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60 Cards in this Set
- Front
- Back
Rabies
-presentation: fever, severe agitation, disorientation, auditory hallucinations, excessive salivation. |
-rhabdoviridae (rabies) are single-stranded RNA viruses enveloped by a bullet-shaped
-capsule that is studded by glycoprotein spikes that bind to nicotinic ACETYLCHOLINE receptors. -once deposited in a wound, virus stays local for period of days/weeks before binding to acetylcholine receptors on peripheral nerve axons and traveling retrograde to CNS. -clinical presentation of agitation, disorientation, pharyngospasm, and photophobia leading to coma and death is strongly suggestive of rabies encephalitis |
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Viral cellular receptors
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-cytomegalovirus binds to cellular integrins
-Epstein-Barr virus binds to CR2 (CD21) -HIV binds to CD4 and CXCR4/CCR5 -Rabies binds to nicotinic acetylcholine receptor -Rhinovirus binds to ICAM-1 (CD54) |
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Psoriasis treatment
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-treatment of psoriasis ranges from topical therapies to systemic treatment with conventional and biological drugs
-topical vitamin D analogs (calcipotriene, calcitrol, and tacalcitol) bind to the vitamin D receptor and inhibit keratinocyte proliferation, and stimulate keratinocyte differentiation. -i.e., calcipotriene = treatment of psoriasis that activates a nuclear transcription factor |
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Acute tubular necrosis
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-acute tubular necrosis can develop following internal hemorrhage (e.g., after MVA)
-clinical course of ATN may be divided into initiation, maintenance (oliguric) and recovery phases. -initiation: renal tubule cell damage begins to evolve, GRF falls, urine output decreases -maintenance (oliguric) phase: renal tubule injury is established, and GFR stabilizes far below normal; urine output is low/absent. --LM in maintenance stage shows granular casts in the tubular lamina --flattening of tubular epithelial cells and tubular epithelial necrosis with denudation of tubular basement membrane also seen. -recovery phase of ATN is characterized by re-epithelialzation of tubules --polyruria and gradual normalization of GFR occur, leading to complete restoration of renal function in most patients. -most patients with ATN experience tubular re-epithelialization and regain renal function -when ATN is associated with multi-organ failure, renal function may be permanently impaired. |
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N-acetylglutamate
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-N-acetylglutamate is an essential activator of carbamoyl phosphate synthase I
-N-acetylglutamate is formed by the enzyme N-acetylglutamate synthase from the precursors acetyl-CoA and glutamate |
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Aortic regurgitation
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-"water hammer pulses" and head-bobbing with each heart beat (de Musset sign) are characteristic findings in patients with aortic regurgitation
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Chronic renal allograft rejection
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-chronic renal allograft rejection can manifest months to years after transplantation
-mediated by recipient antibodies to graft endothelium formed after engraftment, causing an OBLITERATIVE INTIMAL SMOOTH MUSCLE HYPERTROPHY and FIBROSIS OF CORTICAL ARTERIES, i.e., obliterative vascular necrosis -vs. hyperacute rejection involves pre-formed recipient anti-donor endothelial antibodies, causing immediate vascular fibrinoid necrosis, neutrophil infiltration, infarction of graft -vs. acute rejection can be cellular (causing interstitial mononuclear infiltrate) or humoral (causing a graft vasculitis). |
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Skeletal muscle contraction
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-during skeletal muscle contraction cycle, ATP binding to myosin causes release of myosin head from its binding site on the actin filament
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Hyper-prolacinemia
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-hyper-prolactinemia causes hypogonadism, which leads to reduced estrogen in women.
