NBME 11 Answers to All Sections



NBME 1104/07/2014 BLOCK 1 1.FF since TB is a reportable disease 2.CC When blood sugar is low, glucagon signals the adipocytes to activate hormone-sensitive lipase, and to convert triglycerides into free fatty acids 3.EE Ninety percent of patients with gout develop excess urate stores due to an inability to excrete sufficient amounts of normally produced uric acid in the urine (underexcretion). The remaining patients either overconsume purines or produce excessive amounts of uric acid endogenously (overproduction). •In rare cases, overproduction of uric acid is primary, due to a genetic disorder. These disorders include hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome), glucose-6phosphatase deficiency (von Gierke disease), fructose 1-phosphate aldolase deficiency, and PP-ribose-P synthetase variants. •Overproduction of uric acid may also occur in disorders that cause high cell turnover with release of purines, such as meat intake and seafood intake. These disorders include myeloproliferative and lymphoproliferative disorders, psoriasis, chemotherapy (tissue lysis), hemolytic anemias, pernicious anemia, ineffective erythropoiesis (as in B-12 deficiency), excessive exercise, and obesity. •Overproduction of uric acid can occur from overconsumption of foods high in purines. •Common causes of secondary gout due to under excretion of uric acid include renal insufficiency, lead nephropathy (saturnine gout), starvation or dehydration, hypothyroidism, hyperparathyroidism, drugs (including loop and thiazide diuretics and cyclosporine A), low-dose aspirin, and chronic ethanol (especially beer and hard liquor) abuse. These disorders should be identified and corrected, if possible. •Comorbidities, including hypertension, diabetes, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, diabetes, obesity, and early menopause, are associated with a higher incidence of gout. •Consumption of fructose-rich foods and beverages are associated with an increased risk of gout in both men and women Because of no clinical symptoms or history we should think about risk factors that can cause Gout... ....gender...Men more than women .......................age.....elderly more than younger 4.CC Gardenella vaginalis....gram variable rod...cause vaginosis white/gray vaginal discharge Whiff test...add KOH...fishy smell non painful anaerobe overgrowth of bacteria in vagina Clue cells or vaginal epithelial cell covered with bacteria treatment....Metronidazole 5.AA Check 1904 Q in UW 6.CC Lovastatin....-statins HMG-CoA reductase inhibitors...dec. LDL.. Bad cholesterol...mild effect on HDL and triglycerides...inc. mechanism of action.... 1.inhibit cholesterol precursor , mevalonate 2.synthesizing LDL receptors 7.CC 2-Naphthylamine is an aromatic amine. It is used to make azo dyes. It is a known human carcinogen. Aniline dyes...aromatic amines 2-Naphthylamine is found in cigarette smoke and suspected to contribute to the development of transitional cell carcinoma of urinary tract system (It is activated in the liver but quickly deactivated by conjugation to glucouronic acid. In the bladder, glucouronidase re-activates it by deconjugation, which leads to the development of bladder cancer.) 8.DD Presentation •Pin-point pupils, severe respiratory depression/cyanosis and coma. •BP may be low but is often surprisingly well maintained and with pentazocine overdose actually increases. •Although some opiates, e.g. dextropropoxyphene and pethidine, increase muscle tone and cause fits, in general opiates cause marked hypotonia. ....Ferruginous bodies.. And E coli is notorious for that.DD plasmid transfer between bacteria needs cell to cell contact through conjugation.Asbestos bodies with prussian blue iron stain in the lung.It is usually caused by exposure to asbestos. 10... Asbestosis.CC Mesothelioma..9. 11..Bacterial transformation may be referred to as a stable genetic change brought about by the uptake of naked DNA (DNA without associated cells or proteins) and competence refers to the state of being able to take up exogenous DNA from the environment.Nystatin for superficial infection( swish and swallow) Amphotericin B..AIDS and Vulvaginitis..steroides..CC Candida albicans..for serious systemic infection ..neonates...oral and esophageal thrush in immunocompromised.high PH diabetes....chronic mucocutaneous candidiasis Treatment.use of antibiotics Diaper rash and endocarditis in IV drug users. disseminated candidiasis to any organ.diabetes... Two forms of competence exist: natural and artificial. It pierces the palmar carpal ligament. and communicates with the volar branch of the lateral antibrachial cutaneous nerve.CC The palmar branch of the median nerve is a branch which arises at the lower part of the forearm. Therefore. this portion of the median nerve usually remains functioning during carpal tunnel syndrome. the palmar branch travels superficial to the Flexor retinaculum of the hand. The lateral branch supplies the skin over the ball of the thumb. The medial branch supplies the skin of the palm and communicates with the palmar cutaneous branch of the ulnar. and divides into a lateral and a medial branch. .12. Unlike most of the median nerve innervation of the hand. . .. ....AA Albuterol...........> inc.. with pain experienced in different ways or even being completely absent (which is more likely in female patients and those with diabetes)............... the sensation is "atypical".................. or unstable angina (38%) The cardinal sign of decreased blood flow to the heart is chest pain experienced as tightness around the chest and radiating to the left arm and the left angle of the jaw.3-Bisphosphoglycerate: It binds with greater affinity to deoxygenated hemoglobin (e.......g..Protein Kinase A 16 AA 17 CC CMV has a unique method of escaping immune response it dec.....Beta2.....V2 receptors....>inc.. Beta1........ Ref Kaplan Immuno Chap 8[pg 99] viral strategies for evasion of the CMI response ...13.....cAMP..H2...CC 2.......D1......Gs.Beta2 agonist.. The normal for the MHC 1 molecule is that its made in the RER and then transported to the Cell membrane.. as well as shortness of breath.ATP. Some may report palpitations... This may be associated with diaphoresis (sweating)...... If it get translocated to the cytosol......AA Acute coronary syndrome (ACS) is usually one of three diseases involving the coronary arteries: ST elevation myocardial infarction (30%). In many cases...... anxiety or a sense of impending doom and a feeling of being acutely ill....Adenylyl cyclase...used during acute exacerbation .. its likely to be degraded............ 15....... the expression of MHC 1 and also expresses a decoy molecule.. nausea and vomiting...relaxes bronchial smooth muscle ... when the red cell is near respiring tissue) than it does to oxygenated hemoglobin 14. non ST elevation myocardial infarction (25%). Shining a light into one eye should result in equal constriction of the other eye. The neurons in the optic nerve decussate in the optic chiasm with some crossing to the contralateral optic nerve tract.18. 19 DD . This is the basis of the "swinging-flashlight test". as well as his going cross-eyed.GG Pupillary reflex: The oculomotor nerve also controls the constriction of the pupils and thickening of the lens of the eye. his pupils should constrict. By moving a finger toward a person's face to induce accommodation. This can be tested in two main ways. org/elder/lewy_body_disease.org/alzheimers_disease_dementia_with_lewy_bodies. *Cytoplasmic!* Parkinson's disease.alz.. loss of dopaminergic neurons rare cases have been linked with illicit street drug.BB http://www.helpguide.a sp Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson's disease (PD) and Alzheimer's disease (AD) and some other disorders..CC Kernicterus is damage to the brain centers of infants caused by increased levels of unconjugated bilirubin 21. heroin ..degenerative disorder of CNS associated with lewy bodies and depigmentation of the substantia nigra. They are identified under the microscope when histology is performed on the brain...htm http://www.20. .. thyroxine (T4) and triiodothyronine (T3).22. . With higher TSH levels and low free T4 levels.. breaking voice – deepening of the voice can also be noticed. Subclinical hypothyroidism is a state of normal thyroid hormone levels...EE Hypothyroidism is a condition leading to the deficiency in the production of thyroid hormone... increased sensitivity to cold Constipation Rapid thoughts Depression Muscle cramps and joint pain Thin... symptoms become more readily apparent in clinical (or overt) hypothyroidism.. ma. thyroid-stimulating hormone (TSH).. Goiter Slow speech and a hoarse... with mild elevation of thyrotropin.. itchy skin Weight gain and water retention Bradycardia Late. Dry puffy skin. Early.. brittle fingernails Coarse hair Paleness Decreased sweating Dry. Poor muscle tone (muscle hypotonia) Fatigue Any form of menstrual irregularity and fertility problems Hyperprolactinemia and galactorrhea Elevated serum cholesterol Cold intolerance.. especially on the face Thinning of the outer third of the eyebrows Abnormal menstrual cycles Low basal body temperature Thyroid-Related Depression Uncommon. Diminished cardiac output and decreased contractility Reactive (or post-prandial) hypoglycemia Sluggish reflexes Hair loss Anemia caused by impaired hemoglobin synthesis (decreased EPO levels). hands and feet (late. less common symptoms) Gynecomastia Deafness 23. so causes increase in cAMP -Lymphocytosis promotion -Hypoglycemia due to release of insulin. impaired intestinal iron and folate absorption or B12 deficiency Difficulty swallowing Shortness of breath with a shallow and slow respiratory pattern Increased need for sleep Irritability and mood instability Yellowing of the skin due to impaired conversion of beta-carotene to vitamin A Impaired renal function with decreased glomerular filtration rate Acute psychosis (myxedema madness) (a rare presentation of hypothyroidism) Decreased libido in men due to impairment of testicular testosterone synthesis Decreased sense of taste and smell (anosmia) Puffy face. although it is not always present. Chemokines are signaling molecules produced by infected cells and attract neutrophils and macrophages. The muscle is absent in about 14 percent of the population Absence of palmaris does not have any known effect on grip strength 24.DD The palmaris longus is seen as a small tendon between the flexor carpi radialis and the flexor carpi ulnaris. .Impaired memory Impaired cognitive function (brain fog) and inattentiveness.AA Pertussis toxin inhibits Gi. A slow heart rate with ECG changes including low voltage signals. Pertussis Toxin interferes with the early chemokine production and the inhibition of the neutrophil chemotaxis. 25.oxidative phosphorylation.....AA Narrowing renal artery inc.. Present with tearing chest pain radiating to the back.. like codeine. It has therefore been suggested that increased tight junction permeability (reduced barrier function) is a risk factor for development of Crohn's disease...... Mitochondrial pemeability.Marfan's. The cough suppression potency of dextromethorphan in adults is nearly equal to that of codeine.GERD . CXR... 29.2 The drug. .DD irreversible cell injury Plasma membrane damage lysosomal rupture Calcium ion influx..vacualization and phospholipid-containing amorphous density 28.cystic medial necrosis Aortic dissection..BB The addictive potential of codeine encouraged the marketing of dextromethorphan in a variety of cough and cold preparations..EE Bone marrow transplant has been shown to induce tolerance following organ transplant. Renin-Angiotensin-Aldosterone system. 26. Although dextromethorphan is chemically derived from the opiates..Glandular metaplasia. nuclear pycnosis.... 27.. mediastinal widening 31. it has no analgesic or addictive properties.AA The patient is too tall and thin with scoliosis. acts on the central nervous system to elevate the threshold for coughing.often secondary to irritation/or environmental exposure Barrett's esophagous..replacement of non keratinized squamous epithelium with intestinal/columnar epithelium in the distal esophagous due to chronic acid reflux....DD adult cell type is replaced by another. 30......karyolysis.EE Barrier dysfunction is present in patients with Crohn's disease as well as some of their healthy first degree relatives. and does not have a predilection for any particular age group. E Brain Lymphoma (PCNSL). headache.32. altered mental status. is highly associated with Epstein-Barr virus (EBV) infection (> 90%) in immunodeficient patients (such as those with AIDS and those iatrogenically immunosuppressed). usually presents with seizure. or other focal neurological deficits typical of a mass effect Systemic symptoms may include fever. . or weight loss. night sweats. also known as micro glioma and primary brain lymphoma. PCNSLs represent around 20% of all cases of lymphomas in HIV infections (other types are Burkitt's lymphomas and immunoblastic lymphomas). cranial nerve findings. is a primary intracranial tumor appearing mostly in patients with severe immunosuppression (typically patients with AIDS). Other symptoms include • diplopia • dysphagia • vertigo • monocular vision loss • progressive dementia or stupor in patients with a non focal neurologic exam and minimal abnormalities on MRI (more common in AIDS patients) • facial hypoesthesia The definitive diagnosis is arrived at from tissue, i.e. a biopsy, by a pathologist. MRI or contrast enhanced CT classically shows multiple ring-enhancing lesions in the deep white matter. The major differential diagnosis (based on imaging) is cerebral toxoplasmosis, which is also prevalent in AIDS patients and also presents with a ring-enhanced lesion, although toxoplasmosis generally presents with more lesions and the contrast enhancement is typically more pronounced. imaging techniques cannot distinguish the two conditions with certainty, and cannot exclude other diagnoses. Thus, patients undergo a brain biopsy 33. C The patients treated with the new drug the duration of the outbreak was 1 week, instead that the duration of the patients treated with the placebo was 2 week. It mean that the prevalence in the group treated with the new drug ↓ by half. 34. D Hemorrhoids -- vascular structures in the anal canal which help with stool control. They become pathological or piles when swollen or inflamed. In their physiological state they act as a cushion composed of arteriovenous channels and connective tissue that aid the passage of stool. The symptoms of pathological hemorrhoids depend on the type present. Internal hemorrhoids usually present with painless rectal bleeding while external hemorrhoids present with pain in the area of the anus. Recommended treatment consists of increasing fiber intake, oral fluids to maintain hydration, NSAID analgesics, sitz baths, and rest. Surgery is reserved for those who fail to improve following these measures. 35. B Metoclopramide -- antiemetic and gastroprokinetic agent. Thus it is primarily used to treat nausea and vomiting, and to facilitate gastric emptying in patients with gastroparesis. It is also a primary treatment for migraine headaches. 