearing age should be warned not to become pregnant within 2-3 months from the time of immunization. Mild arthralgias and other symptoms may develop in 25% of immunized women. Enteroviral rashes may mimic rubella and rubeola. 
Infectious mononucleosis is caused by the Epstein-Barr virus, a herpesvirus. Classic findings include fever, exudative pharyngitis, generalized lymphadenopathy, severe malaise (most common complaint), and hepatosplenomegaly. A rash is not a characteristic feature unless the patient has been treated with ampicillin. Lyme disease is caused by the spirochete Borrelia burgdorferi. The disease is transmitted by the bite of the tick Ixodes. Reservoirs in nature include the white tailed deer and the white-footed mouse. The initial lesion is an annular rash with central clearing and a raised red border (erythema chronicum migrans) at the bite site. The rash is warm, but not painful or itchy. Patients also have fever, malaise, royal gias, arthralgias, headache, generalized lymphadenopathy, and, occasionally, neurologic findings. Roseola is caused by human herpesvirus 6. Other names include exanthem subitum or sixth disease. Children have a febrile period of 3-5 days with rapid defervescence followed by an erythematous maculopapular rash lasting 1-3 days. Rubeola, or regular measles, is a disease caused by a paramyxovirus. Patients present with an upper respiratory prodrome and characteristic oral lesions (Koplik´s spots) that precede the rash. The non-pruritic maculopapular rash begins on the face and spreads to the trunk and extremities, including palms and soles. The incubation period is 10-14 days. Patients also have a posterior cervical lymphadenopathy. The virus is not associated with risk to a fetus.

Explanation:

The vast majority of cases occur in individuals younger than 30 years. Usually, the symptoms are relatively mild, and death is uncommon. Enteroviruses, arboviruses, and type 2 herpes simplex virus are the most common causes of viral meningitis. Also up to 10% of HIV patients develop an acute meningitis, typically at the time of seroconversion. Adenovirus infection is associated with upper respiratory tract infections (URIs), sinusitis, ocular disease, enteric infections, and bladder infections. It does not typically cause aseptic meningitis. Human papillomaviruses are associated with warts on the skin and genital areas. Poxviruses include the causative agents of smallpox, cowpox, and molluscum contagiosum. These agents do not typically cause meningitis. Reoviruses cause URIs, hepatitis, gastroenteritis, and encephalitis, but not meningitis.

Explanation:

Pasteurella multocida is a gram negative rod that is normal flora of the oral cavity of dogs and cats. It often causes a local abscess following introduction under the skin by an animal bite. Most cases occur in children who are injured while playing with a pet. Bartonella henselae is a very small, gram negative bacterium that is closely related to the rickettsia, although it is able to grow on inert media. It is the cause of cat-scratch disease (a local, chronic lymphadenitis most commonly seen in children) and bacillary angiomatosis (seen particularly in AIDS patients). In this latter patient population, the organism causes proliferation of blood and lymphatic vessels causing a characteristic “mulberry” lesion in the skin and subcutaneous tissues of the afflicted individual. Brucella canis is a gram negative rod that is a zoonotic agent. Its normal host is the dog, but when it gains access to humans, it causes an undulating febrile disease with malaise, lymphadenopathy and hepatosplenomegaly. The normal route of exposure is via ingestion of the organism. Clostridium tetani is a gram positive, spore forming anaerobic rod. It causes tetanus [a spastic paralysis caused by tetanospasmin, which blocks the release of the inhibitory neurotransmitters glycine and gamma aminobutyric acid (GABA)]. There may be no lesion at the site of inoculation, and exudation would be extremely rare. Toxocara canis, a common intestinal parasite of dogs, is a metazoan parasite that causes visceral larva migrans. Young children are most likely to be affected, as they are most likely to ingest soil contaminated with eggs of the parasite.

Explanation:

The tumor is medullary carcinoma of the thyroid, which can occur sporadically or as part of multiple endocrine neoplasia (MEN), types IIa and IIb. The history of pheochromocytoma and the multifocality of this tumor suggest that this is one of the MEN type tumors. Other facts to know about medullary carcinoma of the thyroid include the local production of amyloid (formed in this case from precipitated calcitonin), the secretion of calcitonin (and also other biologically active substances), and the link to a genetic defect on chromosome 10. Parathyroid hormone can be produced by parathyroid tumors or can be a paraneoplastic product of a variety of tumors, including lung cancer.
TSH can be produced by pituitary adenomas. T3, or triiodothyronine, and T4, or thyroxine, can be produced by thyroid tumors composed of follicular cells.

Explanation:

Secondary hyperthyroidism presents in a similar clinical fashion to primary hyperthyroidism. However, secondary hyperthyroidism is the result of a pituitary hyperfunction resulting in an excess production of thyroid stimulating hormone (TSH) and a secondary elevation of thyroid hormones T4 and T3. Some of the symptoms of hyperthyroidism include nervousness, anxiety, heat intolerance, increased sweating, tachycardia, amenorrhea, and infertility.
Decreased thyroxine-binding globulin (TBG) is not by itself diagnostic. Elevated T3 and T4 are found in both secondary and primary hyperthyroidism. The presence of serum thyroid stimulating autoantibodies is diagnostic of Graves disease, a cause of primary hyperthyroidism.

Explanation:

This young man is displaying features of Marfan syndrome, a genetic (often autosomal dominant) disease of connective tissues that affects the skeleton (tall stature, long fingers and toes, hyper-extensible joints), eyes (often subluxation of the lenses bilaterally), and the cardiovascular system (cystic medial necrosis predisposing to aortic dissection, or aortic valve incompetence). Marfan syndrome is due to mutations in the fibrillin gene, leading to defects in the structure of elastic tissue. Lisch nodules are pigmented nodules found on the iris of the eye. They are associated with type I neurofibromatosis. Noncaseating granulomata can be seen in a variety of disorders, including sarcoidosis and berylliosis. Progressive dementia is a feature of a number of disorders, including Alzheimer disease, Huntington disease, and Pick disease.

Explanation:

Options A, C, and D have no prognostic value. White cell count at diagnosis is however important, but most important is the karyotype of bone marrow, as this result stratifies patients into lower risk, standard risk and poor risk, which has prognostic significance.

Explanation:

IgG is the predominant form of immunoglobulin in plasma at a concentration around 10,000 times that of IgE. IgG crosses the placenta to confer immunity to the fetus but IgE does not. IgE is involved in arming mast cells and basophils. IgE causes mast cells to release vasoactive amines, such as histamine, producing an inflammatory response which can result in a type I hypersensitivity reaction. IgE is responsible for allergen mediated diseases such as anaphylaxis, asthma and atopy.
Total serum IgE is frequently increased in those with atopy but serum IgE does not rise acutely during an asthmatic attack

Explanation:

In APL, one of the Retinoic Acid Receptor genes, RARA, is fused to PML in the great majority of patients as a result of the chromosomal translocation t (15; 17).