-low estrogen due to any cause is a risk factor for accelerated bone loss, i.e., osteoporosis. |
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Prolonged ACTH stimulation
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-ACTH is the major trophic hormone of the zone fasciculata and reticular is (vs. zona glomerulosa primarily regulated by angiotensin II)
-prolonged ACTH stimulation causes HYPERPLASIA of zone fasciculata and reticular is, resulting in excessive cortisol production (Cushing syndrome) |
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COPD and erythropoietin
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-COPD can cause hypoxia sufficient to stimulate increased erythropoietin production by the cortical cells of the kidney
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Vertigo
-presentation: 32-yo woman with five episodes of vomiting in last year, with feeling that room is spinning and balance loss -Romberg sign is negative and there is stability during the tandem walk. |
-vertigo is a sensation of excessive motion compared to physical reality
-vertigo is most commonly due to dysfunction within the vestibular system of the inner ear |
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Left atrium
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-left atrium forms majority of posterior surface of heart, and resides adjacent to esophagus.
--left atrium can be analyzed via trans-esophageal ultrasound --enlargment of the left atrium can compress the esophagus and cause dysphagia |
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Descending throacic aorta
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-descending thoracic aorta lies posterior to esophagus and left atrium
-this position permits clear visualization of descending aorta via trans-esophageal echocardiography, allowing for detection of abnormalities such as dissection or aneurysm. |
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Peau d'orange
-presentation: 47-yo female with yellow-red skin rash on chest, plus brawny induration and pitting over right breast |
-Peau d'orange describes présence of pitting edema in subcutaneous breast tissue, accompanied by skin thickening around exaggerated hair follicles
-this pitting edema occurs when neoplastic cells plug the dermal lymphatic channels |
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Pyruvate dehydrogenase
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-hypoxia-induced lactic acidosis is caused by a low activity of pyruvate dehydrogenase (oxidative phsophorylation pathway toward acetyl CoA and Krebs), and a high activity of lactate dehydrogenase (anaerobic pathway toward lactic acid)
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Sporothrix schenckii
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-Sporothrix schenckii is dimorphic: yeast in beast, mold in cold
-seen with gardening, thorn prick ("rose-gardener disease) -pustules, ulcers, subcutaneous nodules along the lymphatics -culture shows branching hyphae, biopsy shows round CIGAR-SHAPED budding yeasts |
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Coccidi oides immitis
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-Coccidioides immitis is dimorphic: yeast in beast, mold in cold
-seen in SW states (desert) – mold form present in soil -pulmonary form: flu-like illness, with cough and erythema nododum -disseminated for: affects skin, bones, lungs -culture: hyphae -biopsy (at 37ºC) forms thick-walled spherules filled with endospores |
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Histoplasma capsulatum
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-histoplasma capsulatus is dimorphic: yeast in beast, mold in cold
-Ohio and Mississippi river valleys – in soil, bird/bat droppings (chicken coops, caves) -pulmonary: similar to tuberculosis (lung granulomas with calcifications) -disseminated: lungs, spleen, liver -culture (25ºC): branching hyphae -biopsy: oval yeast cells WITHIN MACROPHAGES |
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Blastomyces dermatitidis
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-Blastomyces dermatitidis is dimorphic: yeast in beast, mold in cold
-in Ohio and Mississippi River valleys and Great Lakes region – found in soil -pulmonary: pneumonia -disseminated form: common and severe -culture: branching hyphae -biopsy, large round yeasts with DOUBLY REFRACTILE WALL and single BROAD-BASED BUD |
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Paracoccidioides brasiliensis
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-Paracoccidioides brasiliensis is dimorphic: yeast in beast, mold in cold
-found in central and south America -mucocutaneous: chronic mucocutaneous or cutaneous ulcers, which can progress to lymph nodes and lungs -culture: multiple bastoconidia -biopsy: cells covered in budding blastoconidia |
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pCO2 and cerebral vasodilation
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-pCO2 is the most potent cerebral vasodilator
-CO2 decreases cerebral vascular resistance, leading to increased cerebral perfusion and increased intra-cranial pressure -patients with COPD usually have low pO2 (hypoxia) and high pCO2 (hypercapnia) --thus, their cerebral circulation is likely to be increased |
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Antibiotic effective against pseduomonas aeruginosa
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-anti-pseudomonal penicillins: ticarcillin, piperacillin