36. E NNRTI: Nevirapine, Efavirenz, Delavirdine: Mechanism of action: Preferentially inhibit reverse transcriptase of HIV , prevent incorporation of DNA copy of viral genome into the host DNA. ( FA 2010 page 195) 37. C Congenital hearing loss --hearing loss present at birth. Can be hereditary or due to other factors present either in utero (prenatal) or at the time of birth. Treatment: A child with a congenital hearing loss should begin receiving treatment before 6 months of age. Studies suggest that children treated this early are usually able to develop communication skills (using spoken or sign language) that are as good as those of hearing peers. In the United States of America, because of a Federal law (the Individuals with Disabilities Education Act), children with a hearing loss between birth and 3 years of age have the right to receive interdisciplinary assessment and early intervention services at little or no cost. After age 3, early intervention and special education programs are provided through the public school system. 38. B Acidosis Respiratory: ↓ PO2,↓ PH , ↑CO2 39. A The formation of granulation tissue in an open wound allows the re epithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment. Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebacious (oil) glands are the main cells responsible for the epithelialization phase of wound healing. They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle. Keratinocytes migrate without first proliferating. Migration can begin as early as a few hours after wounding. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue. Thus the time of onset of migration is variable and may occur about one day after wounding. Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration. CYP2D6 may be inhibited. Under local anesthesia a catheter is introduced into the femoral artery at the groin and advanced under radiographic control into the uterine artery. D3. If the procedure is done for the treatment of uterine fibroids it is also called uterine fibroid embolization (UFE). although this has only been tested in vitro. benzodiazepine. Ropinirole is metabolized primarily by cytochrome P450 CYP1A2. 41.40. and D4 dopamine receptor agonist with highest affinity for D3. muscarinic.acts as a D2. Uterine artery embolization (UAE) is a procedure where an interventional radiologist uses a catheter to deliver small particles that block the blood supply to the uterine body.non-ergoline dopamine agonist. and at doses higher than clinical. is also metabolized by CYP3A4. At doses greater than 24 mg. α1. B The uterine artery usually arises from the anterior division of the internal iliac artery FemoralExternal Iliac  Internal Illiac Uterine A. and the release of various cytokines in response to an antigen. D Ropinirole -. . GABA. It is weakly active at the 5-HT2. antigen-specific cytotoxic T-lymphocytes. -. and α2 receptors and is said to have virtually no affinity for the 5-HT1. and β-adrenoreceptors. natural killer cells (NK). 42 EE CMI is an immune response that does not involve antibodies or complement but rather involves the activation of macrophages. therefore in cell mediated immunity cytokines are not always present. 2. . enabling them to destroy pathogens. and cancer cells displaying tumor antigens. and 3. Associated with ↑ dopaminergic activity. ↓dendritic branching. T cells cause death by apoptosis without using cytokines. Cellular immunity protects the body by: 1. activating macrophages and natural killer cells. and it is accompanied by significant social or occupational dysfunction. CD4 cells or helper T cells provide protection against different pathogens. for which the protective function of immunization was associated with cells. paranoid or bizarre delusions. or disorganized speech and thinking.immune system separated into two branches: humoral immunity. 43. cells with intracellular bacteria. stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses. for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface. It most commonly manifests as auditory hallucinations. such as virus-infected cells. Marijuana use is a risk factor for schizophrenia in teens. C Schizophrenia: Periods of psychosis and disturbed behavior with a decline in functioning lasting > 6 months. vivax infection if a radical cure (eradication of liver stages) is not given Eradication of the liver stages is achieved by giving primaquine. chills (32%). -voltage-dependent calcium channels to open.myelosuppression. peripheral neurities paralytic ileus Cyclophosphamide.Cardiotoxicity.covalantly x-link DNA at guanine N-7. closely related to sulfa drugs.alkylating agent.. carried by the female Anopheles mosquito..generate free radicals and noncovalantly intercalate in DNA s/e. headache (14%).--inhibition causes cell membrane depolarization.. after checking the patients G6PD status to reduce the risk of haemolysis. in severe G6PD deficiency. require bio activation by liver s/e.. A Plasmodium vivax -. primaquine is contraindicated and should not be used 46.can be prevented by mesna Doxorubicin: .. asthenia (16%).so that mitotic spindle can not form s/e.. and abdominal pain (6%). . 45.areflexia.hemorrhagic cystitis. and is seldom fatal. which is the deadliest of the four.. The most frequent and widely distributed cause of recurring (tertian) malaria one of the four species of malarial parasite that commonly infect humans.protozoal parasite ..toxic extravasation Rituximab: General side effects have included fever (49%). Mechanism of action: works by inhibiting ATP-sensitive potassium channels in pancreatic beta cells..neurotoxicity........ also known as glyburide (USAN).an increase in intracellular calcium in the beta cell. Chloroquine remains the treatment of choice for vivax malaria 32 to 100% of patients will relapse following successful treatment of P.a human pathogen.. A Glibenclamide (INN). which stimulates insulin release......myelosuppression and marked alopesia... -. antidiabetic sulfonylureas.EE vincristine. However.M-phase specific alkaloides that bind to tubulin and block polymerization of microtubules. less virulent than Plasmodium falciparum.44. ..and the RAA system .... the sympathetic nervous system increases the resistance and decreases the flow (Q)..... According to Poiseuille Equation P1-P2(Perfusion pressure)= R multiplied by Q....the gradient between arterial blood pressure and venous pressure in a comparable location in the vascular tree.in this case the perfusion pressure is the pressure gradient between renal artery and renal vein..both work independently even if the end result is the same .even if more on efferent ....AT II is a potent vasoconstrictor throughout the body ...When there is vasoconstriction of the afferent arterioles there will be a decrease in flow (Q).....including the afferent and efferent arterioles ..this causes the activation of the Sympathetic Nervous System ............. The RAA system .. relationship between flow(Q) .Resistance(R).... .and Perfusion pressure(P1P2).47....which further decreases the perfusion pressure according to Poiseuille equation ..Therby decreasing perfusion pressure ( the difference between arterial presuure and venous pressure)..........CC Perfusion pressure.. Sympathetic Nervous System causes Vasoconstriction of arteriolar beds including the renal arterioles ...... P1= Renal artery pressure P2=Renal Vein pressure This patient has Hypotension Secondary to Severe Dehydration ..... 48.there are more people can be identified with positive tuberculin test. This is because the immune system needs to be functional to mount a response to the protein derivative injected under the skin.g.... HbS.g. esp those with HIV and low CD4 T cell counts.) Mycobacteriology lab personnel Persons with clinical conditions that place them at high risk (e. A positive result indicates TB exposure. hospitals. chronic malabsorption syndromes. homeless shelters.CC The child has less opportunity to use her/his gross muscle for movement and development. frequently show negative results from the PPD test. etc. prisons.. and Hb M. so incidence and prevalance will be higher The results of this test must be interpreted carefully.) Children less than 4 years of age. . HbF. low body weight. The most common ones are HbA.AA immunologically compromised.. The person's medical risk factors determine at which increment (5 mm. end-stage renal disease.AA Hb electrophoresis---measures the different types of the oxygen-carrying protein (hemoglobin) in the blood.. prolonged corticosteroid therapy. diabetes.so delayed gross motor development could be occurred 50. 5 mm or more is positive in HIV-positive person Recent contacts of TB case Persons with nodular or fibrotic changes on chest x-ray consistent with old healed TB Patients with organ transplants and other immunosuppressed patients 10 mm or more is positive in Recent arrivals (less than 5 years) from high-prevalence countries Injection drug users Residents and employees of high-risk congregate settings (e.. HbA2. Many different types of hemoglobin (Hb) exist.. Hb H. or 15 mm) of induration the result is considered positive. HbC.. etc.. With the change from 10mm to 5 mm.. leukemia. or children and adolescents exposed to adults in high-risk categories 49. 10 mm. nursing homes. Some people may also have small amounts of HbF (which is the main type of hemoglobin in an unborn baby's body). The symptoms are much milder than they are in sickle cell anemia. or can block small blood vessels. these hemoglobin molecules make up the following percentages of total hemoglobin: •Hb F (newborn): 50% to 80% •Hb F (6 months): 8% •Hb F (over 6 months): 1% to 2% The presence of significant levels of abnormal hemoglobins may indicate: •Hemoglobin C disease •Rare hemoglobinopathy •Sickle cell anemia •Thalassemia BLOCK 2 .Healthy adults only have significant levels of HbA and HbA2. abnormal Hb molecules cause anemias. In people with this condition. HbC is an abnormal form of hemoglobin associated with hemolytic anemia. HbS is an abnormal form of hemoglobin associated with sickle cell anemia. Other. Certain diseases are associated with high HbF levels (when HbF is more than 2% of the total hemoglobin). less common. The cells easily break down. the red blood cells sometimes have a crescent or sickle shape. these hemoglobin molecules make up the following percentages of total hemoglobin: •Hb A: 95% to 98% •Hb A2: 2% to 3% •Hb F: 0.8% to 2% •Hb S: 0% •Hb C: 0% In infants and children. Normal Results In adults. AA The deltoid is innervated by the axillary nerve. via the superior trunk. and the posterior cord of the brachial plexus. a type II topoisomerase. 2.CC Aspirin accetylates and irreversibaly inhibits cyclooxygenase. The axillary nerve originates from the ventral rami of the C5 and C6 cervical nerves. It functions by inhibiting DNA gyrase.both coc1 and cox2 to prevent the conversion of arachidonic acid to thromoxane A2... 3... and topoisomerase iv which is an enzyme necessary to separate replicated DNA.BB . bleeding time .no effect on PT and PTT. dislocated shoulder deep IM injection 4.inc.FF Levofloxacin is a broad-spectrum antibiotic that is active against both Grampositive and Gram-negative bacteria. posterior division of the superior trunk. Axillary nerve lesion ***Sensory supply over deltoid ***Sensory loss small area over deltoid ***Area of pain across shoulder tip ***Motor deficit second 90° of shoulder abduction (deltoid) (teres minor cannot be evaluated) ***Causative lesions # neck of humerus.1. thereby inhibiting cell division. Number Needed to treat..... Choice D..e When Calculated P Value is greater than .05...once you find the difference is STATISTICALLY SIGNIFICANT .and clinical significance MUST ANSWER THE QUESTION ...and the answer was ...And the doctor made the CALL in this case not the researcher..05..Statistical significance= Is determined by P value...EFFECT SIZE ......to treat HYPERCHOLSTEROLEMIA in 1 patient 25 should be INVOLVED .....Due to chance alone......... .And the way u measure CLINICAL SIGNIFICANCE IS by some of the following methods......In general the smaller the p the BETTER....05 u can SAY the difference in the two interventions is due to CHANCE ALONE ... -Already in the question u stated the magnitude of the difference was so small.......Only question sample size if the STUDY is not STATISTICALLY SIGNIFICANT..How do they know ? They calculated NNT...Taking Program A as a control (as u know control groups can get placebo or as in this case STANDARD CARE)....how effective is the intervention or treatment in the CLINICAL SETTING. ---NNT=25 is not clinical significant... Choice C... -This means if the health official decided to change Program B as a STANDARD of CARE .........the sample size should be assumed LARGE and Enough.05.. as u know NNT= 1/49%-45 %=1/4%=25....i.........and Preventive fraction...... And I remember a question on NBME 7 where the computed P value was greater than ..but the scenario was almost the same as this question..Many times the investigator will report the lowest COMPUTED P Value .. about the other choices.hence for sure there is a difference between the two interventions (NOT BY CHANCE ALONE).........and as see the p value is less than ....If the P Value is greater than .....hence choice B..So A is out -Practical Importance means CLINICAL SIGNIFICANCE not Statistical... the secretin peptide is encoded by the SCT 8-E Opioids withdrawal produce. 7-D Secretin is a hormone that controls the secretions into the duodenum. This may also cause pale-colored stool and steatorrhea. nausea. diarrhea (flulike symtoms) and yawning 9-D Raynaud's phenomenon is an exaggeration of vasomotor responses to cold or emotional stress. insomnia. leading to tissue hypoxia Nefedipine vasodilate by releasing nitric oxide in smooth muscle.[1] Its effect is to regulate the pH of the duodenal contents via the control of gastric acid secretion and buffering with bicarbonate from the centroacinar cells of the pancreas as well as intercalated ducts. causing increased in cGMP and smooth muscle relaxation. it is a hyperactivation of the sympathetic system causing extreme vasoconstriction of the peripheral blood vessels. stomach cramps.BB HSV-1 is the more common cause of adult encephalitis. and also separately. rhinorrhea. HSV-2 is the more common cause of newborn encephalitis. The jaundice may be associated with itching as the salt from excess bile can cause skin irritation. water homeostasis throughout the body.[4] Therefore..