Explanation:

Marfan syndrome is a connective tissue disorder that is associated with floppy mitral valve and also with cystic medial necrosis that predisposes to aortic dissection. Autopsy will have shown prolapsed mitral valve with elongation, thinning, and rupture of chordae tendineae.
Abnormalities of the beta-myosin gene may be associated with some form of dilated cardiomyopathy.
The CFTR gene is associated with cystic fibrosis. The obstructive lung disease from widespread bronchiectasis that results from cystic fibrosis involving the lung can lead to pulmonary hypertension with cor pulmonale. The fibroblast growth factor receptor (FGFR) gene mutations can be associated with skeletal dysplasias. BRCA1 mutations are associated with breast cancer.

Explanation:

Dystrophia myotonica is an autosomal dominant condition with variable penetrance. Symptoms characteristically begin from the age of 20-30 with weakness and myotonia.

• Ptosis
• Cataracts
• Frontal baldness
• Gynaecomastia
• Diabetes and
• Reduced reflexes with myotonia are features.
• Progressive external ophthalmoplegia is a feature of ocular muscular dystrophy.

Explanation:

Bacteria develop resistance to antibiotics by gaining genes that encode for particular proteins that offer protection to the organism. Sometimes this is by mutation and other times the gene may be acquired from another bacterial species.
The genes are usually found in plasmids -circular segments of DNA separate from the bacterial chromosome. Plasmids can easily spread from one bacterial to another – a sort of resistance package that bacteria can share.

Explanation:

Most common metastatic tumors to the ovaries are of Mullerian origin: the Uterus, fallopian tube, contralateral ovary, or pelvic peritoneum. The most common extra-mullerian tumors metastatic to the ovary are carcinomas of the breast and gastrointestinal tract. Brenner Tumors are non-metastatic surface derived ovarian tumors whose epithelium mimics transitional urinary epithelium. Gastric carcinoma may metastasize to a number of places, including the left supraclavilcular lymph node (Virchow´s node), an umbilical lymph node (Sister Mary Joseph´s sign), the rectal shelf (Blumer´s shelf), and the ovary (Krukenberg´s tumor). A Klatskin tumor is a pancreatic adenocarcinoma that arises at the confluence of the hepatic ducts. Pseudomyxoma peritonei although is metastatic but arises from the appendix.

Explanation:

Phenylketonuria is a quarter as common as congenital hypothyroidism with an incidence of 1:10,000 live births. It is due either to phenylalanine hydroxylase deficiency or problems with synthesis or recycling of the biopterin co-factor.
The presentation is with infantile spasms or developmental delay between 6 and 12 months of age.
Patients may be musty smelling, fair haired and blue eyed and may develop eczema. Treatment is with restriction of dietary phenylalanine, while ensuring sufficient for physical and neurological growth. Co-factor defects are treated with a diet low in phenylalanine and high neurotransmitter precursors

Explanation:

Amebiasis, caused by Entameba histolytica, is a parasitic diarrheal infection, which forms teardrop-shaped ulcers in the bowel. The organisms may disseminate and cause liver and brain abscesses. Because cell-mediated immunity is requisite for defense against the organism, steroids exacerbate the disease. Typically, the mode of transmission is via ingestion of cysts in contaminated food and water. It is treated with metronidazole (flagyl).

Explanation:

CA-125 may be elevated in ovarian epithelial tumors, such as a cystadenocarcinoma. AFP can be elevated with either an endodermal sinus tumor or embryonal carcinoma. An elevated hCG can be seen with choriocarcinomas. Sertoli-Leydig and granulosa-theca cell tumors do not usually produce an elevated CA- 125, AFP, or hCG level.

Explanation:

In this condition, the levels of parathyroid hormone are elevated but there is relative resistance to the effects of PTH by the kidney, resulting in osteopenia. Postmenopausal osteoporosis, disuse osteoporosis, phosphorus deficiency, and hypocalcitoninemia do not manifest with elevated PTH.

Explanation:

Explanation:

Cobalamin (Vitamin B12 deficiency) probably results from excessive binding of cobalamin by nonintrinsic factor cobalamin binding proteins, which are normally destroyed by pancreatic proteases. Icterus may result from either edema of the head of the pancreas, with compression of the common bile duct, or from chronic cholestasis secondary to chronic inflammation around the intrapancreatic portion of the common bile duct. Although gastrointestinal bleeding may result from pathology of the gastrointestinal tract itself, it may also occur if a pseudocyst erodes into the duodenum. Varices, resulting from splenic vein thrombosis due to inflammation of the tail of the pancreas, may also rupture. Bone pain may occur due to intramedullary fat necrosis. Subcutaneous fat necrosis may present as tender red nodules on the lower extremities.

Explanation:

Medullary thyroid carcinoma is not associated with multiple endocrine neoplasia syndrome type I, but is associated with type II. The other choices are all associated with type I.

Explanation:

Explanation:

Tetralogy of Fallot (TOF), a congenital cardiovascular conditiondefined as infundibular stenosis (RV outflow tract obstruction), RV hypertrophy, ventricular septal defect, and overriding aorta, produces a right to left shunt. The obstruction to RV outflow and obligatory VSD allows blood to move from the RV to LV and then, deprived of oxygen, out to the periphery TOF may present as cyanosis.

Explanation:

Explanation:

Explanation:

Unlike eukaryotic cells in which the electron transport system is located on mitochondria, the electron transport system of bacteria is located on the cytoplasmic (plasma) membrane. Since prokaryotes possess no internal membrane-bound or candies, all biochemical processes that require membrane support must occur on the internal surface of the cytoplasmic membrane. Mesosomes are complex invaginations of bacterial cell membranes that serve in cell division. Bacteria do not have mitochondria or nuclear membranes. Polyribosomes function in bacterial protein synthesis.

Explanation:

Pituitary apoplexy, which is a life-threatening infarction of the pituitary gland, may result after obstetric hemorrhage (Sheehan syndrome), with increased intracranial pressure or during systemic anticoagulation therapy. The anterior pituitary is more susceptible to ischemic injury than the posterior pituitary. The most important hormones that have to be quickly replaced are glucocorticoids (synthesized by the adrenal cortex under pituitary ACTH control) and thyroid hormone, (under, pituitary TSH control), since deficiency of these hormones can result in life-threatening syndromes. Growth hormone, estrogens, and prolactin do not require immediate replacement. Mineralocorticoids can be replaced if diabetes insipidus develops.