-cephalosporins: ceftazidime (3rd generation), cefepime (4th generation) -aminoglycosides effective against P aeruginosa: amikacin, getamicin, tobramycin -fluoroquinolones effective against P aeruginosa: ciprofloxacin, levofloxacin -monobactam effective against P aeruginosa: aztremonam -carbapenems against P aeruginosa: impipenem, meropenem |
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Protein M
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-protein M is the major virulence factor for Streptococcus pyogenes
-protein M inhibits phagocytosis and complement activation; mediates bacterial adherence; and is the target of type-specific humoral immunity to S. pyogenes -i.e., resistance of group A Streptococci to phagocytic killing can be overcome by adding antibodies to Protein M |
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Secondary structure of proteins
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-hydrogen bonds are principal stabilizing force in secondary structure of proteins
-vs. tertiary structure, which is stabilized by not only hydrogen bonds but also ionic bonds, hydrophobic interactions, and disulfide bonds --disulfide bonds are very strong covalent bonds between two cysteine residues within the same polypeptide chain that enhance a protein's ability to withstand denaturation |
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Preventing tissue necrosis due to NE extravasation
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-when norepinephrine is being infused into a vein, blanching of that vein with induration and pallor of tissues surrounding the IV site are signs of NE extravasation and resulting vasoconstriction
-tissue necrosis is best prevented by local injection of an alpha1 blocking drug, such as PHENTOLAMINE |
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Cladribine
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-cladribine is a purine analog that achieves high intracellular concentrations, because it is resistant to degradation by adenosine deaminase
-cladribine is the drug of choice for hair cell leukemia -purine analogs that act as anti-metabolites include cladribine (for hairy cell leukoplakia), 6-thiopurines (such as 6-MP, 6-GP), and fludarabine (for CLL) |
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Parietal cell location
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-parietal cells secrete HCl and intrinsic factor
-primarily found in the superficial (upper) region of the gastric glands -vs. chief cells – synthesize and secrete pepsinogen, and are primarily found in the deeper region of the gastric glands |
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Omalizumab
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-omalizumab is an anti-IgE antibody
-omalizumab is effective and acceptable add-on therapy for patients with severe allergic asthma --shown to reduce dependency on both oral and inhaled steroids |
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Ipatropium
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-Ipatropium and other anti-muscarin agents can reverse VAGALLY-medidated bronchoconstriction
-vs. methylxanthines like theophylline and aminophylline cause bronchial dilation by decreasing phosphodiesterase enzyme activity, thereby increasing intracellular cAMP |
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Beta-blocker mechanism in thyrotoxicosis
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-beta-blockers have dual mechanism of action in treating thyrotoxicosis:
--decrease effect of sympathetic adrenergi impulses reaching target organs --decrease rate of peripheral conversion of T4 to T3 |
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GABAa, GABAb, and GABAc receptors
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-GABAa and c receptors are ion channels, vs. GABAb receptor is linked to a G-protein
-benozodiazepines, barbiturates, and alcohol all bind to different components of the GABAa receptor, thus facilitating GABA's inhibitory action in the CNS |
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Etanercept
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-etanercept is a tumor necrosis factor-alpha (TNF-alpha) inhibitor added to methotrexate to treat moderate-to-severe rheumatoid arthrisi in patients who have failed methotrexate alone
-etanercept is a fusion protein that links a soluble TNF-alpha receptor to the Fc component of human immunoglobulin G1 -etanercept reduces the biological activity of TNF-alpha by acting as a DECOY RECEPTOR |
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Suffices of biological agents
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-suffix of a biological agent indicates whether a medication is a monoclonal antibody (mab), a receptor molecule (cept), or a kinase inhibitor (nib)
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Naloxone
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-naloxone is a pure opioid receptor antagonist used for treating opioid intoxication or overdose
-although naloxone binds to mu, kappa, and delta opioid receptors, it has greatest affinity for mu receptors, making it an ideal agent for treating opioid intoxication |
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Class IA anti-arrhythmics
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-class IA anti-arrhythmics are sodium channel-blocking agents that slow phase 0 of the ventricular myocyte action potential
-this action serves to prolong depolarization, as well as the refractory period of these cells -class IA anti-arrhythmics include quinidine, procainamide, and disopyramide |
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Turner syndrome genetics
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-mitotic error in early development results in 45,XO (complete monosomy) karyotype.
