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cxcr5
Forum Newbie  Topics: 4 Posts: 83 |
personality problems - frontal lobe brai lobes - indulent indiscrete and indescent temporal lobe- get sizeures with aura- smelll of burnt urubber- ringing and smell delusion occipital lobe- visual field defects cannot identify with eyes closed parietal lobe problems cerebellar- problems with cooordinatiopn - 3 mo vomininting in the morning - headache -- rest of the day shes -- cant do heel shing movement and diffificulty mocewment optic disc fuzzy0- waves in retina wb ecayuse of the swelling-- pappilaedema - headaches and hypertension- big tumors healing- exploains her symptoms- beain tumor - 6 yo children with large tumors- neuroblastomas-- meudlloblastoma - classical cdommon brain tumor. MG secondary to synrengiomyelia long track signs? NF1- ocular NF2- bilateral 22- acioustic neuroma palmar of lateral 3.5 is spared . kumpkleys - interosseous muscles of the hand T1 to erbs- roots5 and 6 peripheral neurophathies- 1. have this before diabetes increase in ischemia and porotein kinase C - alanine redutase pathways - ischemia all increase during diabetes- which nerves are adffected- Sensory motor , caranial and autonomic neves. starts with sensory - vibrartion and proprioception---> comie in talking about cant drive or feel = burning pain and nigh crapms is a neuronal issue. they feel like they are walking on cotton wool = big time debetes - pt with ulcer - ball of the foot which is the weight bearing pressure related ulcer. this is sa peripheral neuropathy ulcer because the patient cant feel - sensory ulcer.smell of rotten feet from the diabetes. not jsut the seonsory but also autonomic. delayed gastric emptying because the nerves for paristalss are destroying so carrot vominitng. a lot of uriniary retention. Cranial neuropathy = 3 or 6 problems- oftern do not have have horners syndrome - because its neural ischemia - the sympathetic component travels outside , they have single nerve involvemnet usally the yee.
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
other causes of peripheral neuropathies- lead- causing sickling in RBCs post infectious == guillialne barree hypothyroid-- gives peripheralneuropathy - thyroid drugs isoniaazied --- can give u resp signs===and they get peripheral neyuropahty phosphates infections- shingles- parasthesias and tingling in the nasal and opthalmic of trigem never vit D MG. guillain barre mostly motor autoimmune - start witha foot drop - cant stand frrom chair- need help getting off the bed - sensation is preserved - dorsal; adffected= vibration - iurine dysfunction - erectile dysfunction - influenza virus cross reactivicity of the gangliosides and myelin sheaths break down motor ascending problems give u flaccid paralysis eventually cant cought or breathe -- 30% end up on a ventrilator campylobacter infection before hand ascending flaccid paralysis starting in foot-- foot drop-- things get wose in 7-20 ays until 6 weeks- 4-6 weeks- antibodiest hat cross react with gangliposides that deteriorate the myelin sheaths - ant horn- cells- polio- fecal oral - plexopathioes - thorracic outlet syundromes - UMN+ LMN = ALS = - carpal tunnel- erb klumplkes ** charcot marie schwann cells degeneration cause - genetic problemw ith making the myelin very casssic - high arch motor problem-- drop foot perineal nerve-- palsy foot tendons get shortened -- charracted hamatose like a N shape - - very high arch as a result of the foot drop - first symptom of charcot marie tooth first it is the foot drop then u get the abnormalities as a result of that. ambulatory problems neuromuscular junction - eaton lambert- paraneoplastic. autoantibodies against ca channel in the -- weakness in the shoulder girldle presede onset of cancer by 3 years small cell carcinoma of the lungs MG- - slurred speech - weakness cant swlaoing choking autoimmune disorder antibodies ach receptors occasionaliy drugs cause it too females slightly more common autoimmune- arnd 30s eyes wide ptosis look parkinsonian monotonian seppeech diagnosie- anticholineesterase rapid on and rapiod off oinstantly they are fine-- for 15 mins and then gone atrophoniaum then long acting ones. drug induced MG- prganophosphate poison - sludge- urinating pooing, peeing, sweating and drooling iirereversible atrophonium to someone who doesnt have MG-- they will get poopoing, peeing etc oorganophosphates is irreversible. atropponioum is given to reversse their probkems muscular dystrophies deuchenne - severe hypertrophy of the weak muscles replaced with fat-- bnorn fine0 w- -- at 3 they start to regress-- have a distinctinve standup- walk up their bodies--enofldment of the paraspinal muscles ans scoliosis muscle fibers are reduced pseudophypertrophy in the peroipheral l msuchesla nd also in their tongues x linked recessive pt with deuchennes inheritance- dont make it past 15-20 friedereicks ataxia - inherited- x linked recessive - look it up - gives u cerebellar sgns - also LMN signs and flaccid paralysis and difficuilty iwth the speech. 15-30 yo and classic cerebeally glit- hypotonia flaccid paralysis heart -- get diabetes-- more than 40% have heart problems--rhytms obstructive and hypetrophic cardiomyopathy