Explanation:

This patient most likely has obstructive sleep apnea, which is a transient airway occlusion that causes apnea (periodic cessation of breathing), progressive asphyxia, and arousal from sleep. This occurs many times during the night and leads to increased cardiac after load, pulmonary and systemic vasoconstriction, acute carbon dioxide retention, transient arterial hypoxia, cerebral dysfunction, sleep fragmentation and excessive motor activity. Arterial oxygen and carbon dioxide return to normal between periods of apnea. Options A and B are incorrect because this disorder does not alter the diffusion characteristics of the lungs. It neither increases thickness of the diffusion barrier nor decreases surface area. Hyperpnea is incorrect because ventilation decreases during apnea. Shunt occurs when blood passes through a region of the lung in which there is no ventilation or there is no diffusion. It refers specifically to a regional disorder. This is not the same as decreased ventilation throughout the lungs, which is called hypoventilation; that is what occurs during periods of apnea.

Explanation:

The patient has renovascular hypertension. There are two principal mechanisms of the hypertension. First, there is increased vascular resistance caused by high levels of angiotensin II; this is a direct consequence of the elevated renin level. Severe stenosis of renal arteries may cause decreased renin, angiotensin, and aldosterone if necrosis has progressed to the point that the juxtaglomerular cells are dead; this has not happened in this patient since renin activity is above normal. The level of ADH tends to decrease if blood pressure is elevated. Volume expansion by aldosterone also suppresses ADH, but this is partially offset by a stimulatory effect of angiotensin II. The main reason for volume expansion in this disorder is elevated aldosterone. Volume expansion typically does not cause edema, unless cardiac pumping ability is impaired.
Sympathetic activity is suppressed via the baroreflex when arterial pressure rises; however, normal sympathetic activity is expected in this case, since adaptation of the baroreflex would have allowed it to return to normal. Volume contraction is not to be expected since aldosterone is increased by renal artery stenosis.

Explanation:

Isolated ACTH deficiency is a pituitary disorder characterized by decreased secretion of ACTH, but not of the other hormones of the anterior pituitary. Because of the decreased drive to the inner two zones of the adrenal cortex the secretion of adrenal androgens is decreased. Since pubic and axillary hair in females is dependent on ad renal androgens, ACTH deficiency would lead to a decrease in both. Like primary adrenal insufficiency isolated ACTH deficiency would lead to low serum levels of cortisol (not increased). However, unlike primary adrenal insufficiency, serum levels of aldosterone are usually unchanged with isolated ACTH deficiency. This is because ACTH is not long term regulator of aldosterone secretion (angiotensin II and potassium are the main long term regulators). Since aldosterone is unchanged, serum sodium and serum potassium are normal. Hyperpigmentation is associated with increased, not decreased, serum levels of ACTH.

Explanation:

The patient data showing a decreased maximum flow rate and the total volume exhaled in addition to decreased total lung capacity (4 liters compared to 7 liters) is consistent with restrictive lung disease. Restrictive lung disease reduces not only total lung capacity and vital capacity, it also markedly reduces functional residual capacity (FRC) and, to a lesser extent, residual volume. In restrictive lung disease, both FEV and FVC are reduced, but typically the FEV1/FVC% is normal or increased. A decreased ratio is characteristic of obstructive lung disease. A patient with advanced restrictive disease is more likely to have reduced arterial oxygen and increased carbon dioxide due to low ventilation; if not, blood gases would be normal not reflecting higher than normal alveolar ventilation as in choice C. Anatomic dead space remains relatively constant at different lung inflations. The increased elastic recoil of the lung in a patient with restrictive lung disease decreases pulmonary compliance.

Explanation:

This patient has diabetic ketoacidosis (DKA), as noted by the acetone smell on the breath. Metabolic acidosis tends to cause a shift of potassium from the intracellular compartment to the extracellular fluid. This increases plasma potassium concentration and, along with other effects of chronic acidosis, causes increased urinary potassium excretion. The result is progressive depletion of potassium from the body; patients in severe DKA have been found to have as much as 60% reduction of total body potassium while still displaying hyperkalemia. Volume depletion caused by diuresis can potentially cause hypernatremia however glycosuria increases sodium excretion. The combination of natriuresis with large volume consumption of water strongly suggests that hyponatremia will be present. Hyperphosphatemia is incorrect, because diabetic ketoacidosis
causes excessive loss of phosphate in the urine, and therefore hypophosphatemia. Hypokalemia is incorrect, because, as noted above, metabolic acidosis causes a shift of potassium from the intracellular fluid into the extracellular fluid; hyperkalemia is expected. Positive potassium balance is in correct in the setting of chronic ketoacidosis (duration greater than about 24 hours). The patient´s condition is consistent with DKA of several days duration. It is important to remember that although acute metabolic acidosis decreases urinary potassium excretion, sustained acidosis has the opposite effect.

Explanation:

A 26 year old woman is giving birth. During the birth, the placental membranes tear and amniotic fluid is expressed into a lacerated cervical vein. The woman would most likely experience immediately which one of the following events?

Explanation:

Question Explanation:
The nephrotic syndrome describes the clinical presentation associated with glomerular diseases, which share the common characteristic of “leaky glomeruli.” Large biochemicals, normally unable to cross out of glomerular capillaries into Bowman´s space are lost in to the urine. Serum proteins are lost in large quantities and can be detected as both hypoproteinemia and massive proteinuria. The final component of the nephrotic syndrome (besides generalized edema, hypoalbuminemia, and massive proteinuria) is hyperlipidemia. It is multifactorial in pathogenesis and results from increased synthesis of lipoproteins in the liver, abnormal transport of circulating lipid particles, and decreased lipid catabolism. Increased cholesterol, triglycerides, and low density lipoproteins are found in the serum with membranous glomerulonephritis. Interestingly, there is a decrease of high density lipoproteins in most patients. In addition to albumin the glomerular capillary wall also becomes permeable to lipid producing lipiduria. Furthermore, important plasma proteins lost across leaky capillaries may include immunoglobulins and anticoagulant factors (antithrombin III) that result in vulnerability to infection and venous thrombosis. Albumin a relatively small plasma protein (MW 66,000) is lost very readily, leading to hypoalbuminemia. Serum concentrations of small compounds, such as potassium and glucose which are highly permeable in the normal glomerulus, are unaffected by glomerulonephritides, thus producing the nephrotic syndrome. Similarly blood urea nitrogen is unaffected, and serum ammonia levels are unchanged

Explanation:

The pathologic picture is classic for papillary necrosis. This complication develops most commonly in diabetic patients, but other conditions may result in this renal complication. Among these, analgesic abuse, urinary tract obstruction, and sickle cell disease are the most important. Papillary necrosis may lead to acute renal failure. Fragments of tissue that slough off necrotic papillae may become impacted into the ureters and cause ureteral colic. Gout may cause two renal complications: interstitial nephritis due to deposition of urate crystal within the renal interstitium, and formation of urate calculi within the pelvis. Miliary tuberculosis often involves the kidney. Tubercular infection will give rise to whitish, seedlike nodules most apparent in the renal cortex and consisting of caseating granulomas. Mural thrombosis in the heart frequently leads to systemic thromboembolism. Consequently, embolic infarcts develop in peripheral organs, including kidney, spleen, brain, and the heart itself. In the kidneys, infarcts manfiest grossly as wedge shaped areas of pale coagulative necrosis in the cortex. Recent streptococcal infection may be associated with postinfectious glomerulonephritis (manifesting with nephritic syndrome). The kidneys are edematous and enlarged, and microscopically there is acute glomerulonephritis.