-this accounts for the majority of cases of Turner syndrome |
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Small-cell lung carcinoma
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-small cell carcinoma of lung is the most aggressive lung neoplasm
-SCC is though to have a neuroendocrine origin -tumor cells express NEUROENDOCRINE MARKERS, and contain neuro-secretory granules in the cytoplasm -i.e., neurofilaments would be present in a small cell carcinoma of the lung |
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Hypertrophic cardiomyopathy
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-hypertrophic cardiomyopathy often presents as sudden cardiac death in a young athlete
--almost all cases are due to autosomal dominant mutations in cardiac sarcomere proteins --the most common of protein involved is BETA-MYOSIN HEAVY CHAIN -vs. about 1/3 of cases of DILATED cardiomyopathy are genetic --these cases are mostly due to autosomal dominant mutations of cardiac myocyte cytoskeletal proteins (dystrophin) or mitochondrial enzymes |
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Primary myelofiborisis
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-primary myelofiborsis presents as severe fatigue, splenomegaly (causing early satiety/abdominal discomfort), hepatomegaly, anemia, and BONE MARROW FIBROSIS
-associated with JAK2 mutation -a JAK2 inhibitor (ruxolitinib) is approved for treatment of primary myelofibrosis |
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Polycythemia vera presentation
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-polycythemia very presents with pruritus, erythromelalgia, splenomegaly, thrombotic complications, ERYTHROCYTOSIS, and thrombocytosis
-also associated with JAK2 mutation |
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Essential thrombocytosis presentation
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-essential thrombocytosis presents with hemorrhagic and thrombotic symptoms (easy bruising, microangiopathic occlusion), THROMBOCYTOSIS, and megakaryocytic hyperplasia
-also associated with JAK2 mutation |
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Chronic myelogenous leukemia presentation
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-CML presents with constitutional symptoms (fatigue, weight loss, sweating), splenomegaly, and LEUKOCYTOSIS WITH MARKED LEFT SHIFT (i.e., mylocytes, metamyelocytes, band forms)
-associated with mutation of Philadelphia chromosome t(9:22) BCR-ABL fusion protein |
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Chronic myeloproliferative disorders (general)
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-chronic myeloproliferative disorders (polycythemia vera, essential thrombocytosis, primary myelofibrosis) often have a mutation in the cytoplasmic tyrosine kinase, Janus kinase 2 (JAK2)
--this results in constitutive tyrosine kinase activity, with consequent cytokine-independent activation of STAT transcription factors |
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Progressively weakening diaphragmatic contractions
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-progressively weakening diaphragmatic contractions during maximal voluntary ventilation with intact phrenic nerve stimulation indicate neuromuscular junction pathology (e.g., myasthenia gravis) and/or abnormally rapid diaphragmatic muscle fatigue (e.g., restrictive lung disease, or chest wall disease).