[4] and the later symptoms are usually nonspecific and varied. possibly in combination with darkened urine) when a cancer of the head of the pancreas (about 60% of cases) obstructs the common bile duct as it runs through the pancreas. It is notable for being the first hormone to be identified. anxiety. pancreatic cancer is often not diagnosed until it is advanced. More specifically. anorexia. dilate veins more than arteries and dicreased the preload . The encephalitis affects the temporal lobes of the brain in most cases 6. In humans. fever. It is produced in the S cells of the duodenum in the crypts of Lieberkühn. sweating dilated pupils. piloerection (cold turkey).BB Pancreatic cancer is sometimes called a "silent killer" because early pancreatic cancer often does not cause symptoms. Painless jaundice (yellow tint to whites of eyes and/or yellowish skin in serious cases.5. Decreased colloid osmotic pressure Inflammation Appearance Clear Cloudy Specific gravity < 1. platelets and (in the case of local vascular damage) red blood cells.9 g/dL fluid protein serum protein < 0.2 g/dL < 1. Its composition varies but generally includes water and the dissolved solutes of the main circulatory fluid such as sap or blood. white blood cells.6 or < ⅔ > 0.10.5 > 0.6[5] or > ⅔ Cholesterol content < 45 mg/dL > 45 mg/dL[5 .2 g/dL fluid LDH upper limit for serum < 0.012 > 1. In the case of blood: it will contain some or all plasma proteins.020 Protein content < 2 g/dL > 2.C An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation.5 Difference of albumin content with blood albumin > 1. Transudate Exudate Main causes Increased hydrostatic pressure. due to inc venous pressure . (See below for difference between transudate and exudate) Malignant (or cancerous) pleural effusion is effusion where cancer cells are present.. and can usually be seen in certain disease states like tuberculosis. white blood cells. It is usually classified as exudate. Often.... it will contain some or all plasma proteins. fibrinogen..specific gravity >1020 ***Types*** Purulent or suppurative exudate consists of plasma with both active and dead neutrophils. Protein poor Specific gravity 11. Fibrinous exudate is composed mainly of fibrinogen and fibrin. large amounts of antibiotics are necessary for resolution. It is characteristic of rheumatic carditis. Its consistency resembles that of serum. Serous exudate (sometimes classified as serous transudate) is usually seen in mild inflammation.Exudate. Fibrinous inflammation is often difficult to resolve due to the fact that blood vessels grow into the exudate and fill the space that was occupied by fibrin. with little protein content. Trasudate versus Exudate Hypocellular..An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation.. This kind of exudate is consistent with more severe infections. platelets and (in the case of local vascular damage) red blood cells protein rich..sacral edema .. Catarrhal exudate is seen in the nose and throat and is characterized by a high content of mucus. and necrotic parenchymal cells. and is commonly referred to as pus.Jugular venous distantion and bilateral Ankle.DD Rigt heart failure. but is seen in all severe injuries such as strep throat and bacterial pneumonia. but the rise in 2. This mechanism allows for the body to adapt the problem of supplying more oxygen to tissues that need it the most.12.. thus enhancing the ability of RBCs to release oxygen near tissues that need it most.FF The dissociation curve shifts to the right when carbon dioxide or hydrogen ion concentration is increased. Rise in 2. This facilitates increased oxygen dumping.It has asked the effect of shift of the O2 dissociation curve to the right due to an increase of H+.. .i.3 BPG will also have the same effect.. The answer should definitely be F..The unloading of O2 becomes easier in tissue capillaries.They have not mentioned anything regarding hypoxia in the question which u mentioned here.3 DPG is not solely due to rise in H+. 2. The general equation for the Haldane Effect is: H+ + HbO2 ←→ H+Hb + O2 ..3-Bisphosphoglyceric acid . release of oxygen in tissue capillaries..interacts with deoxygenated hemoglobin beta subunits by decreasing their affinity for oxygen. so it allosterically promotes the release of the remaining oxygen molecules bound to the hemoglobin. That's what happens when pH falls and the curve shifts to the right.e... 13.CC . com/imgres? imgurl=http://missinglink.html 14. Fat emboli occur in almost 90% of all patients with severe injuries to bones. http://library. The release of free fatty acids from the fat globules causes local toxic injury to endothelium.utah.A fat embolism is a type of embolism that is often (but not always) caused by physical trauma like fracture of long bones.0CEAQ9QEwAw .edu/lm/ids_104_ce. The pathogenesis occurs due to both mechanical obstruction and biochemical injury. The risk of fat embolism syndrome is thought to be reduced by early immobilization of fractures and especially by early operative correction.ucsf.edu/WebPath/HISTHTML/STAINS/STAIN011. It is aggravated by local platelet and erythrocyte aggregation. The vascular damage is aggravated by platelet activation and recruitment of granulocytes. The mortality rate of fat-embolism syndrome is approximately 10-20%.med. The microemboli cause pulmonary and cerebral microvasculature occlusion..AA http://www. There is also some evidence that steroid prophylaxis of high-risk patients reduces the incidence.google.. although only 10% of these are symptomatic. soft tissue trauma and burns. .California.AA In statistics. and therefore generalizes t-test to more than two groups. in which the observed variance in a particular variable is partitioned into components attributable to different sources of variation.. three or more means. ANOVAs are useful in comparing two... Can disseminate to bone and skin Culture.Hyphe with doubly reflective wall Biopsy Thick -wall spherules filled with endospores 16.Southwestern US. and their associated procedures.. For this reason..BB Coccidioidmycosis.15..25degree. In its simplest form ANOVA provides a statistical test of whether or not the means of several groups are all equal. ...causes pneumonia and meningitis(very rare). analysis of variance (ANOVA) is a collection of statistical models.mold in soil.. Doing multiple twosample t-tests would result in an increased chance of committing a type I error. ANOVAs are helpful because they possess an advantage over a two-sample t-test.... .(Two Nominals ) e...g comparing B.*got 3 groups Now what's the difference B/W t-Test and ANOVA ...... Weight.... Middle-age and Children) etc *Race------a Nominal that can have many groups Two groups (African Americans and Latino) Three groups(African Americans.. *Gender ---is a Nominal that has Two Groups (Male and Female) *AGE-------is a Nominal that we can have either TWO groups (Elderly and Middle age) or THREE Groups(Elderly....P measurements) *NOMINAL variable ("GROUPS" ) so to compare MEANS of B... Latino and Asian) and so forth e.P. comparing the BP means b/w (Latinos) and (African Americans) *for a t-Test it will be a wrong statement to say e.....g we compare Blood Pressure measurements *INTERVAL variable ("MEANS" of B. measurements of B... (African Americans) and (Asians)...P..... b/w two are more groups we do these tests t-Test: 1 Interval (Blood pressure Means) 1 Nominal with "ONLY TWO GROUPS" e....P means b/w (Latinos)......... *"GENDER"(Men and Women)....g......g....g..1-"Interval variable" (values from where we can drive their "Mean") e......g. Cholesterol levels etc 2-"Nominal variable" ( different categories or "GROUPS") e.(Single Nominal) *"GENDER"(Men and Women) n "RACE"(Caucasian and African). ...g as above comparing B.. just the NOMINAL data) best example.. Gender (Men and Women) *AND Race (Caucasians and African Americans) ---->we do these tests to see If there is a Difference b/w groups ? t-statistics (t-Test) and f-statistics(ANOVA) will be compared to get a p-value If p-value = 0... 1 Interval and 1 Nominal with TWO Groups One-way ANOVA.... we are not using any Interval variable here ....t-Test or One-way ..... how many Nominals..... How many groups and If Interval variable is used or not? 1 Interval and 1 Nominal (Two Groups)...... Chi-square: we compare b/w "TWO NOMINAL" (with ANY # of GROUPS) (Note..........3 groups Two-way ANOVA: 1 Interval 2 Nominal e....(Recovered group) and(Not recovered group) ***I think this is all u have to do is recognize what kind of data is presented ....05 or less -----it is said to be "Statistically Significant' and we say that there is a Difference in these Groups.."Testing Drug Efficacy" First Nominal.....(New drug group) and (Placebo group) Second Nominal .. (African Americans) and (Asians)...........P means b/w (Latinos)..t-Test------>ONLY TWO Groups comparison ANOVA------------>TWO Groups or more than Two Groups comparison NOTE:these two will give u the Identical results if comparing "TWO Groups" t-Test.1 Interval and 1 Nominal with TWO Groups and for the above reason they rather use One-way ANOVA when more than two groups are there to be compared e...g... .. Diagnosis is made based on these findings in an individual with a history of recent streptococcal infection.......LM.............One-way ANOVA 1 Interval and *2 Nominal (many groups)..Chi-square 17.....Lumpy -Bumpy appereance Em.. but classically occurs after infection with Streptococcus pyogenes.DD Post-infectiousPost-infectious glomerulonephritis can occur after essentially any infection..IgM............glumeruli enlarged and hypercelullar Neutrophiles...Subepithelial IC humps.Two-way ANOVA ....ANOVA 1 Interval and 1 Nominal (More than Two groups)...C3 IF........IgG.granular resolve spontaneously .. It typically occurs 10–14 days after a skin or pharyngeal infection with this bacterium......... Patients present with signs and symptoms of glomerulonephritis. Streptococcal titers in the blood (antistreptolysin O titers) may support the diagnosis causes Nephritic syndrome......*2 Nominal (any# of Groups)...... HIT. Haematopoietic progenitors derived from haematopoietic stem cells populate the thymus and expand by cell division to generate a large population of immature thymocytes. Positive selection "selects for" T-cells capable of interacting with MHC. whereas the other 2% survive and leave the thymus to become mature immunocompetent T cells.osteoparosis... Immadiate anticoagulation for pulmonary embolism. B: Interfere with Carboxylation of Coagulation Factors. before initiating warfarin therapy we start heparin to obtain immediate anticoagulation as warfarin takes time for it action.bleeding Thrombocytopenis.EE The thymus..drug-drug interactions For rapid reversalof heparinization.. and are therefore classed as double-negative (CD4-CD8-) cells. About 98% of thymocytes die during the development processes in the thymus by failing either positive selection or negative selection..Enoxaparin act more on Xa have better bioavilibility without laboratory monitoring 20-E "Drug Y alone no effect" ( partial agonist are incapable of eliciting a maximal response and are less efecctive than the full agonist .acute coronary syndrome Toxicity.stroke . As they progress through their development they become double-positive thymocytes (CD4+CD8+). and finally mature to single-positive (CD4+CD8or CD4-CD8+) thymocytes that are then released from the thymus to peripheral tissues. Negative selection removes thymocytes that are capable of strongly binding with "self" peptides presented by MHC.. is the principal organ responsible for the T cell's maturation.18. The earliest thymocytes express neither CD4 nor CD8.PROTAMINE SULFATE ****Newer low molecular weight heparin. The answer should be B as they have asked which drug is to be given for 6 months after initiating therapy with heparin... 19.. All T cells originate from haematopoietic stem cells in the bone marrow. Typically. This partially dissociates. The effectiveness of lactulose in treating hepatic encephalopathy is somewhat controversial.. lactulose helps "draw out" ammonia (NH3) from the body. only "Potency decreases"(as needed higher dose of Drug X) ---------------------------------Graph on the Right-------------------------But at "High Dose" of of NCA (Drug Y).g all the 10 spare receptors---->result *Efficacy(Emax) of Drug X decreases *there are non of the spare receptors left unoccupied since there are no extra receptors left.. and now consider. trapping NH3 in the colon and effectively reducing plasma NH3 concentrations.[ Lactulose for hepatic encephalopathy generally requires oral dosage three or four times a day with diarrhea almost a certain side effect.D-Noncompetitive Antagonist This is the case on the concept of "Spare Receptors" Assume . 21-E In treating hepatic encephalopathy.[5] Lactulose is metabolized in the colon by bacterial flora to short chain fatty acids including the production of the lactic acid and acetic acid..[6] This favors the formation of the nonabsorbable NH4+ from NH3.100% receptor occupancy required by an Agonist to exert Maximum Effect (Emax) /Optimal effect... it won't be able to increase it's Efficacy back to Emax. there for "No Change in Efficacy" . even if we raise the Drug "X" dosage. if Emax is achieved with result *Efficacy of Drug X decreases *5 of the spare receptors are still Unoccupied Now if we raise the drug "X" dosage. it will bind to e.it will bind to the remaining unoccupied spare receptors and brings it Efficacy back to to the Emax.. . acidifying the colonic contents (increasing the H+ concentration in the gut). The signs and symptoms of a pheochromocytoma are those of sympathetic nervous system hyperactivity. another clue to the presence of pheochromocytoma is orthostatic hypotension (a fall in systolic blood pressure greater than 20 mmHg or a fall in diastolic blood pressure greater than 10 mmHg on making the patient stand) Palpitations Anxiety often resembling that of a panic attack Diaphoresis (excessive sweating) Headaches Pallor Weight loss Localized amyloid deposits found microscopically Elevated blood glucose level (due primarily to catecholamine stimulation of lipolysis (breakdown of stored fat) leading to high levels of free fatty acids and the subsequent inhibition of glucose uptake by muscle cells. including paroxysmal (sporadic. or severely high blood pressure. including: Skin sensations Flank pain Elevated heart rate Elevated blood pressure. usually noradrenaline (norepinephrine). A pheochromocytoma can be fatal if it causes malignant hypertension. stimulation of beta-adrenergic receptors leads to glycogenolysis and gluconeogenesis and thus elevation of blood glucose levels). This hypertension is not well controlled with standard blood pressure medications 23. or extra-adrenal chromaffin tissue that failed to involute after birth [1] and secretes excessive amounts of catecholamines. episodic) high blood pressure. which sometimes can be more difficult to detect.22-E A pheochromocytoma or phaeochromocytoma (PCC) is a neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells). A pheochromocytoma can also cause resistant arterial hypertension. and adrenaline (epinephrine) to a lesser extent TO ADD.DD . Further. .................................. 