Explanation:

This patient has Wernicke aphasia, which is caused by a lesion of Wernicke´s area, located in the posterior part of the superior temporal gyros (area 22) of the language dominant hemisphere. Lesions of the basal ganglia produce extrapyramidal motor symptoms. Lesions of the diencephalon, which includes the thalamus, hypothalamus, subthalamus, and epithalamus, can lead to myriad sensory, endocrine, and motor defects, but would not selectively affect language. Lesions of the frontal lobe can produce spastic paralysis, Broca´s aphasia (expressive, nonfluent aphasia), disorders of higher order thinking, and deviation of the eyes. (Mnemonic: Broca´s aphasia is associated with broken speech). Lesions of the occipital lobe can produce visual disturbances.

Explanation:

A little knowledge, such as the “knee-jerk” association between asbestos exposure and malignant mesothelioma, can get you into trouble on this question. Malignant mesothelioma is a very rare tumor that is much more common in individuals with a history of asbestos exposure. However, bronchogenic carcinoma is more common than malignant mesothelioma in asbestos exposed individuals, as well as in the population at large. Asbestos exposure is also associated with pulmonary interstitial fibrosis and pleural reactions. Bladder carcinoma is associated with cigarette smoking and exposure to naphthalene dyes. Lymphomas and leukemias are often associated with chromosomal rearrangements (e.g., translocations) that alter the locations of proto-oncogenes (e.g., c-myc, c-abl, bcl-1, bcl-2). The association between scrotal carcinoma and hydrocarbon exposure was first noted by Percival Pott, who noticed an increased incidence of scrotal cancer in chimney sweeps in London.

Explanation:

Microscopic examination of heart muscle from a patient with hypertrophic cardiomyopathy would reveal short, thick myofibrils arranged in circular patterns admixed with normal tissue. On electron microscopy, myofibrils and myofilaments appear disarrayed. Aschoff bodies appear in rheumatic myocarditis and consist of degenerating material and leukocytes. These occur along with Anitschkow myocytes, which contain “ribbon-like” nuclei and eosinophilic cytoplasm. Infiltration by inflammatory cells would be expected in association with an infectious process, such as acute bacterial endocarditis. Localized fibrous scarring is associated with myocardial healing after infarction. Structures resembling poorly formed vessels are found in cardiac myxoma, the most common primary tumor of the heart. The tumor cells are derived from primitive multipotent mesenchymal cells. They may be sessile or pedunculated masses.

Explanation:

BMI is one of the most important calculations of anthropometry, is calculated as weight over (height) squared and measured in kg/m2. BMI can be defined as underweight (less than 18.5), normal (18.5-24.9), overweight (25-29.9) and obese. A BMI above 30 diagnoses obesity and has prognostic value indicating increased propensity to develop diabetes, cancer, osteoarthritis and depression.

Explanation:

Campylobacter infection is one of the commonest causes of inflammatory diarrhoea. Abdominal pain is often a prominent feature of the illness, frequently localising to the right iliac fossa. Diarrhoea may be mild or very severe, often with passage of blood. Symptoms may last a week or longer. Reactive arthritis and Reiter´s syndrome can develop following infection with a number of enteric pathogens, including Shigella, Salmonella, Campylobacter and Yersinia.

Explanation:

The history is suggests a five year history of gastro-oesophageal reflux.
This can cause a columnisation of the oesophageal mucosa known as Barrett´s oesophagus, which is a premalignant state. Surveillance endoscopies are recommended every three years. The development of dysphagia for solids and weight loss suggests the presence of oesophageal carcinoma.

Explanation:

Cholera toxin has two parts, A and B.
B binds while A activates G protein, which activates adenylate cyclase. Elevated cyclic adenosine monophosphate (CAMP) results in unrestricted chloride secretion from villous crypts.

Explanation:

The product of the bcr/abl gene that is seen 97% cases of Chronic Myeloid Leukaemia, is a constitutively active Tyrosine Kinase, this is responsible for the leukaemic process.

Explanation:

DiGeorge syndrome (DGS) consists of congenital thymic aplasia, and thymic hypoplasia.

Explanation:

Approximately 1/4,000 males have Fragile X Syndrome and many of them have never been diagnosed. Males with Fragile X Syndrome almost always exhibit mental retardation and it is the commonest cause. FXS is the most common known cause of autism or “autistic-like” behaviors. Symptoms can also include characteristic physical and behavioral features and delays in speech and language development.
Behavioral characteristics in males include attention deficit disorders, speech disturbances, hand biting, hand flapping, autistic behaviors, poor eye contact, and unusual responses to various touch, auditory or visual stimuli.

Explanation:

Other conditions producing Malabsorption include disaccharidase deficiency, Cystinuria, hypogammaglobulinemia, scleroderma and abetalipoproteinemia. Endocrine disorders, including diabetes mellitus, hypoparathyroidism, adrenal insufficiency, and carcinoid, are also associated with Malabsorption. The steatorrhea of hyperthyroidism is thought to result from ingestion of particularly large amounts of fat in the presence of rapid gastric emptying and intestinal transit. Malabsorption may result if there is an inadequate intestinal absorptive surface. This occurs following extensive surgical resections in conditions such as regional enteritis or after jejunal ileal bypass for morbid obesity. Bacterial overgrowth may produce changes in bile salt metabolism, leading to steatorrhea. This may occur in hypomotility states, such as scleroderma, diabetes, and intestinal pseudoobstruction, as well as in conditions such as blind loops, strictures, and small bowel diverticula. Biochemical and genetic abnormalities may also produce malabsorption. In persons with celiac sprue, administration of gluten
Results in steatorrhea with associated mucosal changes. Abnormalities in mucosal function may also produce Malabsorption. Abdominal radiation may produce extensive morphologic damage to the small intestinal mucosa, which is associated with diarrhea and impaired absorption. Other conditions associated with mucosal defects include arnyloidosis, eosinophilic enteritis, mastocytosis, and collagenous sprue.

Explanation:

Venous thrombosis is attributed to three predisposing factors. The first factor is stasis of blood, which may occur with prolonged immobilization, such as prolonged travel or which may occur in any condition associated with prolonged bed rest, such as a cerebrovascular accident or during surgery requiring more than 30 minutes of anesthesia. The second factor is hypercoagulability of blood, such as that occurring with Antithrombin III deficiency protein S. and protein C deficiencies. The third factor is abnormality of the vessel wall, resulting in endothelial injury, such as that caused by chronic venous insufficiency. Estrogens, but not progestins, are associated with an increased risk of venous thrombosis, with the risk apparently related to dose.