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Von Willebrand factor
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-vWF is made by endothelial cells and stored in endothelium and platelets
-vWF binds GP Ib-IX receptors on the platelet membrane and mediates platelet aggregation and adhesion to subendothelial collagen -vWF also serves as a carrier for factor 8 -deficiency of vWF causes both impaired platelet function and coagulation pathway abnormalities -the ristocetin aggregation test is used to measure vWF-dependent platelet aggregation --ristocetin activates GP Ib-IX receptors on platelets and makes them available for vWF binding --when the vWF level is DECREASED, there is poor platelet aggregation in the presence of ristocetin -since vWF serves as carrier for factor 8 (and prolongs its half-life), low vWF causes prolonged bleeding after minor surgeries, and PROLONGED PTT |
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Glanzmann thrombasthenia
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-hereditary deficiency of GP IIb-IIIa receptors
--> mucocutaneous bleeding and increased bleeding time -platelet aggregation is decreased with addition of ADP |
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Thromboxane A2 deficiency
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-deficiency of thromboxane A2 is associated with aspirin treatment, due to irreversible inactivation of COX in platelets
--> decreased platelet adhesion and aggregation |
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Congenital deficiency of Hageman factor
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-congenital deficiency of factor 12 (Hageman) does not cause symptoms
-usually incidental finding because it causes PTT prolongation |
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Risk
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-risk is probability of getting a disease over a certain period of time
-to calculate risk, divide number of diseased subjects by total number of subjects in the corresponding group (i.e., all of the people at risk). |
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Opioid withdrawal
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-opioid withdrawal is marked by abdominal pain, nausea, vomiting, diarrhea, piloerection, lacrimation, and diaphoresis
-yawning, dilated pupils, lacrimation, hyperactive bowel sounds seen on physical exam -can occur after cessation or very reduced use of narcotics -opioid withdrawal is generally not life-threatening, and does not result in seizures like withdrawal from alcohol and benzodiazepines. |
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Alcohol withdrawal
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-symptoms of alcohol withdrawal: tremors, agitation, anxiety, delirium, psychosis
-findings: seizures, tachycardia, palpitations |
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Benzodiazepine withdrawal
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-benzo withdrawal: tremors, anxiety, perceptual disturbances, psychosis, insomnia
-same findings as alcohol withdrawal: seizures, tachycardia, palpitations |
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Withdrawal from stimulants
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-withdrawal from stimulants (cocaine, amphetamines): increased appetite, hypersomnia, intense psychomotor retardation, severe depression ("crash")
-no significant physical findings |
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Nicotine withdrawal
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-nicotine withdrawal: dysphoria, irritability, anxiety, increased appetite
-no significant physical findings |
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Granulomatosis with polyangiitis (Wegener's)
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-granulomatosis with polyangiitis is a cause of rapidly progressive (crescentic) glomerulonephritis (RPGN) type 3 (pauci-immune)
-symptoms of nephritis are accompanied by signs of upper and lower respiratory tract involvement -crescents on light microscopy, absence of deposits on immunofluorescence, and elevated serum c-ANCA are diagnostic. -but immunofluoresence will show reaction to neutrophils |
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Granulomatous inflammation
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-foreign bodies (e.g., retained sutures) can elicit a granulomatous response, which can present as tender erythematous brown/purple papule, nodule, or plaque
-granulomatous inflammation is a form of chronic inflammation, characterized by aggregates of activated macrophages that assume an epithelioid appearance -persistent grnulomatous inflammation with subsequent fibrosis can cause organ dysfunction, which is seen in various granulomatous diseases |
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Granulomatous inflammation
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-microscopically, granulomas characterized by aggregates of activated macrophages that assume an epithleioid appearance
-often surrounded by rim of lymphocytes that synthesize cytokines responsible for continued macrophage activation -multi-nucleated giant ells, derived from fusion of several macrophages, may also be found in granulomas -granulomas associated with certain infection organisms (TB) can develop a central zone of necrosis due to hypoxia and free-radical injury --this appears grossly as a granular and cheesy (caseating) necrosis |
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Granuloma formation
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-granuloma formation is a complex process that occurs over several days to weeks in response to an antigen that can't be eradicated by the usual immune mechanisms
-activated Th1 CD4+ cells secrete interferon-gamma, which activates macrophages -macrophages then secrete TNF-alpha, which results in further macrophage maturation and formation of the granuloma -the granuloma serves to wall off the offending agent -but agent is not always eradicated, as certain pathogens (TB) are resistant to killing -persistent granulomatous inflammation with subsequent fibrosis can cause organ dysfunction. |
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Anemia in women of child-bearing age
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-anemia in women of childbearing age is usually caused by iron deficiency, secondary to menstrual blood loss.
-may present with conjunctival pallor and fatigue -leads to: -decreased bone marrow iron stores (ferritin and hemosiderin) -decreased serum ferritin -increased serum total iron binding capacity, reflecting increased serum transferrin -decreased serum iron concentration -decreased blood hemoglobin -appearance of MICROCYTIC, HYPO-CHROMIC RBCs |