2 pounds=7000cal she needs to loss 1000 cal per day.so if she decreases 500 cal in her diet and gets 1 hour brisk walking then she will loss 1000 cal/day.......if she walked 2 hours per day...........we need to cut 2lb=7000 cal (3500*2) 1 hr walk/d will cut 3500 cal In the meanwhile she is also getting 1800*7 calories=12600 in a week decrease intake for 500 cal /d * 7 days=3500 cal so 3500+3500=7000 It is a mathematic calculation........she could lose 1000 calories but between choices there is no 2 hours..... She is asked to loss 2 pounds weight weekly...each pounds=3500 cal and brisk walking consums 500cal per hour so.............and 7000/week .. Each protein is a link on the autoimmune chain. SLE is triggered by environmental factors that are unknown. C Systemic lupus erythematosus often abbreviated to SLE or lupus. The immune system must have a balance (homeostasis) between being sensitive enough to protect against infection. some genetic combinations result in autoimmunity.24. the body's immune system produces antibodies against itself. according to Crow. the immune system attacks the body's cells and tissue. and viruses. and their role in the immune system. SLE most often harms the heart. is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body. In SLE. such as the glomeruli of the kidney. Researchers are now identifying the individual genes. "All the key components of the immune system are involved in the underlying mechanisms [of SLE]" according to Rahman. in some people the immune system attacks these nuclear-related proteins and produces antibodies against them. and nervous system. . These stimuli cause the destruction of cells and expose their DNA. resulting in inflammation and tissue damage. and being too sensitive and attacking the body's own proteins (autoimmunity). histones. The course of the disease is unpredictable. particularly against proteins in the cell nucleus. the population must have enough genetic diversity to protect itself against a wide range of possible infection. Because of genetic variations in different components of the immune system. particularly parts of the cell nucleus. these antibody attacks are the cause of SLE. skin.[1] It is a Type III hypersensitivity reaction caused by antibody-immune complex formation. liver. drugs. blood vessels. As occurs in other autoimmune diseases. kidneys. the proteins they produce. lungs. From an evolutionary perspective. The likely environmental triggers include ultraviolet light. and researchers are trying to find drugs to break each of those links. with periods of illness (called flares) alternating with remissions. and SLE is the prototypical autoimmune disease. In the end. these antibody complexes damage blood vessels in critical areas of the body. and other proteins. joints. thinning hair. A histological hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities. Histologically a wire-loop lesion will be present. SLE can also damage the skin.[1] Kwashiorkor was thought to be caused by insufficient protein consumption but with sufficient calorie intake. irritability. micronutrient and antioxidant deficiencies have come to be recognized as contributory. joints.Renal Painless hematuria or proteinuria may often be the only presenting renal symptom. distinguishing it from marasmus. anorexia. leading to acute or end-stage renal failure. Acute or chronic renal impairment may develop with lupus nephritis. More recently. nervous system and virtually any organ or system in the body. Apart from the kidneys. an enlarged liver with fatty infiltrates. skin depigmentation and dermatitis. Other signs include a distended abdomen. . Because of early recognition and management of SLE. Children with kwashiorkor often develop irritability and anorexia. leading to a typical granular appearance in immunofluorescence testing. a disease of the immune system.[16] This finding is due to immune complex deposition along the glomerular basement membrane. E Kwashiorkor (pronounced /kwɑːɑ iɑɑrkər/) is an acute form of childhood protein-energy malnutrition characterized by edema. The wire loop lesion is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop. ulcerating dermatoses. loss of teeth. The presence of edema caused by poor nutrition defines kwashiorkor. Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE). The defining sign of kwashiorkor in a malnourished child is pedal edema (swelling of the feet). end-stage renal failure occurs in less than 5% of cases. 25. and an enlarged liver with fatty infiltrates. Cases in the developed world are rare. Other common characteristics include dry skin. A child with marasmus looks emaciated. loose skin folds hanging over the glutei. In extreme episodes.[citation needed] Marasmus occurrence increases prior to age 1. axillae. The malnutrition associated with marasmus leads to extensive tissue and muscle wasting. [1] It is usually associated with a patient's increasing fluid intake due to the sensation of having a dry mouth. There is also drastic loss of adipose tissue from normal areas of fat deposits like buttocks and thighs. 26. the patient's kidneys will be unable to deal with the fluid overload. This urine will have a low electrolyte concentration. irritable. Marasmus is a form of severe protein deficiency and is one of the forms of proteinenergy malfunction (PEM). Marasmus is generally known as the gradual wasting away of the body due to severe malnutrition or inadequate absorption of food. C Primary polydipsia or psychogenic polydipsia is a special form of polydipsia. it implies that the condition is caused by mental disorders. It can be distinguished from kwashiorkor in that kwashiorkor is protein wasting with the presence of edema. . and voraciously hungry. as well as variable edema. Clinical presentation Patients have been known to seek fluids from any source possible. which dilutes the extracellular fluid. decreasing its osmotic pressure. When the term "psychogenic polydipsia" is used. The afflicted are often fretful. However.Marasmus is a form of severe protein-energy malnutrition characterized by energy deficiency. It is a severe form of malnutrition caused by inadequate intake of proteins and calories. The word “marasmus” comes from a Greek word meaning starvation. The body responds to this by decreasing the level of vasopressin (antidiuretic hormone). the dry mouth is often due to phenothiazine medications used in some mental disorders. with a resultant increased production of urine (polyuria). rather than the underlying condition The patient drinks large amounts of water. Body weight may be reduced to less than 80% of the average weight that corresponds to the height . and weight gain will be noted. etc. whereas kwashiorkor occurrence increases after 18 months. Primary polydipsia can be life threatening as serum sodium is diluted to an extent that seizures and cardiac arrest can occur. and some contain XXY chromosomes. there are cases where the trisomy occurs in only a selection of the cells. where two or more genotypes arise from the fusion of more than one fertilized zygote in the early stages of embryonal development. Another form of somatic mosaicism is chimerism. called 46/47 XY/XXY mosaic wherein some of the patient's cells contain XY chromosomes. self-limiting necrotizing vasculitis in infants/ children. changes in lips/ oral mucosa (“strawberry tongue”). 28.[2][3] The most common form of mosaicism found through prenatal diagnosis involves trisomies. desquamative skin rash. Association with Asia ethnicity. such as in calico cats. while complete monosomy (45 XO) occurs in about 50–60% of cases. A Kawasaki disease: Acute.27. resulting in a loss of a chromosome from some trisomic cells.[4] Generally this leads to a milder phenotype than in non-mosaic patients with the same disorder. different genotypes arise from only a single fertilized egg cell. May develop coronary aneurysms. lymphadenitis. and the XXY cells have 47 total chromosomes. True mosaicism should not be mistaken for the phenomenon of Xinactivation. Somatic mosaicism Somatic mosaicism occurs when the somatic cells of the body are of more than one genotype. In the more common mosaics. In rare cases. Around 30% of Turner's syndrome cases demonstrate mosaicism. The 46/47 annotation indicates that the XY cells have the normal number of 46 total chromosomes. a mosaic or mosaicism denotes the presence of two populations of cells with different genotypes in one individual who has developed from a single fertilized egg. where all cells in an organism have the same genotype. D In genetic medicine. due to mitotic errors at first cleavage. This may be caused by a nondisjunction event in an early mitosis. Fever. intersex conditions can be caused by mosaicism where some cells in the body have XX and others XY chromosomes.[1] Mosaicism may result from a mutation during development which is propagated to only a subset of the adult cells. . but a different copy of the X chromosome is expressed in different cells. An example of this is one of the milder forms of Klinefelter's syndrome. conjuntivitis. Although most forms of trisomy are due to problems in meiosis and affect all cells of the organism. .C PaCO2=metabolic CO2 production/Va So if Ventilation increases to match up with CO2 production. PCO2 remains the same 30-F The classic triad for congenital rubella syndrome is: Sensorineural deafness (58% of patients) Eye abnormalities—especially cataract and microphthalmia (43% of patients) Congenital heart disease—especially patent ductus arteriosus (50% of patients) Other manifestations of CRS may include: Spleen. seizures.29. microcephaly. and can cause complications such as low birth weight. liver or bone marrow problems (some of which may disappear shortly after birth) Mental retardation Small head size (microcephaly) Eye defects Low birth weight Thrombocytopenic purpura (presents as a characteristic blueberry muffin rash) Hepatomegaly Micrognathia Children who have been exposed to rubella in the womb should also be watched closely as they age for any indication of the following: Developmental delay Autism spectrum disorders[1] Schizophrenia[2] Growth retardation Learning disabilities Diabetes Glaucoma Note:NO a congenital cytomegalovirus Generalized infection may occur in the infant. and moderate hepatosplenomegaly (with jaundice). petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome. Occurs in hot humid weather. oropharyngeal colonization. large capsule. Malassezia is naturally found on the skin surfaces of many animals. selenium sulfide. meningitidis capsular antigen in CSF. spread to meninges via blood stream. Malassezia (formerly known as Pityrosporum) is a genus of fungi. B strain is most common strain in US.31. meningitidis: Gram neg. some species can cause hypopigmentation on the trunk and other locations in humans. latex particule agluttination ( or Counter immunoelectrophoresis ( CIE) to identify N. T: Topical Miconazole. 32. 5 common serogrups : B is not strongly immunogenic( sialid acid). A N. C Pityriasis or tiña versicolor caused by malassezia furfur. Degradation of lipids produces acids that damage melanocytes and cause hypopigmented patches. including humans. Pathogenesis: Important virulent factor: Polysacharide capsule: antiphagocytic. Reservorio: Human nasopharynx Transmision: Respiratory droplets. antigenic. Yeast clusters & and short curved septate hyphae KOH scaping shows “spaghetti and meatballs”. In occasional opportunistic infections. (Kaplan Microbiology book page 257) . kidney bean shaped diploccoci. the process is normal in every respect except the unusually early age. may also be used.33. D Leuprolide As a medical term.5 standard deviations below the population mean). and often simplified as early puberty. the early development is triggered by a disease such as a tumor or injury of the brain. GnRH agonists cause a decreased release of FSH and LH. One possible treatment is with anastrozole. unusually early puberty can have adverse effects on social behavior and psychological development. However. occurring earlier than the usual age. Histrelin acetate (Supprelin LA). allowing for a physiologic release of FSH and LH. Even in instances where there is no disease. In most of these children. GnRH produced by the hypothalamus is pulsatile. especially when it is being considered as a medical problem. . A common definition for medical purposes is onset before 8 years in girls or 9 years in boys. The term is used with several slightly different meanings that are usually apparent from the context.g. 2. and may shift some life-long health risks. or based on opinion as to the age at which early puberty may have adverse effects.[1] on expert recommendations of ages at which there is more than a negligible chance of discovering an abnormal cause. In its broadest sense. precocious puberty describes puberty occurring at an unusually early age. In a minority of children. Central precocious puberty can be treated by suppressing the pituitary hormones that induce sex steroid production. "precocious puberty" sometimes refers to any physical sex hormone effect. when used regularly. GnRH agonists stimulate the pituitary to release Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). can reduce adult height potential. and simply represents a variation of normal development. Triptorelin or Leuprolide. due to any cause.. Stricter definitions of "precocity" may refer only to central puberty starting before a statistically specified age based on percentile in the population (e. any GnRH agonists. the resulting facilitated diffusion of ions (chloride IN.34-B Inhibitory synapses ↓ Postsynaptic CA2+ Influx The neurotransmitter at inhibitory synapses hyperpolarizes the postsynaptic membrane. taking as long as 1 second. As you might expect. this is a slower response. This increased membrane potential is called an inhibitory postsynaptic potential (IPSP) because it counteracts any excitatory signals that may arrive at that neuron. •Binding of GABA to GABAB receptors activates an internal G protein and a "second messenger" that leads to the opening of nearby potassium (K+) channels. In both cases. potassium OUT) increases the membrane potential (to as much as −80 mv). Example: gamma aminobutyric acid (GABA) at certain synapses in the brain. This is a fast response — taking only about 1 millisecond. Actually. A hyperpolarized neuron appears to have an increased threshold. It is simply a question of whether the depolarization produced by excitatory synapses on the cell minus the hyperpolarizing effect of inhibitory synapses can reach this value or not. the threshold voltage (about −50 mv) has not changed. •The GABAA receptor is a ligand-gated chloride channel. Mutation of the GABA. Binding of GABA to the receptors increases the influx of chloride (Cl−) ions into the postsynaptic cell raising its membrane potential and thus inhibiting it. (no receptor) secundary to the mutation DECREASED THE influx of Cl- . caused by a deficiency of arginine vasopressin (AVP). which is caused by an insensitivity of the kidneys to ADH.35-F (DCT!) ADH is secreted in response to increased plasma osmolarity and dicreased blood volume. each with a different cause. The second common type of DI is nephrogenic diabetes insipidus. also known as antidiuretic hormone (ADH). ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules. causing increased number of water channels and increased water reabsortion in the collecting tube. thus concentrating the urine. There are several different types of DI. Diabetes insipidus (DI) is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine. FA pag 396 The main effector organ for fluid homeostasis is the kidney. This increase in permeability allows for reabsorption of water into the bloodstream. . specifically it acts on proteins called aquaporins which open to allow water into the collecting duct cells. binds to receptors on principal cells. with reduction of fluid intake having no effect on the latter. It can also be an iatrogenic artifact of drug use. The most common type in humans is central DI. which can eventually lead to blindness. D -zona reticularis. These damages change the formation of the blood-retinal barrier and also make the retinal blood vessels become more permeable.BB Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus. E -adrenal medulla 39..blunt trauma. The fluid makes the macula swell.. called nonproliferative diabetic retinopathy (NPDR).tentorium venous bleeding with delayed onset . An overaccumulation of glucose and/or fructose damages the tiny blood vessels in the retina. It occurs when the damaged blood vessels leak fluid and lipids onto the macula. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more. caput medusae.36.. most people do not notice any change in their vision.shaken baby 37 A esophageal varices liver cirrhosis -->portal hypertension -->Ascites. 40 B chemokine receptor HIV entry requires interaction with CD4 receptors and CCR5 receptors 41 C its not A for sure ..cn not cross falx. During the initial stage.. Diabetic retinopathy is the result of microvascular retinal changes. haemarrhoids 38 B Zona glomerulosa -->Aldosterone other options C -zona fasciculata.alcoholics.seen in elderly.CC Subdural hematoma. the part of the retina that lets us see detail.rupture of bridging vein crescent -shaped hemorrhage that crosses suture lines. Small blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar (blood glucose) control. esophageal varices. which blurs vision. Hyperglycemia-induced intramural pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. splenomegaly. Some people develop a condition called macular edema. Commonly lesions are found near the pleural surface (peripheral) which is retracted (puckered) over the neoplasm. 43. . While muscle cells generally break down glycogen to power their immediate activity.AA Adenocarcinoma is a type of cancer that develops in cells lining glandular types of internal organs.DD Physiologically.peripheral. and/or mucus production by the tumor cells. Adenocarcinomas grossly present with the "three P's" ."Currently the WHO recognizes four categories of adenocarcinoma: acinar papillary bronchioloalveolar solid carcinoma with mucus formation The majority of adenocarcinomas occur at the periphery of the lung. They frequently lie just below the pleura. Often adenocarcinomas are discovered on routine chest x-rays or in a primary search for distant metastases. and.42. the regulatory mechanisms of PhK activity vary somewhat depending on cell type.no germ cells bosted by nf2011 to add Genetic mosaicism (46XX/45XO) is most often implicated. This activity is particularly important in liver and muscle cells. and cause pleural retraction and thickening on x-ray.The cut surface is often white .The World Health Organization (WHO) defines adenocarcinoma as "a malignant epithelial tumor with tubular. alongside nondisjunction (45XO) and partial monosomy (46XX). 44 A oocyte donation turners sundrome --. as a resultare often asymptomatic until late in their course. liver cells are responsible for maintaining glucose concentration in the bloodstream. acinar. Thus. or papillary growth patterns. pigmented and puckered. though for somewhat different purposes.streak ovaries-. phosphorylase kinase plays the important role of stimulating glycogen breakdown into free glucose by phosphorylating glycogen phosphorylase and stabilizing its active conformation. .like wegner but lacks granuloma.EE Ureters paa under uterine artery and under ductus deferens.....P-ANCA positive All affect small vessels .Turner syndrome is characterized by primary amenorrhea.accidental ligationof the Ureter 47.. streak gonads and infertility. 45 B inheritance of amplified CYP2D6 locus rule out A induction --->increased dose should induce a response C inactive alleles & D inhibitor --> small doses should do the trick E tolerance ----> initiall doses should induce a response 45 B inheritance of amplified CYP2D6 locus rule out A induction --->increased dose should induce a response C inactive alleles & D inhibitor --> small doses should do the trick E tolerance ----> initiall doses should induce a response ************************************************************* ******************************** 46. technology (especially oocyte donation) provides the opportunity of pregnancy in these patients...ligation the ovarian vasculature in the suspensory lig. Complication in surgery. However. premature ovarian failure..EE Microscopic Polyangitis... corticospinal fibers contralateral hemiparesis and typical upper motor neuron findings corticobulbar tract difficulty with contralateral lower facial muscles and hypoglossal nerve functions oculomotor nerve fibers ipsilateral oculomotor nerve palsy with a drooping eyelid and fixed wide pupil pointed down and out. leading to a movement disorder of the contralateral body.48.DD Weber's syndrome (superior alternating hemiplegia) is a form of stroke characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia. This lesion is usually unilateral and affects several structures in the midbrain including: substantia nigra contralateral parkinsonism because its dopaminergic projections to the basal ganglia innervate the ipsilateral hemisphere motor field. This leads to diplopia It is caused by midbrain infarction as a result of occlusion of the paramedian branches of the posterior cerebral artery or of basilar bifurcation perforating arteries . . the left parietal lobe in the region of the angular gyrus. The pain associated with thalamic syndrome may be made worse by exposure to heat or cold and by emotional distress. a lack of understanding of the rules for calculation or arithmetic (acalculia or dyscalculia). slurred speech. It is a rare neurological disorder in which the body becomes hypersensitive to pain as a result of damage to the thalamus. It may occur after a stroke or in association with damage to the parietal lobe. Pain or discomfort may be fel after being mildly touched or even in the absence of a stimulus. Lateral medullary syndrome (also called Wallenberg syndrome and posterior inferior cerebellar artery syndrome) is a disease in which the patient has a constellation of neurologic symptoms due to injury to the lateral part of the medulla in the brain. there is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face. this may include even such emotions as those brought on by listening to music.Thalamic syndrome (or thalamic pain syndrome)It is also known as "Dejerine-Roussy disease" is a condition that can be associated with inadequate blood supply from the posterior cerebral artery. or dysphagia. an inability to distinguish right from left. Primary symptoms include pain and loss of sensation. Clinical symptoms include swallowing difficulty. arms. Specifically. resulting in tissue ischemia and necrosis. This syndrome is characterized by sensory deficits affecting the trunk (torso) and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side with the infarct. Gerstmann's syndrome is a cognitive impairment that results from damage to a specific area of the brain -. The thalamus has been described as the brain’s sensory relay station. a part of the brain that affects sensation. This crossed finding is diagnostic for the syndrome. It is characterized by four primary symptoms: a writing disability (agraphia or dysgraphia). a type of transmissible spongiform encephalopathy. The disorder should not be confused with Gerstmann-Sträussler-Scheinker disease. usually in the face. . Sometimes. and an inability to identify fingers (finger agnosia). and/or legs. by binding to GABAA receptors at the same location as benzodiazepines. It is a short-acting nonbenzodiazepine hypnotic that potentiates gamma-aminobutyric acid (GABA). an inhibitory neurotransmitter. Zolpidem has not adequately demonstrated effectiveness in maintaining sleep. vertigo. however it is effective in initiating sleep . nystagmus. and possibly palatal myoclonus. Horner syndrome. diplopia. It works quickly (usually within 15 minutes) and has a short half-life (2–3 hours). facial pain.ataxia. as well as some brain disorders. 49 E zolpidem Zolpidem (Ambien) is a prescription medication used for the short-term treatment of insomnia. pysical protection.production and secretion of gastric mucous barrier and dic acid production A. In normal individuals.. Block 3 1..inc.a PGE1 analog.dec H+ secretion by parietal cells 2. effectively silencing the expression of the FMR1 protein.folding of the CFTR protein in the endoplasmic reticulum is affected by this mutation .and allow bicarbonate secretion to restablish PH gradient in the mucous layer Misoprostol. FMRP is believed to regulate a substantial population of mRNA: FMRP plays important roles in learning and memory.H2 blocker.....EE Sucralfate and bismuth.. FMRP..can affect absorbtion......bind to ulser base.AA CFTR gene on chromosome 7 ..... Mutation of the FMR1 gene leads to the transcriptional silencing of the fragile X-mental retardation protein.B...bioavailibility or urinary excreation of other drugs by altering gastric and urinary PHor by delaying gastric emptying Ranitidin.. Expansion of the CGG repeating codon to such a degree results in a methylation of that portion of the DNA.BB Fragile X syndrome is a genetic disorder caused by mutation of the FMR1 gene on the X-chromosome....deletion of Phe 508.50.reversible block of histamine H2 receptors.. ... Cystic Fibrosis..lidocain.secretion abnormally thick mucous that pluge lung .CC The concept they are testing is if a disease has a high heterozygote frequency then the chances of a female carrier and a male carrier meeting are higher...parasympathetic activity.....failure to thrive in infancy ...BB Digoxin toxicity.folding of the CFTR protein in the endoplasmic reticulum is affected by this mutation defective Cl....scooping of STad T-wave inversion Antidote.inc.vomitingdiarrhea. 4.... It is referring to the particular gene frequency in the population.chanel...anti-dig fragments. and thus chances of having a child with a recessive disorder in a family where none of the grandparents had a disease are also higher. most common lethal genetic disease of caucasians.slowly normalize K+and Mg+. For example....blurry yellow visionand arrhythmia may cause inc...pancreas and lver.deletion of Phe 508..3..nausea..PR and decQT.. the gene frequency for cystic fibrosis is high in Caucasians...recurent pulmonary infection.AR with high heterozigot frequency.Fat-soluble vitamine deficiency.. central and peripheral nervous system manifestations. optic nerve inflammation can occur in stage 2. cardiac. renal failure. meningoencephalitis. and neurological manifestations. fever. and jaundice. • Ocular manifestations occur in the majority of patients.CC Spirochete Infections: Lyme Disease and Leptospirosis • Lyme disease is characterized by dermatological. 6. and ophthalmic manifestations that result from tick-borne transmission of the spirochete Borrelia burgdorferi • Three chronological stages: 1. Leptospirosis is a zoonotic infection of worldwide distribution caused by pathogenic Leptospira species. • Corneal. peripheral neuropathy. subconjunctival hemorrhages. Biphasic disease. ASSOCIATED FEATURE • Weil’s disease—severe disease with hemorrhages. • Immune phase—high fever. most common manifestation in stage 1.Tertiary or late stage—arthritis. uveitis. rheumatic. meningismus. uveal.DD the bullet is seen inside the spleen . carditis.Primary or initial phase—rash at the site of tick bite (erythema chronicum migrans) and flu-like symptoms. and retinal inflammation can occur in stage 3. • Cranial nerve palsies.Secondary or dissemination stage—further dermatological. cranial neuropathy. • Leptospiremic phase—severe headache. cardiac. ASSOCIATED FEATURES • Conjunctivitis. • Conjunctivitis. neurological. myalgia. 3.5. 2. wikipedia. retroaortic. omentum minus) is the double layer of peritoneum that extends from the liver to the lesser curvature of the stomach and the start of the duodenum. Viruses such as respiratory syncytial virus (RSV) and those that cause the common cold may also result in otitis media by damaging the normal defenses of the epithelial cells in the upper respiratory tract. The most common bacterial pathogen is Streptococcus pneumoniae. anterior to the spine.7. and right and left lateral aortic.org/wiki/File:Gray1104. gastrohepatic omentum.BB The lesser omentum (small omentum. http://en. The retroaortic group drains from the lateral and preaortic glands.CC The paraaortic lymph node group is divided into three subgroups: preaortic.EE Otitis media is most commonly caused by infection with viral. The lateral group nodes are located adjacent to the aorta. The lesser omentum is extremely thin. bacterial. and superiorly to the crura of the diaphragm. . and other pelvic organs. and Moraxella catarrhalis. 9. Others include Pseudomonas aeruginosa. The preaortic group drains the abdominal part of the gastrointestinal tract above the mid-rectum. and is continuous with the two layers of peritoneum which cover respectively the antero-superior and posteroinferior surfaces of the stomach and first part of the duodenum. The lateral group drains the iliac lymph nodes. extending laterally to the edge of the psoas major muscles. Among older adolescents and young adults. the most common cause of ear infections is Haemophilus influenzae.png 8. nontypeable Haemophilus influenzae. the ovaries. or fungal pathogens. ... anxiety.inability to synthetize melanin from tyrosine.......AA most human rabies cases in the United States were caused by bat bites that probably were unrecognized or undetected.3 .... and cannot quench his or her thirst.CC Albinism... Negri bodies are 100% diagnostic for rabies infection. terror. insomnia. in which the patient has difficulty swallowing because the throat and jaw become slowly paralyzed.Rabis is a viral disease that causes acute encephalitis .odds of having disease in exposed group divided by odds of having disease in unexposed group 250/50/250/150. shows panic when presented with liquids to drink.10.. hallucinations. paranoia.. 