Explanation:

Cerebral emboli are often preceded by such factors as mitral valve prolapse, infective endocarditis, mitral stenosis, and regurgitation. There is typically no prior history of transient ischemic attacks in the cerebral embolic patient. The progression of cerebral emboli typically occurs very rapidly (within seconds) and happens while the patient is awake.

Explanation:

Factitious hypoglycemia occurs in medical personnel and family members of persons with insulin-dependent diabetes mellitus. C-peptide is released on an equimolar basis with endogenous insulin into the portal vein. In insulinoma, the level of C-peptide parallels the high insulin levels. With exogenous insulin administration, endogenous insulin secretion, and along with it, C-peptide secretion is suppressed. Plasma insulin levels are high in both conditions. As a consequence of raised insulin levels, plasma glucose levels are suppressed in both conditions. Sulfonylurea levels are absent in both conditions. Because insulinoma cells frequently do not process proinsulin completely, the proinsulin levels are often elevated in the serum of persons with these tumors.

Explanation:

Any prolonged systemic overload of iron results in a condition called hemosiderosis. This may result from hemolytic anemias, repeated blood transfusions or (rarely) increased iron absorption. Patients with severe forms of sickle cell anemia or thalassemia are especially prone to this complication. The pigment appears as coarse, golden-brown granules within the cytoplasm. Despite some pathologists claim to the contrary, it is often difficult to distinguish between different types of pigments based on their light-microscopic features. Bilirubin is the normal pigment in the bile. Excess bilirubin can be appreciated on tissue sections of the liver in cases of cholestatic jaundice. Inhalation of carbon particles is an inevitable consequence of living in polluted urban areas and of cigarette smoking. Carbon particles are taken up by alveolar macrophages and transported to the regional lymph nodes, causing a dark discoloration of hilar lymph nodes and lung interstitium known as anthracosis. Homogentisic acid is a black pigment occurring in alkaptonuria. The pigmentation, referred to as ochronosis, especially involves connective tissue and cartilage. Lipofuscin is a brown pigment that accumulates in aging postmitotic cells such as cardiac myocytes and neurons. It results from lipid peroxidation of polyunsaturated fatty acids in the plasma membranes and represents an epiphenomenon of free radical injury. As far as we know, lipofuscin is harmless.

Explanation:

True statement regarding phenylketonuria is which one of the following?

Explanation:

Explanation:

With respect to gastric cancer, men are affected twice as commonly as women. H. pylori infection, chronic atrophic gastritis, pernicious anemia, and history of partial gastric resection are all risk factors for gastric cancer.

Explanation:

Explanation:

This case describes a pandemic of influenza A, which is caused by the ability of the virus to undergo dramatic genetic changes of type by reassortment of its segmented RNA genome a trait called genetic shift. The only virus on the list that possesses a segmented genome is the rotavirus, in the reovirus family, which possesses 10-11 segments in its genome. Coronavirus is not segmented and is a cause of the common cold. HIV is not segmented and is known for its genetic drift (minor mutational changes over time due to an error prone polymerase), not genetic shift. Measles virus is not segmented and is controlled largely by vaccination. Rabies virus is not segmented

Explanation:

The tuberculin response is the classic example of type IV hypersensitivity, which is mediated by TH1 cells and macrophages. The initial recognition signal involves interaction between MHC class II and the T cell receptor. The B7 molecule on the cell surface of the antigen presenting cell reacts with the CD 28 molecule on the T cell surface for maximal costimulatory signals. The B7 molecule on the surface of the antigen presenting cell reacts only with CD 28 and does not react with LFA-1 adhesion molecule. The ICAM-I on the surface of an antigen presenting cell reacts with the LFA- I on the surface of a T cell for the purpose of cell-to-cell adhesion and does not function for costimulation. LFA-3 (CD58) is an adhesion molecule on the surface of an antigen presenting cell. It does not react with a CD28 costimulatory molecule on the T cell surface. The MHC class II molecule with its epitope does interact with a specific T cell receptor (TCR) but this is not termed costimulatory. However, the interaction does stimulate the T cell to produce interleukins for further cell division.

Explanation:

A full term neonate is born after a normal pregnancy and is well for the first 2 years of his life. He receives all his immunizations without any complications. Around his second birthday his mother notes him having frequent upper respiratory tract infections and he is hospitalized three times for pneumonia. Investigations would most likely reveal a deficiency of which immunoglobulin?

Explanation:

Blocking antibody is generally an IgG antibody against the allergen. It is induced in the allergic patient by administering small amounts of allergen over a period of time. When the person is again exposed to the allergen, the IgG reacts with the allergen before it can reach the IgE-coated mast cell. Antihistamines would block histamine receptors out would not react with the allergen before it could reach the IgE-coated mast cell. Cromolyn sodium is a drug that stabilizes mast-cell membranes, thus inhibiting degranulation, but would have no effect on allergen binding to IgE on mast cells. Epinephrine is the mainstay of therapy in severe cases of immediate hypersensitivity (anaphylaxis). It increases intracellular cyclic AMP thus decreasing mast-cell degranulation, and causes smooth-muscle dilation in the airways. Epinephrine would have no effect on the binding of the allergen to IgE on mast cells. Cyclic AMP is degraded in cells by the enzyme phosphodiesterase. Theophylline inhibits this enzyme, thereby increasing mast-cell cyclic AMP levels and making degranulation less likely without affecting the binding of the allergen to IgE on mast cells.

Explanation:

Swelling and inflammation at an inoculation site within 1 to 2 days reflects that the individual has “seen” this immunogen before and is mounting a secondary immune response to it. This is known as Arthus reaction which is a type III hypersensitivity reaction resulting from the formation of immune complexes of the vaccines on this list, the one that a young military recruit will have been previously exposed to (probably multiple times) is the tetanus toxoid. This vaccine is routinely administered at 10 year intervals, or even shorter intervals in cases in which there is fear of serious exposure. Adenovirus is a live non attenuated vaccine administered in enteric-coated capsules. Hepatitis A is not the best choice because at the beginning of a course of immunizations there would be no underlying preexisting immune response and thus no inflammation and swelling caused by previously sensitized lymphocytes. The final booster of the series might be expected to cause such inflammation, but not the beginning ones. Hepatitis B is not the best choice because at the beginning of a course of immunizations, there would be no underlying preexisting immune response and thus no inflammation and swelling caused by previously sensitized lymphocytes. The final booster of the series might be expected to cause such inflammation, but not the beginning ones. The typhoid vaccine is single dose and administered to individuals likely to travel to endemic areas. It is unlikely to have been administered to this individual before his recruitment into the military, so he is unlikely to have previously sensitized immune cells.

Explanation:

This patient is suffering from toxic shock syndrome which resulted from growth of Staphylococcus aureus in the surgical packing associated with his tonsilioadenoidectomy. S. aureus produces an exotoxin, TSST-1 which acts as a superantigen, cross-linking the T-cell receptors and major histocompatibility complex class II antigens of unrelated T lymphocytes and macrophages (in the absence of antigen recognition) causing their polyclonal stimulation and the production of dangerous amounts of their cytokines. The cytokines that are overproduced during superantigen pathogenesis are interleukin-1, interleukin-6, and tumor necrosis factor-alpha (from macrophages) and interleukin-2 and interferon-gamma (from T helper lymphocytes). The pathogenesis of endotoxin shock (gram- negative sepsis) results from the direct stimulation of macrophages because of the binding of bacterial lipopolysaccharide (endotoxin) to the endotoxin receptor (CD14) and would only involve T-helper lymphocyte stimulation as a secondary effect. Therefore, a patient suffering from superantigen pathogenesis will have higher leveis of cytokines from T-helper lymphocytes (interleukin-2 and interferon-gamma) than will a patient suffering from gram-negative sepsis. Both forms of pathogenesis will cause elevation of the macrophage cytokines, interleukin-1, interleukin-6, and tumor necrosis factor-alpha. Interleukin-1 is a product of activated macrophages and would be elevated to similar degrees in both toxic shock syndrome and endotoxin shock. This cytokine is also known as endogenous pyrogen and plays a major role in the development of the fever in these cases. Interleukin-4 is a product of T-helper-lymphocytes that stimulates the activation of B lymphocytes in the humoral immune response. It would not be produced in abnormal amounts in either superantigen or endotoxin shock pathogenesis. Interleukin-6 is a product of activated macrophages and would be elevated to similar degrees in both toxic shock syndrome and endotoxin shock. This cytokine is a second pyrogenic product and also mediates the acute phase response. Tumor necrosis factor-alpha is a product of activated macrophages and would be elevated to similar degrees in both toxic shock syndrome and endotoxin shock. This cytokine is pyrogenic and plays a role in cancer cachexia.

Explanation:

Herpes simplex is one of the most common etiologic agents of infective esophagitis. The disease may manifest in immunocompetent hosts, although it is more frequent in immunocompromised (e.g., AIDS) patients. Punched out ulcers are highly characteristic. The histology is rather nonspecific (chronic inflammatory infiltrate) except for the presence of glassy intranuclear eosinophilic inclusions Cytomegalovirus is the other common viral etiology of esophagitis.-This form would be characterized by purple intranuclear inclusions combined with granular cytoplasmic inclusions, and markedly enlarged cell size.
Candida albicans gives rise to esophagitis in immunocompromised hosts or develops superimposed on CMV/herpes ulcers. Candida organisms are easily identified admixed with squamous cells and neutrophils. Chemical injury is usually due to accidental or suicidal ingestion of corrosive agents, such as lye acids, and detergents. The mucosa shows diffuse erythema, edema, and (in severe cases) extensive ulcerations. The intestinal microbe Escherichia coli does not usually cause disease in the esophagus. Helicobacter pylori does not cause esophagitis. This gram negative organism is associated with chronic gastritis of the antrum, peptic ulcer, gastric adenocarcinoma, and lymphoma.

Explanation:

Primary adrenal insufficiency occurs when the adrenal glands fail to produce adequate cortisol. Cortisol secretion is normally stimulated by ACTH release from the anterior pituitary. Once cortisol is released, it feeds back to the pituitary to inhibit further ACTH secretion. Therefore, if cortisol secretion was impaired, ACTH levels would be elevated rather than reduced.
Elevated cortisol does not occur in adrenal insufficiency. Instead, cortisol secretion would be decreased. Epinephrine is released by the adrenal medulla and could be reduced by adrenal insufficiency rather than increased by it. CRH is released by the hypothalamus and acts on the anterior pituitary to stimulate the secretion of ACTH from the anterior pituitary. It is inhibited when cortisol feeds back to turn off its production in the hypothalamus. Therefore CRH levels would be elevated in the absence of cortisol rather than decreased.

Explanation:

A small segment of DNA containing drug resistance genes and three pairs of indirect repeats is a description of a group of three transposons. Transposons, or “jumping genes,” are segments of DNA capable of movement from one location to another inside a cell. When they become accumulated in one location, particularly if that location is inside a fertility factor plasmid, then they can be transferred to new bacteria by conjugation. This is how multiple drug resistance plasmids are formed. Transposons are flanked by indirect repeats, which are sequences that are complementary and antiparallel to one another. Inside the indirect repeats, they carry the coding for the enzymes that mediate the actual movement from place to place, transposase genes, and other genetic coding (such as the drug-resistance genes described here). A temperate phage is a bacterial virus that incorporates its genome into the chromosome of the bacterium during its life cycle (lysogeny). There is no reason to expect that viral DNA would be found within a transposon. OriT is the genetic locus at which a break in the double-stranded DNA of either plasmid (fertility factor) or episome (Hfr chromosome) is made to begin transfer of DNA across a conjugal bridge. Transposons are not involved in the process of conjugation, although they can be transferred passively across a conjugal bridge if they become inserted in a fertility factor. The tra operon is the set of genes found in a fertility factor and that mediates the actual mechanism of conjugation. They encode sex pill, the enzymes of DNA metabolism, and those that mediate formation of the conjugal bridge. Because transposons move by site specific recombination, it is not possible that the tra operon could be found inside the margins of a transposon. Three pairs of direct repeats could not be found inside the segment of DNA that includes three transposons. Direct repeats are formed by repair of the staggered breaks made in the recipient DNA when a transposon lands. Thus, with three transposons landing in a small area of DNA, two sets of direct repeats could be inside the margins, but the third set would have to be outside the outermost set of indirect repeats.

Explanation:

This woman sustained an obstruction of a major airway such that the area of the lung distal to the obstruction was perfused, but not ventilated. In this area of lung, there will be no gas exchange, and the V/Q ratio will approach zero. As a result, the PO2 and PCO2 of the pulmonary blood (and alveolar gas) approaches that of venous blood (PO2 = 40 mm Hg, PCO2 = 45 mm Hg). Therefore, the PO2 will be lower, and the PCO2 will be higher than normal. Because the PCO2 is high, pH Al be low. The amount of dissolved oxygen will be lower than nor-mal, not greater. Dissolved oxygen is equal to 0.003 mL 02/100 mL blood times PO2. Because the PO2 is low in this situation, so must be the dissolved oxygen. PCO2 will be elevated and pH will be diminished in this lung area. Both of these factors cause the curve to shift to the right, not to the left. PCO2 will be higher than normal, not lower. PO2 is decreased and approaches that of venous blood, not arterial blood.