12.DD Viral vaccines that living strains elicit both-cell mediated and humoral immunity. progressing to delirium The production of large quantities of saliva and tears coupled with an inability to speak or swallow are typical during the later stages of the disease.amount of tyrosin and thus melanin 13. cerebral dysfunction.FF .Congenital deficiency of either ** Tyrosinase . this can result in hydrophobia.. Soon after.. but are found in only about 80% of cases 11.. The period between infection and the first flu-like symptoms is normally two to twelve weeks... whereas killed viral vaccines elicit predominantly an antibody respond. agitation. confusion... the symptoms expand to slight or partial paralysis..Autosomal recessive or ** Defective tyrosine transporter. abnormal behavior.induce humoral immunity/antibody respond.dec.so common features of these two types. sabin and salk . but can be as long as two years.. •Intentional avoidance of responsibility. . especially toward authority figures •Easily offended •Resentful of useful suggestions from others •Blames others •Chronically impatient •Unexpressed anger or hostility 16. This personality disorder is a chronic condition. but he purposely performs in a manner that is not useful and sometimes even damaging.AA supernumerary nipples (polythelia) more than the normal number of nipples.CC Decreased ATP causes decreased action of Na+ / K+ pumps in the cell membranes. leading to increased Na+ and water within the cell (cell swelling).FF Individuals with passive-aggressive personality disorder appear to comply or act appropriately. may be on the breast or other parts of the body-found along the "milk line" from axilla to groin. meaning that it lasts throughout life. sulky. and hostile. 15. Occasionally. Usually. fluctuating swelling. It is derived from epithelial tissue .14. or pregnancy cause increased pigmentation. or even lactation. Some behaviors that may be used to avoid responsibility include: •Procrastination—to delay or postpone needlessly and intentionally •Deliberate inefficiency—purposefully performing in an incompetent manner •Forgetfulness •Feelings of resentment toward others •Stubbornness •Argumentative. the supernumerary nipple is noticed only when hormonal changes during adolescence. These accessory nipples resemble raised nevi (commonly called "moles"). tenderness. but actually behave negatively and passively resist. the supernumerary nipple remains undetected or asymptomatic. Symptoms include: •Contradictory and inconsistent behavior—An individual with passiveaggressive personality disorder may appear enthusiastic to carry out others’ requests. menstruation. such as bacteria.17. immune system cells cause inflammation and cluster to form lumps called granulomas. This can cause signs and symptoms. Genetics also may play a role in sarcoidosis. they can affect how the organ works. Signs and symptoms vary depending on which organs are affected. . Some researchers think that sarcoidosis develops when the immune system responds to a trigger. or chemicals. viruses. If many granulomas form in an organ.BB In people who have sarcoidosis. Many people who have sarcoidosis have no symptoms or mild symptoms. dust. eye movement(SR..CC Oculomotor nerveIII.single stranded. it can bind to the IgE on the mast cells.eyelide opening(Levator Palpebrae) 20. it also can release dopamine from intact nerve terminal. via various interactions..IR.MR.promote viral entery and Neuroaminidase antigen. and throat can also be involved.. Allergic rhinitis is the most common cause of rhinitis.is used forr parkinson's disease 19..18.enveloped.. Contain: Hemagglutinin antigen. Exposure to certain foreign proteins leads to allergic sensitization.Orthomyxovirus.BB Allergic Rhinitis is defined as inflammation of the nasal membranes and is characterized by a symptom complex that consists of any combination of the following: sneezing. a specific pollen grain) is inhaled into the nose.. which is characterized by the production of specific IgE directed against these proteins. sinuses. The mediators that are immediately released include histamine. ..pupillary constriction . ears. which are present in the nasal mucosa... and heparin. including leukotrienes and prostaglandin D2. chymase.... kinins..promotes progeny viral release Amantadine is DOC for prophylaxis and treatment It blocks viral penetration/uncoating. leading to immediate and delayed release of a number of mediators.CC Influenza viruses.. nasal itching. tryptase.accommodation. The mast cells quickly synthesize other mediators. When the specific protein (eg. These mediators. ultimately lead to the symptoms of rhinorrhea .. nasal congestion...RNA viruses with segmented genome.IO).. and rhinorrhea. A pet that is isolated to one area of the house may still cause significant problems for an person with allergic rhinitis because the dander can be airborne and move to any part of the home through the ventilation system.The eyes. This specific IgE coats the surface of mast cells. bone marrow transplant. serious CMV infections can occur in people with weakened immune systems due to AIDS. A CMV infection may affect different parts of the body.DD ITs tricuspid Valve.BB Most humans are exposed to CMV in their lifetime. So even by exclusion its tricuspid .21. Usually. Infections include: •CMV esophagitis (infection of the esophagus) •CMV gastroenteritis (infection of the stomach or intestines) •CMV retinitis (infection of the eye) •CMV pneumonia (infection of the lung) •Mononucleosis-like illness 22. Its too low for aortic valve and you dont do pulmonary artery replacement in adults. organ transplants. chemotherapy. However. or medicines that suppress the immune system. CMV produces no symptoms. The other is mitral valve. but typically only individuals with weakened immune systems become ill from CMV infection. volvulus and intussusception. usually within about 60100 cm (2 feet) of the ileocecal valve The most common presenting symptom is painless rectal bleeding such as melena-like black offensive stools. severe pain in the upper abdomen is experienced by the patient along with bloating of the stomach region. Meckel's diverticulitis may present with all the features of acute appendicitis. bleeding occurs without warning and stops spontaneously. often mistaken as just belly pain resulting from not eating or constipation. The symptoms can be extremely painful. At times. and is the most frequent malformation of the gastrointestinal tract Meckel's diverticulum is located in the distal ileum. is a small bulge in the small intestine present at birth. It is a vestigial remnant of the omphalomesenteric duct (also called the vitelline duct or yolk stalk).FF A Meckel's diverticulum. . followed by intestinal obstruction. Most of the time. a true congenital diverticulum. Occasionally.23. Also. the symptoms are so painful such that they may cause sleepless nights with extreme pain in the abdominal area. . Alternate day use may not prevent this complication.24. Mechanisms of SIOP include: Direct inhibition of osteoblast function Direct enhancement of bone resorption Inhibition of gastrointestinal calcium absorption Increased urine calcium loss Inhibition of sex steroids . Some professional guidelines recommend prophylaxis in patients who take the equivalent of more than 30 mg hydrocortisone (7. The synthetic glucocorticoid prescription drug prednisone is a main candidate after prolonged intake. Treatment of Chlamydia: Azithromycin Doxycycline Treatment of Gonorrhea: Ceftriaxone Cefixime 25 Steroid-induced osteoporosis (SIOP) is osteoporosis arising due to use of glucocorticoids . especially when this is in excess of three months.analogous to Cushing's syndrome and involving mainly the axial skeleton.5 mg of prednisolone).BB Because dual infection is common. unless the other infection has been ruled out. patients diagnosed with either Gonorrhea or Chlamydia should receive empiric treatment for both infections. lightheadedness.Galactitol accumulates if galactose is present in diet... confusion.. At first the drug is rapidly redistributed so the plasma level falls suddenly. there is a marked discrepancy between cortical and medullary blood flow and oxygen delivery and consumption.. cataracts and mental retardation Galactokinase deficiency.DD Classic galactosemia.due to Galactose-1-phosphate Uridyltransferase Smptos:failure of thrive. nausea and vomiting.26.. Characteristic of rapidly redistributed drug.CC Although the kidneys receive nearly a quarter of the cardiac output and extract relatively little oxygen. Typically. unless there has been an episode of severe acute poisoning 27.. This is followed by normal elimination which causes the characteristic change in the slope. It is unknown whether low-level chronic exposure may cause permanent neurological damage. 28.. Jaundice. symptoms usually resolve themselves. depression.Answer should be DD. hepatomegaly.. 29.. upon removal from exposure to carbon monoxide.. memory loss.DD Chronic exposure to relatively low levels of carbon monoxide may cause persistent headaches. In the medulla.. blood flow and oxygen supply are restricted by a tubulovascular anatomy specifically designed for urinary concentration.mild condition .. CC At a single locus.wikipedia.30.deletion of active allele.the other is inactive(imprinted/inactivated by methylation).DD http://en.png 32...>disease .org/wiki/File:Gray784.CC retroviruses (HIV and HTLV) have reverse transcriptase 31.only 1 allele is active...... .. fluoroquinolones and their derivatives (e.>DIC 35.33. ciprofloxacin. clarithromycin). azithromycin.high Alkaline phosphatase. and is related to cold agglutinin disease. allowing it to retain a simple structure.Peroxide positive cytoplasmic inclusion in granulocytes and myeloblasts Treatment of AML M3 can release Auer rods. This species lacks a peptidoglycan cell wall. which act by disrupting the bacterial cell wall.. (↓ P O2  ↑ VEGF) 34.. similar to eukaryotic cells....due to chronic renal failure..CC AML-M3.BB The cold agglutinins test is used to confirm the diagnosis of certain diseases that stimulate the body to produce cold agglutinins.. these organisms are resistant to the effects of penicillins and other beta-lactam antibiotics. doxycycline).. Lacking a cell wall. . mycoplasma pneumonia....high PTH 36.. it has a cell membrane that incorporates sterol compounds..CC Vascular endothelial growth factor (VEGF) is a signal protein produced by cells that stimulates vasculogenesis and angiogenesis.. Instead.g.causes secondary hyperplasia of parathyroid due to dec Calcium ion absorption and inc phosphorous HYpocalcemia.DD Secondary Hyperparathyroidism. levofloxacin).High circulating myeloblasts on peripheral smear Auer bodies... Antibiotics with activity against these organisms include certain macrolides (erythromycin. It is part of the system that restores the oxygen supply to tissues when blood circulation is inadequate. It obtains these sterols from the host serum. a form of atypical bacterial pneumonia...g. and tetracyclines (e..Hyperphosphatemia. 37. social anxiety disorder) and panic attacks. It is the result of the eventual depletion of almost all of the oocytes and ovarian follicles in the ovaries. and it was estimated that the risk of infection is 7000 times higher in such individuals. meningitidis infection than complement-satisfactory persons.EE Menopause is a term used to describe the permanent cessation of the primary functions of the human ovaries.the nasal septum... insomnia and mood changes. This causes an increase in circulating follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels because there are a decreased number of oocytes and follicles responding to these hormones and producing estrogen. This decrease in the production of estrogen leads to the perimenopausal symptoms of hot flashes.. complement component-deficient population frequently experience frequent meningococcal disease.C5-C9) are more susceptible to N.g..formation of primary palate Cleft palate...failure of fusion of the maxillary and medial nasal process ... It is primarily used to treat moderate to severe anxiety disorders (e. and/or the median palatine process. 39.CC Persons with component deficiencies in the final common complement pathway (C3...AA Alprazolam is a potent short-acting drug of the benzodiazepine class.EE Cleft lip.formation of secondary palate .. and is used as an adjunctive treatment for anxiety associated with moderate depression. 40.failure of fusion of the lateral palatine processes .. In addition. 38.. Long term effects may include osteoporosis and vaginal atrophy.. .pericarditis 46 E Right Main Lobe Foreign Body Obstruction . the difference O2 saturation% between right atrium ......5......is a nonselective beta agonist.. symmetric joint involvement.............****no DIP....there is a significant change.............alpha1>alpha2>beta1....75%..alpha1>alpha2.. ulnar deviation..DD 43.pleuritis. 83% shows there is a opening/shunt between two ventricles that causes to move oxygenated blood from left to right ventricle.....after using drug X.fatigue.after using drug X ..there is no significant change Phenylephrine......5 So drug X must be an alpha 1 antagonist.....morning stiffness improving with use..is an alpha agonist..MCP and PIP..... and systemic symptoms.8 Isoproterenol..DD Drug X is an alpha1 blocker NE.anti-antiG antibody strong association with.1...... subluxation Baker's cyst......between choices Prazosin is an alpha 1 antagonist 42..CC Secoundary hyperparathyroidism..so VSD. ↓ Ca2+....DD Failure of Fusion of IVS with Endocardial cushions.to..after using drug X.. loudest at tricuspid area 44.Autoimmune inflammatory disease affecting synovial joints with pannus formation in joint..DD Rheumatoid arthritis.41....HLA-DR4 clinical presentation..force dec...Osteoarthritis*** Subcutaneous rheumatoid nodules. ↑ PTH 45.Behind the knee nodules 80% have Positive Rheumatic factor.. from 15... force from 13.and right ventricle.look at Q35 ↑ PO4+.tempreture....6....Holosystolic .....has high alpha1 agonist power....dec.....harsh sounding murmur. and there is a genetic predisposition for the disease. if the new born Male low threshold mean more susceptible to have the disease it's tricky Q Males are more commonly affected than females.so if this Patient is a female the chance of her brother is much more than other ones .47 B Brother. African Americans.org/wiki/Pyloric_stenosis I think A.[3] Pyloric stenosis is more common in whites than Hispanics. and has multifactorial inheritance patterns..because the chance of getting of this abnormality in males more than females.. or Asians..wikipedia. with firstborn males affected about four times as often. http://en.[2] It is commonly associated with people of Jewish ancestry. Bosentan has a slightly higher affinity for ET-A than ETB. Bosentan is a competitive antagonist of endothelin-1 at the endothelin-A (ET-A) and endothelin-B (ET-B) receptors. endothelin-1 binding of ET-A or ET-B receptors causes pulmonary vasoconstriction. if Newborn Female b/c Female unlikely. so if get that then male very likely! 