Explanation:

Myocardial infarction is the leading cause of death in diabetics. The advanced glycosylated products associated with long-standing diabetes mellitus accelerate the atherosclerotic process. Other risk factors for coronary artery disease (CAD) include hypertension, smoking, hypercholesterolemia, family history of CAD at a young age, male sex, or being a postmenopausal female. Diabetic ketoacidosis (DKA) carries a high mortality rate for type 1 diabetics. However, this patient had type 2diabetes, which is associated with hyperosmolar coma, not with DKA. Although the remaining choices are all common causes of morbidity and mortality in diabetics, myocardial infarction is the most frequent cause.

Explanation:

The history of nosebleeds and menorrhagia, the petechiae, thrombocytopenia, and increased bleeding time all suggest a platelet disorder. The decreased platelet count suggests a thrombocytopenic disorder rather than a platelet function disorder. The absence of antinuclear antibody argues against systemic lupus erythematosus (a significant cause of thrombocylopenia). The negative drug history rules out drug-associated thrombocytopenia. After other causes have been ruled out, a tentative diagnosis of idiopathic thrombocytopenic purpura can be made. This disorder, also called immune thrombocytopenic purpura, is an acquired thrombocytopenia caused by formation of autoantibodies directed against the platelet membrane proteins glycoprotein IIb/IIIa, followed by splenic destruction of opsonized platelets. The disease typically occurs in women from 20 to 40 years of age. Splenectomy and immunosuppressive therapy can generally control the thrombocytopenia. Antibodies to the acetylcholine receptor are seen in myasthenia gravis. Antibodies to erythrocyte membrane proteins are seen in autoimmune hemolytic anemia. Antibodies to intrinsic factor are seen in pernicious anemia. Antibodies to Type IV collagen are seen in Goodpasture syndrome.

Explanation:

The forced vital capacity (FVC) is the vital capacity measured with a forced expiration (which may be less than that measured without straining). The forced expiratory volume in one second (FEV1) is the amount of air that can be expelled from the lungs during the first second of a forced expiration. The FEV1 /FVC ratio has diagnostic value for differentiating between normal, obstructive, and restrictive patterns of a forced expiration. The FEV1 /FVC for the normal individual A is 4 L/5 L = 80% and 1.5 L/3.0 L = 50% for the individual B. Individual B is a patient with chronic obstructive pulmonary disease. Notice that the rate of expiration is slower and the total volume exhaled is reduced. This is typical of obstructive disease. Patients with restrictive disease also have a reduced FVC, but exhale a large percentage of it in the first second, increasing their FEV1 /FVC ratio.

Explanation:

Explanation:

Pernicious anaemia is usually a megaloblastic anaemia but may also be associated with a pancytopaenia. The platelet count is usually normal in chronic renal failure but there is a platelet function abnormality.

Explanation:

CLL is commonly complicated by panhypogammaglobulinaemia. Although immunoglobulin prevents recurrent infections it does not prolong survival.

Explanation:

Neisseria gonorrhoea occurs in young adults and is often preceded by a migratory tendonitis or arthritis. Gram´s stain is positive in 25% and culture positive in 50%. Neisseria gonorrhoeae is a species of Gram negative bacteria responsible for the disease gonorrhoea. They are highly fastidious gram negative cocci, that is, they require special nutrients to survive. These cocci typically appear in pairs (diplococci).

Explanation:

Lithium can produce diabetes insipidus and also raise calcium. Neither Seroxat nor angiotensin-converting enzyme (ACE) inhibitors are related to hypercalcaemia. Excess of vitamin D causes elevated calcium. Furosemide lowers calcium but thiazides reduce excretion and so can exacerbate hypercalcaemia.

Explanation:

This food poisoning with no vomiting and an incubation period between 9-13 hours is typical of Clostridium perfringens. The history is too long for a typical Staph, aureus infection (vomiting a typical feature, incubation period 1-6 hours) and rather short of enterovirus (24 hours).
The predominant symptom of B.cereus (incubation period 1-5 hours) is marked vomiting with diarrhoea occasionally seen.
Most infections with C. neoformans consist of a lung infection and not diarrhea.
Rotavirus is the most common cause of severe diarrhoea among infants and young children.
Supportive treatment is all that is generally required with symptoms resolving after 24 hours.

Explanation:

The alpha-fetoprotein (AFP) tumor marker may be elevated in HCC. Prostate specific antigen (PSA) may rise in prostate carcinoma. CA- 125 can be elevated in ovarian carcinoma. Urinary metanephrines are elevated in Pheochromocytoma. Carcinoembryonic antigen (CEA) may be elevated in colon carcinoma. PSA is prostrate specific and not cancer specific and may be elevated in prostatitis, etc.

Explanation:

This patient´s condition is a classic third-trimester complication referred to as toxemia of pregnancy or preeclampsia. Preeclampsia is defined as “sustained elevation of HP >140/90 after 20 weeks of pregnancy with proteinuria.” It occurs in 6% of all pregnancies but is more frequent in primiparas. Although the pathogenesis is still unclear, the first event appears to be placental ischemia, probably due to abnormalities in the trophoblast and alterations in the maturation of placental vessels. The trophoblast of invading placental vessels fails to acquire the characteristics of normal endothelial cells, with subsequent alterations in blood flow. Placental ischemia then triggers the release of thromboplastic substances, increases renin synthesis, and reduces prostaglandin E levels.
Chorioamnionitis (choice A) is an infection of chorioamnionic membranes due to bacteria that ascend through the vaginal canal. This is an important cause of spontaneous abortion in the second and third trimesters but plays no role in the pathogenesis of toxemia of pregnancy, The release of thromboplastic substances may cause disseminated intravascular coagulation (DIC) (choice B)
Increased renin and reduced prostaglandin E mediate increased sensitivity to angiotensin, leading to maternal hypertension (choice C)
Ischemic damage to maternal organs, including brain, liver, and kidneys (choice D) results from thrombotic occlusion of arterioles and capillaries as a consequence of DIC.
Overall, the clinical picture of toxemia is due to DIC mediated ischemic damage to brain (changes in mental status and convulsions), liver (elevated liver enzymes), and kidneys (proteinuria, leading to peripheral edema).A manifestation of toxemia is HFLLP syndrome which stands for hemolysis, elevated liver enzymes, and low platelets.

Explanation:

Trypanosomiasis, or sleeping sickness, is most often caused by Trypanosoma brucei. Winterbottom´s sign, or post-cervical nodal adenopathy and a blank look smile are commonplace in trypanosomiasis. None of the other parasitic infections causes the characteristic Winterbottom´s sign and blank look smile.

Explanation:

This patient has cryptosporidiosis. The causative protozoan, most often Cryptosporidium parvum, infects the brush border of the small intestine. Although the disease is usually self limited in healthy individuals, in AIDS patients it can cause severe diarrhea with fluid losses in the 5 to 10 liters/day range. The mechanism of causation of diarrhea is through the direct lysis of cells of the brush border as the intracellular parasites multiply there. The diarrhea may continue persistently or intermittently until the patient´s death. Stool concentration techniques increase the chance of indenting the characteristic acid fast oocysts in stool. Invasion into the submucosa is observed with organisms such as Entamoeba histolytica and Shigella dysenteriae among others. Invasive organisms cause diarrhea that is bloody and filled with neutrophils. Stimulation of neutrophilic infiltrate is also a finding in invasive organisms because neutrophils are attracted to the area of bowel wall destruction. Intracellular organisms such as Cryptosporidium are not major attractors of neutrophils. Toxins that inactivate the 60S ribosomal subunit include the Shiga toxin of Shigella dysenteriae and the verotoxin of enterohemorrhagic Escherichia coil. Most intracellular parasites such as Cryptosporidium do not produce exotoxins. A toxin which ribosylates Gs is produced by enterotoxigenic .Escherichia colt Cryptosporidium is not known to produce any exotoxins.

Explanation:

The description of large ameboid trophozoites tells us this patient is infected with Plasmodium vivax malaria. P. vivax and P. ovale are both capable of causing relapse following recovery from the primary infection because both organisms leave dormant forms in the liver, called hypnozoites. P. falciparum and P. malariae do not possess these forms and thus are incapable of causing relapses, but if drug treatment of the erythrocytic stages is inadequate, the symptoms can “recrudesce” due to renewed multiplication in the bloodstream. Relapses and recrudescences look the same symptomatically because once parasites begin multiplying again in the bloodstream, the cyclic fevers return. This distinction is medically important, because relapses can be prevented by destruction of hypnozoites with primaquine, by so called “radical cure.” Radical cure is not necessary following Infection with the two species of Plasmodium that do not produce hypnozoites. Gametocytes of P. falciparum and P. vivax are the haploid forms of the malaria parasite, which must be ingested by mosquitoes in a blood meal so that fertilization can occur in the mosquito stomach and a new generation of infectious sporozoites can be produced. Gametocytes die if they are not taken up by mosquitoes, and they play no role in the human with reinitiating symptoms. Hypnozoite of P. falciparum is not a possible answer since neither P. falciparum nor P. malariae leaves these dormant stages in the liver. Merozoites of P. falciparum and P. vivax are parasite daughter cells. Exoerythrocytic merozoites are produced by the process of schizogony (asexual fission) in the liver, and erythrocytic merozoites are produced by schizogony in erythrocytes. Although the release of merozoites from red blood cells is associated with the release of pyrogens and a spike of fever these forms are not responsible for the potential for relapse.

Explanation:

Patients with hyper IgM syndrome (HIGM) experience very little, if any, isotype switching. The B cells in these patients cannot undergo the switch from IgM to IgG, IgA or IgE that normally occurs during B-cell maturation. When B cells undergo isotype switching, they require two factors: IL-4, which binds to a specific receptor on the B cell, and the CD40 molecule on the B-cell surface, which binds to the CD40 ligand (CD40L) on an activated T cell surface. The deficiency is due to mutations in the CD40L and results in patient: who are IgG and IgA deficient, but synthesize, large amounts of polyclonal IgM. Affected individuals are susceptible to pyogenic infections, and often form IgM autoantibodies to neutrophils, platelets, or tissue antigens. The disease is inherited as an X-linked recessive in 70% of the cases. Another form of HIGM, does involve CD40 itself; however, it usually presents later in childhood The problem in this patient is due to mutations in the CD40L, not the CD40 molecule on the B cell. Gamma-interferon is primarily a type I helper T cell (TH1) cytokine, although it does inhibit the TH2 lineage response to specific antigens. A decrease in IL-2 would inhibit the cell mediated immune response, and the patient would be susceptible to infection with intracellular microorganisms. IL-3 is considered a growth factor for hematopoietic stem cells and mast cells. The patient had a normal CBC, except for slight neutropenia and thrombocytopenia.

Explanation:

Two types of free-living amoeba can infect the brain and meninges: Naegleria fowleri and Acanthamoeba species. The former affects healthy adolescent or adult divers while the latter causes infection in patients with immunosuppression because of diabetes, alcoholism, cancer, or HIV infection. The brain infection characteristically has a prominent perivascular character, which causes a multifocal hemorrhagic necrotizing meningoencephalitis. Skin ulcers, nasal infection, or pneumonia may also be present. It is thought that the organisms may release a toxin causing host tissue necrosis. Systemic antifungal agents (e.g. amphotericin) have some activity against this organism, but most cases are fatal. Entamoeba histolytica causes amoebic dysentery and liver abscess. Giardia lamblia is a flagellate, rather than an amoeba, and causes diarrhea. Naegleria fowleri is an amoebic cause of meningoencephalitis in previously healthy swimmers and divers. Trichomonas vaginalis is a flagellate, rather than an amoeba, and causes vaginitis

Explanation:

Mild renal failure is a common cause of hyperkalemia (excess serum potassium). The mechanism appears to be deficient renin production by the damaged kidney which in turn causes lower than normal secretion of aldosterone by the adrenal cortex. The relative lack of aldosterone causes hyperkalemia because there is less than normal exchange of Na for of by the renal tubules (Na+ is comparatively lost while K+ is comparatively saved). Treatment can be either with a mineralocorticoid, such as hydrocortisone, or more easily with a potassium-wasting diuretic such as furosemide. The combination of high renin and high aldosterone can be seen in secondary hyperaldosteronism due to processes such as renal ischemia, renal juxtaglomerular cell, hyperplasia, and edema. Clinically secondary hyperaldosteronism produces sodium retention and potassium wasting. The combination of high renin and low aldosterone can be seen in nonrenal causes of hypoaldosteronism, such as with biosynthetic defects or following surgical ablation of the adrenal glands. The combination of low renin and high aldosterone can be seen in primary hyperaldosteronism (Conn syndrome) and produces sodium retention and potassium wasting. Hyperkalemia with normal renin and normal aldosterone levels can be seen when potassium-sparing diuretics are coupled with high dietary intakes and as a drug side effect (e.g.ACE inhibitors).

Explanation:

Weight loss of more than 5% of body weight is considered a very adverse prognostic feature in cancer since it usually indicates the presence of widespread disease. (Uncommonly, a relatively small primary lesion that has not yet metastasized can cause cachexia.) Both tumor necrosis factor (TNF) and interleukin 1-beta have been implicated in the production of cachexia with weight loss, loss of appetite, and alteration in taste. Large tumor burdens may additionally alter protein and energy balance, often with negative nitrogen balance. Therapy, in whatever form (surgery, radiation, chemotherapy), may also contribute to cachexia late in the course secondary to effects on the digestive system. Clathrin is a protein that helps to form pinocytotic vesicles. Histamine is released by mast cells and basophils and contributes to allergic responses. Interferon is important in the body´s response to viral infection. Interleukin 1-beta, not 2, is produced by activated monocytes and macrophages and has been implicated in cachexia. Interleukin 2 is released by helper T cells and augments B-cell growth as well as antibody production.