48.EE The thymus and parathyroid. By blocking this interaction.Male Lower threshhold of liability = easily get Dz= Greatest risk: Brother. . bosentan decreases pulmonary vascular resistance.CC Bosentan is a dual endothelin receptor antagonist used in the treatment of pulmonary artery hypertension (PAH). both derivatives of the 3rd pharyngeal pouches 49. Under normal conditions. this curve is the same for Lymphoproliferative disorders. early tewnties. onsets in late teens. immunoglobulin levels decreased with time. unknown molecular defect. B cells presents in peripheral blood. the albumin can be normal or low. increased autoimmunity. congenital immunodeficiencies ..50-D Common variable hypogammaglobulinemia. but the gamma globulin always is low. inflammatory bowel disease. Patients who have one or more antiphospholipid antibodies and those that are diagnosed with antiphospholipid syndrome have an increased risk of having recurrent thrombotic episodes. C. and thrombocytopenia. flushing. also MDD Treated with SSRI (Fluoxetine). according to the question there is no decreased between both group ---MI and placebo group----the study get the information in retrospective condition.EE PD. antiphospholipid testing may be ordered to help determine the cause of a positive VDRL/RPR test for syphilis. such as pain and swelling in the extremities. no enough time with the study to place en practice----.CC Antiphospholipid antibody testing may be ordered when a patient has symptoms suggestive of a thrombotic episode. recurrent miscarriages. Cardiolipin antibodies (IgG. S/S-diarrhea.. and headaches. shortness of breath.BLOCK 4 1. the patient are follow forward in time. Don't Give __ FOR PD: Selegiline (b/c MAO I = Serotonin Syn) MAO inhibitors are contraindicated with SSRI's. It also may be ordered when a woman has had recurrent miscarriages and/or as a follow-up to a prolonged PTT test. D. and sometimes IgA) are frequently ordered as they are the most common antiphospholipids. If a patient has a prolonged PTT test. E discarded to precoz. the population should be follow long enough for incidence to appear. 3. muscle spasm. then it is likely that the patient is positive for the lupus anticoagulant. The reagents used to test for syphilis contain phospholipids and can cause a false positive result in patients with antiphospholipid antibodies 2. Occasionally.A NO because cross sectional is used to determine prevalence or to establish etiology . further lupus anticoagulant testing is usually indicated If the tests indicate the presence of the lupus anticoagulant and it persists when retested. etc. IgM.BB Cohort study by concept is prospective. May cause serotonin syndrome due to excess synaptic serotonin.. The signs and symptoms of syphilis vary depending on which of the four stages it presents in (primary. latent. and tertiary).DD Syphilis is a sexually transmitted disease caused by the spirochetal bacteria Treponema pallidum subspecies pallidum. or cardiac symptoms. . secondary. secondary syphilis with a diffuse rash. The primary route of transmission of syphilis is through sexual contact however it may also be transmitted from mother to fetus during pregnancy or at birth resulting in congenital syphilis.4. specifically intramuscular penicillin G. and tertiary with gummas. neurological. It can be effectively treated with antibiotics. Diagnosis is usually via blood tests. latent with little to no symptoms. The primary stage typically presents with a single chancre. 5. which are specialized vesicles. Release of surfactant in lamellar bodies occurs from an infant's first breath onwards. a group of phospholipids that reduce the alveolar surface tension. Surfactant phospholipids are stored in Type II pneumocytes in lamellar bodies. Type II pneumocytes can replicate in the alveoli and will replicate to replace damaged Type I pneumocytes. .EE Type II cells are responsible for the production and secretion of surfactant (the majority of which are dipalmitoylphosphatidylcholine). A low serum ferritin is the most sensitive lab test for iron deficiency anemia Serum iron levels (i. .e.CC Body store iron deficiency is diagnosed by diagnostic tests as a low serum ferritin. an elevated serum transferrin and a high total iron binding capacity (TIBC)..6. however the manifestation of iron deficiency occurs in several stages.e. but these levels increase immediately with iron supplementation. mean corpuscular volume less than 80 μm3 [80 fL]) and hypochromic. iron not part of the hemoglobin in red cells) may be measured directly in the blood.. The diagnosis of IDA requires that a patient be anemic and show laboratory evidence of iron deficiency. Red blood cells in IDA are usually described as being microcytic (i. a low serum iron level. DD IgG is the only Ig that transports through the placenta .Hypercalcemia http://courses..edu/bonephys/hypercalU/opthiazide.DD Hydrocholorothiazide .html 8....7..washington. It may occur spontaneously in people without chronic lung conditions ("primary") as well as in those with lung disease ("secondary"). C Pneumothorax (plural pneumothoraces) is a collection of air or gas in the pleural cavity of the chest between the lung and the chest wall. In a small proportion. or as a complication of medical treatment.9. The diagnosis can be made by physical examination in severe cases but usually requires a chest X-ray or computed tomography (CT scan) in milder forms. blast injury. and many pneumothoraces occur after physical trauma to the chest. progressing to cardiac arrest unless treated. the pneumothorax leads to severe oxygen shortage and low blood pressure. they may include chest pain in most cases and shortness of breath in many.[1][2] The symptoms of a pneumothorax are determined by the size of the air leak and the speed by which it occurs. this situation is termed tension pneumothorax . In individuals without a family history of HCM. family-specific genetic testing can be used to identify relatives atrisk for the disease (HCM Genetic Testing Overview). "male impotence") is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual performance. while approximately 35% involve the cardiac myosin binding protein C gene. B Hypertrophic cardiomyopathy is a disease of the myocardium (the muscle of the heart) in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause. 11. the most common cause of the disease is a de novo mutation of the gene that produces the β-myosin heavy chain. and for this reason some suggest routinely screening certain populations for this disease. Myosin heavy chain mutations are associated with development of familial hypertrophic cardiomyopathy. Younger people are likely to have a more severe form of hypertrophic cardiomyopathy HCM is frequently asymptomatic until sudden cardiac death. HCM is most commonly due to a mutation in one of 9 sarcomeric genes that results in a mutated protein in the sarcomere. Whenever a mutation is identified through genetic testing. B Dmg Blood and Nerve supply to Erectile Tissue! Erectile dysfunction (ED.[7] The occurrence of hypertrophic cardiomyopathy is a significant cause of sudden unexpected cardiac death in any age group and as a cause of disabling cardiac symptoms. The number of hours on a bike and/or the pressure on the penis from the saddle of an upright bicycle is directly related to erectile dysfunction . the sarcomeres (contractile elements) in the heart replicate causing heart muscle cells to increase in size. which results in the thickening of the heart muscle. With hypertrophic cardiomyopathy (HCM). A study in 2002 found that ED can also be associated with bicycling. the primary component of the myocyte (the muscle cell of the heart).2-3. children of an HCM parent have 50% chance of inheriting the disease-causing mutation. Since HCM is typically an autosomal dominant trait. About 50-60% of patients with a high index of clinical suspicion for HCM will have a mutation identified in at least 1 of 9 sarcomeric genes.10. In addition. Approximately 45% of these mutations occur in the β myosin heavy chain gene on chromosome 14 q11.[1][2][3][4][5][6] It is perhaps most well-known as a leading cause of sudden cardiac death in young athletes. HCM also causes disruptions of the electrical functions of the heart. the normal alignment of muscle cells is disrupted. a phenomenon known as myocardial disarray. [8] A cardiomyopathy is a primary disease that affects the muscle of the heart. panic disorder. schizophrenia. 13.[9] Kidney failure Diseases such as diabetes and multiple sclerosis (MS). multiple sclerosis. surgery of the colon.72 hrs). prostate. mental disorders (clinical depression. While these two causes have not been proven they’re likely suspects as they cause issues with both the blood flow and nervous systems.          Causes Drugs (anti-depressants (SSRIs) and nicotine are most common) Neurogenic disorders (spinal cord and brain injuries. D Tumor Best Prog : Poorly differentiated carcinoma confined to mucosa . and stroke[4]) Cavernosal disorders (Peyronie's disease[5]) Psychological causes: performance anxiety. substance abuse. Lifestyle: smoking is a key cause of erectile dysfunction. personality disorders or traits[6]). [10][11] Smoking causes impotence because it promotes arterial narrowing 12. Activate macrophages. causes inflammation. psychological problems. Alzheimer's disease.[7][not in citation given] Surgery (radiation therapy. stress. generalized anxiety disorder. common in chronic intracellular inflammation. which increases the risk for impotence [8]) Ageing. negative feelings. (Kaplan micro immuno book page 158). D Type IV Hypersensitivity: Delayed type ( 48 . or rectum may damage the nerves and blood vessels involved in erection. nerve disorders such as Parkinson's disease. CD4 +TH1 cells mediate. It is four times higher in men in their 60s than in men in their 40s. Prostate and bladder cancer surgery often require removing tissue and nerves surrounding a tumor. bladder. any N. with mild cases followed conservatively. It is the most common cause of bladder outlet obstruction in male newborns. Any T. D Posterior urethral valve (PUV) disorder is an obstructive developmental anomaly in the urethra and genitourinary system of male newborns. any N. Any T. Stage III-C any T. Stage IV any T. http://en. . cancer-in-situ Stage I T1 N0 M0 T1: Tumor invades submucosa Stage I T2 N0 M0 T2: Tumor invades muscularis propria Stage II-A T3 N0 M0 T3: Tumor invades subserosa or beyond (without other organs involved) Stage II-B T4 N0 M0 T4: Tumor invades adjacent organs or perforates the visceral peritoneum Stage III-A T1-2 N1 M0 N1: Metastasis to 1 to 3 regional lymph nodes. requiring intensive care and close monitoring.[1] A posterior urethral valve is an obstructing membrane in the posterior male urethra as a result of abnormal in utero development. N2 M0 N2: Metastasis to 4 or more regional lymph nodes. a thickened bladder wall with thickened smooth muscle trabeculations. Stage III-B T3-4 N1 M0 N1: Metastasis to 1 to 3 regional lymph nodes. Abdominal ultrasound is of some benefit.wikipedia. and bladder diverticula. T1 or T2. The disorder varies in degree. More severe cases can have renal failure and even respiratory failure from lung underdevelopment as result of low amniotic fluid volumes.org/wiki/Colorectal_cancer#Staging 14.Stage 0 Tis N0 M0 Tis: Tumor confined to mucosa. T3 or T4. Features that suggest posterior urethral valves are bilateral hydronephrosis. M1 M1: Distant metastases present. but not diagnostic. 15.BB B.....100% sensitivity C.....most accurate D....100%specificity 16.DD Hepatitis- Hep B. Direct dmg to hepatocytes by Cytotoxic T Lymphocytes. Natural killer cells (or NK cells) are a type of cytotoxic lymphocyte that constitute a major component of the innate immune system. NK cells play a major role in the rejection of tumors and cells infected by viruses. NK cells are cytotoxic; small granules in their cytoplasm contain proteins such as perforin and proteases known as granzymes. Upon release in close proximity to a cell slated for killing, perforin forms pores in the cell membrane of the target cell, creating an aqueous channel through which the granzymes and associated molecules can enter, inducing either apoptosis or osmotic cell lysis. 17.CC Ehler-Danlos syndrome...faulty collagen synthesis causing: Hyper extensible skin tendency to bleed hypermobile joint...may be associated with joint dislocation, berry aneurism and organ rupture Type III collagen is most frequently accented Can be AR or AD 18.CC Increased estrogen produces higher levels of thyroid-binding globulin, a protein that transports thyroid hormone in the blood. These normal hormonal changes can sometimes make thyroid function tests during pregnancy difficult to interpret. Low TSH levels may occur in a normal pregnancy, however, especially in the first trimester. If TSH levels are low, another blood test is performed to measure T4 and T3. Elevated levels of free T4—the portion of thyroid hormone not attached to thyroid-binding proteins—confirm the diagnosis. Rarely, free T4 levels are normal in a woman with hyperthyroidism but T3 levels are high. Because of normal pregnancy-related changes in thyroid function, test results must be interpreted with caution. 19.BB The ureter passes under the uterine artery in females and the ductus deferens in the males in the pelvis. The gonadal arteries cross the ureter in its middle 1/3 in the abdominal cavity where it overlies posas major. In pelvic surgery, particularly during hysterectomy, the ureter is at risk when the uterine artery is ligated and divided . DD Tay-Sac Disease is caused by insufficient activity of an enzyme called hexosaminidase A that catalyzes the biodegradation of fatty acid derivatives known as gangliosides. the lipids accumulate in the brain and interfere with normal biological processes. Hexosaminidase A is a vital hydrolytic enzyme. Patients and carriers of Tay–Sachs disease can be identified by a simple blood test that measures hexosaminidase A activity. The term is often used to refer to a single gene defect that is expressed as problems in multiple systems of the body. that breaks down phospholipids. 23. peripheral neuropathy and trigeminal and glossopharyngeal neuralgias.AA High levels of AFP may suggest that the developing baby has a neural tube defect such as spina bifida or anencephaly. Trisomy 18 (Edwards Syndrome) or another type of chromosome abnormality 21. GM2 Gangliosides are made and biodegraded rapidly in early life as the brain develops. the most common reason for elevated AFP levels is inaccurate dating of the pregnancy. Baclofen is widely used for the treatment of spastic movement disorders. found in the lysosomes.However. spastic diplegia cerebral palsy.BB pleiotropy the production by a single gene of multiple phenotypic effects. where the gene causes defects in several different systems that contain collagen. Low levels of AFP and abnormal levels of hCG and estriol may indicate that the developing baby has Trisomy 21( Down syndrome). 22. such as in osteogenesis imperfecta.CC Baclophen is an agonist for the GABAB receptors. When Hexosaminidase A is no longer functioning properly. amyotrophic lateral sclerosis . . Its beneficial effects in spasticity result from actions at spinal and supraspinal site. especially in instances of spinal cord injury. High levels of AFP may also suggest defects with the esophagus or a failure of the baby's abdomen to close. multiple sclerosis.20. a male hormone.EE Gynecomastia is overdevelopment of the male breast.. and (ii) the tripartite protein toxin.. The lethality of the disease owes itself to the bacterium's two principal virulence factors: (i) the polyglutamic acid capsule.For febrile neutropenia: Adults dosage is 5—10 µg/kg IV or SC once daily is sufficient to support the Absolute Neutrophil Count during an episode of febrile neutropenia. 1). Anthrax toxin is a mixture of three protein components: (i) protective antigen (PA).. 26.adducts and laterally rotates arm Subscapularis.For the treatment of congenital..DD Anthrax is a disease caused by Bacillus anthracis..24.BB . called anthrax toxin.. (ii) edema factor (EF). . teen boys. and cyclic neutropenia and hastens the recovery of marrow from neutropenia after cancer chemotherapy 27... It occurs in babies.GM-CSF . and (iii) lethal factor (LF).. The glandular tissue of the breast swells. idiopathic. which is anti-phagocytic. and older men. 25.innervated by Axillary n.AA It is Sargramostim. Gram positive.. a spore-forming.. Infraspinatus . rod-shaped bacterium (Fig. usually in response to an excess of the female hormone estrogen or a lack of testosterone.CC Supraspinatus helps deltoid abduct arm.latealyrotate arms Teres Minor.medially rotates and adducts arm 28. inc.liver failure) 3. ophthalmoplegia. often resulting from inadequate intake or absorption of thiamine (vitamin B1). interstitial fluid colloid osmotic pressure(lymphatic blockage) 31. capillary pressure and heart failure) 2. 29. CC . dysarthria and loss of consciousness. dysphagia. mammillary bodies.. infection.. Reovirus (Colorado tick fever) Rotavirus is number 1 cause of fetal diarrhea in children less than 2.. confusion. and superior cerebellar vermis... capillary pressure (inc. Wernicke encephalopathy is a syndrome characterized by ataxia.DD Edema is caused by. nephrotic syndrome .FF Reovirus family. consumption resulting in thiamine deficiency. burns) 4. no envelope...nonbloody .watery stool and ELISA+ 30. 1.inc.Rotavirus(children diarrhea) and 2.1.Rapid correction of hyponatremia causing Central Pontine myelinosis which is characterized by acute paralysis.. plasma colloid osmotic pressure.DS RNA .(dec..low plasma proteins. and impairment of short-term memory. It is caused by lesions in the medial thalamic nuclei. periaqueductal and periventricular brainstem nuclei. It is most commonly correlated with prolonged alcohol. capillary permeability (toxin. especially in conjunction with carbohydrate ingestion... inc..10-12 segments . . The mediastinal space which is present between the parietal layer of serous pericardium and the fibrous pericardium contains both the phrenic N and the vagus N.So it can be both phrenic and vagus which are given in the options but i guessed it and i got it right.Right Phrenic nerve and i got it right. Approximately one in four patients with malignant pericardial effusions has breast cancer. progressive disorder in which brain cells (neurons) deteriorate. Hematologic malignancies such as leukemia.The answer should be C Dx of this CT picture really big pericardial effusion . judgment and reasoning. The cerebral cortex is an extremely convoluted and complicated structure associated with the "higher" functions of the mind—thought. the most frequent source of neoplastic pericardial disease. and autopsy findings indicate that of all patients with breast cancer. sensation. and pattern recognition. reasoning. movement coordination. primarily memory. Damage to the hippocampus produces global amnesia . Lung cancer. mediastinal pleura. In advanced stages of the disease. the primary. approximately one in four had malignant pericardial effusion. Hodgkin disease.[1] Both of these nerves supply motor fibers to the diaphragm and sensory fibers to the fibrous pericardium. resulting in the loss of cognitive functions. The hippocampus plays a crucial role in learning and in processing various forms of information as long-term memory. all memory and mental functioning may be lost.full On both sides the phrenic nerve runs posterior to the subclavian vein and posterior to the internal thoracic artery as it enters the thorax. PLEASE check this video:http://radiographics.org/content/21/2/439.AA significant factor in AD is the greatly reduced presence of acetylcholine in the cerebral cortex. Acetylcholine is necessary for cognitive function.rsna. Alzheimer's disease (AD) is an irreversible. and motion. accounts for about one-third of cases. and non-Hodgkin lymphoma make up the third largest group (15% of cases). Breast cancer is the second most common cause of malignant pericardial effusions. and diaphragmatic peritoneum. Open to more explanations 32. also known as myeloid metaplasia.EE Myelofibrosis.There may also be urgency for bowel movements.CC The primary symptoms of IBS are abdominal pain or discomfort in association with frequent diarrhea or constipation. smoking. People with IBS more commonly than others have gastroesophageal reflux. Some studies indicate that up to 60% of persons with IBS also have a psychological disorder. 35. backache and psychiatric symptoms such as depression and anxiety. diabetes mellitus. a feeling of incomplete evacuation (tenesmus). and its onset is caused by a number of small strokes or sometimes. symptoms relating to the genitourinary system. is a disorder of the bone marrow. a change in bowel habits.33. headache. one large stroke preceded or followed by other strokes. impairing the patient's ability to generate new blood cells resulting in a progressive pancytopenia . Abdominal fullness related to an enlarged spleen (splenomegaly). and cardiovascular and cerebrovascular disease 34. chronic fatigue syndrome. typically anxiety or depression. hypercholesterolemia. Bone pain Bruising and easy bleeding due to inadequate numbers of platelets Fatigue Increased susceptibility to infection. fibromyalgia. Vascular dementia is the second most common form of dementia after Alzheimer's disease (AD) in older adults. is one type of vascular dementia. hyperuricemia and gout may also complicate the picture The bone marrow is replaced by collagen fibrosis. Multi-infarct dementia (MID) is thought to be an irreversible form of dementia. such as pneumonia or diarrhea Pallor and shortness of breath while doing physical work due to anemia Because of a high rate of cell turnover. bloating or abdominal distention. or the replacement of the marrow with collagenous connective tissue fibers. It is currently classified as a myeloproliferative disease in which the proliferation of an abnormal type of bone marrow stem cell results in fibrosis. Risk factors for vascular dementia include hypertension.DD Multi-infarct dementia. which is a mutation in the oxidative phosphorylation enzymes (which are on both the mtDNA and the nuclear DNA). and fatty acids into adenosine triphosphate (ATP). in rare cases. to function improperly. teenagers and adults as well. located on the X chromosome It is an inherited disorder that usually affects infants between the age of three months and two years. Mitochondria carry their own DNA. mutations in mitochondrial DNA (mtDNA) or in nuclear DNA (gene SURF1[2] and some COX assembly factors) cause degradation of motor skills and eventually death. This causes a chronic lack of energy in the cells. Mitochondria are an essential organelle in eukaryotic cells. In the case of Leigh's disease. which. In the case of the disease. Leigh's disease. in turn. and the machinery to manufacture their own RNAs and proteins. part of the pyruvate dehydrogenase complex. but. Mutations in the mtDNA that cause the mitochondria to fail. creating poorly functioning mitochondria. amino acids. a person is at risk for a number of disorders. is a rare neurometabolic disorder that affects the central nervous system.36.wikipedia. Their function is to convert the potential energy of glucose. The information stored in the mtDNA is used to produce several of the enzymes essential to the production of ATP. also known as Subacute Necrotizing Encephalomyelopathy (SNEM).org/wiki/Leigh's_disease . crucial cells in the brain stem have mutated mtDNA. C Mitochondria have their own genetic material. affects the central nervous system and inhibits motor functions. The X-linked Leigh's disease is a mutation of a gene encoding PDHA1. called mitochondrial DNA [mtDNA]. There is another form of this disease called the X-linked Leigh's syndrome (OMIM 308930). including Leigh's disease. http://en. thread worm. 38. B Mebendazole or MBZ is a benzimidazole drug developed by Janssen Pharmaceutica and marketed as Vermox. tapeworms. Antiox. and by destroying extant cytoplasmic microtubes in their intestinal cells: thereby blocking the uptake of glucose and other nutrients. including round worm. roundworms. and whipworms Mechanism of action Mebendazole is thought to work by selectively inhibiting the synthesis of microtubules in parasitic worms. and hook worm. and Pripsen. resulting in the gradual immobilization and eventual death of the helminths. hookworms. whip worm. A . The drug is a highly effective broad spectrum antihelminitic indicated for the treatment of nematode infestations. Ovex. C 39. It is poorly absorbed and has no systemic effects. It is used to treat infestations by worms including pinworms.37. CVA tenderness. nausea and vomiting. Acute pyelonephritis is characterized by neutrophilic infiltration and abscess formation within the renal interstitium.Acute pyelonephritis: Affects cortex with relative sparing of glomeruli /vessels white cells cast in urine are classic. introduction collections of white cells to the tubular lumen. A . 40. Abscess may rupture. Present fever. The MCA is the most common site for the occurrence of ischemic stroke Signs and Symptoms 1. leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal. the corona radiata. globus pallidus. Hemiparesis or hemiplegia of the lower half of the contralateral face[2] 2. arm and leg*[2] 4.x Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted. temporal and parietal lobes. Sensory loss of the contralateral face. caudate and putamen. Hemiparesis or hemiplegia of the contralateral upper and lower extremities*[2] 3. Ataxia of contralateral extremities*[1] . The classical symptoms are polyuria (frequent urination). apraxia. Individual risk factors can have separate pathophysiological processes to.[2] The subsequent lack of insulin leads to increased blood and urine glucose. DKA results from a shortage of insulin. involving an expansion of autoreactive CD4+ and CD8+ T helper cells. cause this beta cell destruction. in response the body switches to burning fatty acids and producing acidic ketone bodies that cause most of the symptoms and complications. unneeded cells undergo apoptosis. polydipsia (increased thirst). Diabetes mellitus type 1 (Type 1 diabetes. the wound is made smaller by the action of myofibroblasts. and weight loss. anosognosia. contralateral homonymous hemianopsia. When the cells' roles are close to complete. 42. If contraction continues for too long. juvenile diabetes) is a form of diabetes mellitus that results from autoimmune destruction of insulin-producing beta cells of the pancreas. and spatial disorganization as a result of a non-dominant hemisphere lesion (usually the right brain)[1][3] 7. a gaze preference towards the side of the lesion. Pathophysiology The pathophysiology in diabetes type I is basically a destruction of beta cells in the pancreas. regardless of which risk factors or causative entities have been present. It happens predominantly in those with type 1 diabetes. polyphagia (increased hunger). but it can occur in those with type 2 diabetes under certain circumstances. Speech impairments/aphasia: Broca's.5. Still. 41. B Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. formerly. a process that appears to be common to most risk factors is an autoimmune response towards beta cells. it can lead to disfigurement and loss of function. C In contraction. Perceptual deficits: hemispatial neglect. which establish a grip on the wound edges and contract themselves using a mechanism similar to that in smooth muscle cells. IDDM. in turn. or. Wernicke's or Global aphasia as a result of a dominant hemisphere lesion (usually the left brain)[1][2][3] 6. autoantibody-producing B cells and activation of the innate immune system. . Visual disorders: deviation conjugée. 46. ↓LH. Acts to ↓ bone reabsorption. and electrolyte disturbances. leading to body weight < 85% below ideal body weight.43. Sen primarily in adolescent girls. body imagen distortion. Regulation: ↑ serum Ca causes calcitonin secretion.severe weight loss. Associated with ↓ body density. amenorrhea ( ↓ GnRH. ( FA 2010 page 289) . anemia. ↓FSH. Anorexia nerviosa: excessive dieting +/. or expected value). subacuted combined degeneration) due to anormal myelin. D Vitamine B12 defficiency: Macrocytic . A low standard deviation indicates that the data points tend to be very close to the mean. whereas high standard deviation indicates that the data are spread out over a large range of values. metatarsal stress fractures. and ↑ exercise . neurologic symptoms ( paresthesias. It shows how much variation or "dispersion" there is from the average (mean. E Standard deviation is a widely used measurement of variability or diversity used in statistics and probability theory. megaloblastic anemia. Prolonged deficiency leads to irreversible nervous system damage 45. B. hypersegmented PMN. ( FA 2010 page 447) 44.purging intense fear of gaining weight . Commonly coexist with depression. ↓ estrogen). A Calcitonin: Source: Parafollicular cells ( C cells ) of thyroid. Folic acid is needed for the de novo synthesis of the nucleoside thymidine. Thymidylate synthetase (EC 2.1. it therefore has a greater toxic effect on rapidly dividing cells (such as malignant and myeloid cells. eg. Also. 5. and gastrointestinal and oral mucosa). ( FA page 107) 49. BP . Nutrasweet) and thyrosine in diet. yielding dihydrofolate as a secondary product. which replicate their DNA more frequently. which is subsequently phosphorylated to thymidine triphosphate for use in DNA synthesis and repair. growth retardation. and thus it is cytotoxic during the S-phase of the cell cycle. DHFR catalyses the conversion of dihydrofolate to the active tetrahydrofolate. inhibits the synthesis of DNA. eczema. so all purine synthesis will be inhibited. Treatment: ↓ phenylalanine ( contained in aspartame. and proteins. A 48. ↑ Parasympathetic. an enzyme that participates in the tetrahydrofolate synthesis. folate is needed for purine base synthesis. ↓ HR. D Phenylketonuria: Due to ↓ phenylalanine hydroxylase. E Carotid Massage: ↑ afferent activity. Facing a scarcity of dTMP. ↓ sympathetic activity. therefore. and thus inhibits the growth and proliferation of these noncancerous cells. Methotrexate acts specifically during DNA and RNA synthesis. musty body odor.[4] The affinity of methotrexate for DHFR is about one thousand-fold that of folate.47. ↓. thymidylates. Methotrexate. 50.10-methylenetetrahydrofolate + dUMP dihydrofolate + dTMP By means of reductive methylation. seizures. deoxyuridine monophosphate (dUMP) and N5. D Methrotexate: mechanism of action The similar structure of dihydrofolic acid (top) and methotrexate (top) suggests that methotrexate is a competitive inhibitor Methotrexate competitively inhibits dihydrofolate reductase (DHFR). Logically. or ↓ tetrahydrobiopterin cofactor. Findings: mental retardation. Tyrosine becomes essential.45)[1] is the enzyme used to generate thymidine monophosphate (dTMP).1. rapidly dividing cancerous cells undergo cell death via thymineless death.N10-methylene tetrahydrofolate are together used to form dTMP. required for DNA synthesis. RNA. as well as causing the side effects listed below. fair skin.
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