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
Disorders of consciousness Disturbed consciousness--- awake and aware- Clouding of consciousness - awareness of surrpunding. Confusion-disoriented in time place and personSleepStupor - difficult to be arousedDelirium- ecxtreme loss of conciousness. Coma- unarousalble- wakefulnes is a issueDeliriumAcute confusional state( delirium) vs Dementia[font class="Apple-style-span" face="monospace"] [/font] Q1 29 yr old male found in bus stop dazed and confused. He was disorientated in TPP and believed that he could control the traffic through his thoughts- delusional. He appeared drowsy. His parents claimed that he had been fine the day before. List three characteristics of an acute confusional stateAcute confusional state=deliriumRapid onset- Consciousness impairedDisorientated TPPBehaviour disruptiveThinking muddledMood labilityMemory impairedPerception disturbed - see things= in tremensnot awake disrupted were fine early on emotionally labile [/font] He had no PMH and was on no meds. He had no evidence of a head injury. On exam his temp 38.5C, BP 130/90, p 150. He was confused and drowsy, with choreiform movements of all limbs. He had poor attendion span. He had generalised hyperreflexia and a small goitre.deliriumChanged level of consciousness with confusion & illusionsNot an end diagnosisUp to 15% surgical patientsRF’s include age, underlying dementiaPain important cofactorCauses:Infection,drugs, electrolyte imbalance, hypoxiacauses of delirium- hyperthyroidism, trauma, pain , infections in old people- nemornia and UTI-- hiding infection- disruptve little old ladies, underlying dementia, drugs opiates and hypoxia with nemonia, thyroid storm, deficinecie confused and growsy --- presentation]- metabolic-- nuchal rigidity- meningitis encephalitis Delirium tremens
Wernicke’s encephalopathy and Korsakoff psychosis0- STEP 1
Q2A 72 yr old man is found lost in the street. He gives his name & address but cannot remember how to get there. This is the third time he has been found like this in the past three months. On examination he appears well with no physical abnormalities however he becomes aggressive during the examination and has to be sedated with haloperidol.What features of dementia does he have?List two types of dementia? DementiaImpaired cognition with intact consciousness5-10% over 65 yrs, 70%>100yrsGradual onsetPrimary causes & secondary causesTreatable causes – B12, folate, syphilis, hypothyroid, HIVdementiaa decreases with marriageDementia incidence with agePrimary dementia causesDementia typesAlzheimers- beta amyloidVascular dementia- deteriotration from infarctsLewy bodiesPick’s diseaseCreutzfeldt Jacob diseaseParkinson’s diseaseHuntington diseaseAlzheimer’sLeading cause of dementia7yr mean survivalWidespread cortical atrophyVisual-spatial skills, memory, cognition- no recent memoryNeurofibrillary tangles and amylod deposits- tau proteins- make neurofib taqngles- extracellular amyloid plaquesLoss of acetylcholine NTDrug treatment?Amyloid deposition in alzheimersVascular dementiaStep wise deteriorationUsual ischaemic RF’sLacunar infarcts may cause smoother progressionLewy body dementia - overlapping gives depressionLB=Alpha-synuclein cytoplasmic inclusionsLB in and frontal cortex BGOverlap with Alzheimers & PDPicks disease - younger individualsFrontotemporal dementiaPronounced degeneration in frontal lobesPick bodies Early personality changeDifferential of AD[font class="Apple-style-span" face="monospace"] [/font] A wife brings her 67 yr old husband for an evaluation. She is concerned because he has become increasingly forgetful over the past 2 yrs. He even managed to get lost driving to his daughter’s house where she has been living for the past 5 yrs. You perform a MMSE to assess cognition and he scores 18 (he loses points in verbal recall). Is this:A. Alzheimers DementiaB. Normal agingC. Huntingdons type dementiaD. Vascular dementiaMini Mental State Exam(MMSE)Used to screen for dementiaFollows course of cognitive changes20 questions testing memory, arithmetic, orientationMax score 30>27 = Normal20-26 + moderate impairment10-19 + moderate-to severe impairment<10 = very severe impairmentQ3A 22 yr old women is brought to the emergency room in a drowsy and confused state. Her friends say that she complained of a strange smell and then had convulsions of all 4 limbs. She was incontinent of urine.What features of epilepsy does she haveWhat type of epilepsy does she have ? Can you list another?epilepsyEpilepsy2% of populationFirst convulsion may occur in adultsCan be generalised or partial seizuresDx from good Hx and EEGAuraSeizure Post ictal stuporepilepsy classificationSeizure typeEpilepsy subtypesTemporal lobe – aura w/ generalization = classic - smell soemthing Absence seizure – childhood, 3Hz spike - child not doing good in the school. being disruptiveNocturnal – frontal lobe, childhood onset, inheritedJacksonian march – partial epilepsy which travels through primary motor cortex simple partial never generalizedDiagnosis of epilepsyA good history, Were they post ictal?Electroencephalogram - 3 hz spikeCT/MRIDX - Syncope- hypoxic featureMigraineMovement disorders eg choreoathetosisAlcoholic blackouts, hypoglycaemiaDrugs & side effectsEpilepsy differentialMovement disordersPsychiatric disordersSleep disordersSyncopeVascular diseaseSeizure CausesQ4 A 29 yr old man is found unresponsive in his bed. He has a pmh of IDDM.On exam he does not respond to questions, but flexes & grimaces to pain. His eyes remain closed.Is this man in a coma, PVS or does he have locked in syndrome?List two differences between a coma and LISPersistent locked in syndrome and vegetative stateComa – profound unconsciousness, with damage to reticular formationPVS – do not recover by 30 days--widespread cortical damage, brainstem normalLocked in syndrome – damage to brainstem below level of third nuclei, normal and functioning cortex-- they can think and beathe.Brainstem deathComa- Profound state of unconsciousnessInjury to brainstem, reticular formation or cerebral cortexThree mechanismsDiffuse brain injury eg drugs, ureamiaBrainstem lesion eg haemorrhagePressure effects in brainstem eg tumourComa cont’dInitially lessened brain responsiveness- Loss of reflexes - No response to painGlasgow coma scale ( eyes, verbal, movement)Reversible causes (drugs, hypothermia, metabolic )PrognosisPVS vs improvement (30dys)Locked in syndrome Normal cognition, sensation and proprioceptionCaused by Brainstem lesionTraumaStrokeMedication ODBrainstem deatnSyndrome of deep coma, absence of brainstem reflexes and dependence on mechanical ventilation.Diagnosis important re: organ donationabsent corneal reflex, pupils fixed, gag reflex, pain grimace, Caloric testing (COWS), oculocepalic reflex, Neuro exam of coma patientNote trauma, neck stiffnessPupils?FundusOccular movement (Lost dolls eye and COWS)Blood & urineSpace occupying lesionsSymptoms – headache, vomiting, seizuresSigns – features of raised intracranial pressure with focal neurologyCauses - tumour, aneurysm, abscess, cyst, intracranial bleed,Differential – CVA, head injury, vasculitis, post ictalTest – CT, MRI, avoid lumber punctureSpace occupying lesionpapilloedemaNo sharp edge to optic discAsk about morning headache/vomiting
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
Connective Tissue Disorders Giant Cell (Temporal) Arteritis- rheuma has giant granule and large on her ESR zen and her muscles had a ache and proximal muscles/neck and shoulder because of all the swimming--Tenderness/erythema/cord like thickening over the temporal artery/scalpPolymyalgia Rheumatica - SHELFMuscular pain/ stiffness affecting proximal muscles neck/shoulder/hipSystemic symptoms: weight loss/malaise/fever Case scenario30 yrs korean female complains of fever, weight loss, joint pains, claudication and myalgia. You detect absent carotid/radial pulses but femoral pulse is present takayasuTakayasu’s ArteritisYoung Asian women Pulse less disease: weak pulses felt in the upper extremities (carotid and radial) and decreased blood pressureCharacterized by stenosis of the main branches of Aorta due to fibrous thickeningSymptoms include light headedness, limb claudication, malaise, fever, arthralgia, ocular disturbancesAngiography diagnosticCase 40 yrs lady with past history of hep B presents with severe weight loss, fever and painful nodules on her fingers. Over a few weeks you see her again and she has developed gangrene of her digits. Lab work shows p- ANCA and biopsy reveals a necrotising vasculitis of medium sized vesselsQ: what biopsy findings are expected? What is your diagnosis? PAN35 yrs man has abdominal pain and rectal bleeding. He has lost 10 pounds recently. 2 months later comes with wrist drop and muscle pain/weakness. biopsy shows necrotising vasculitis PANPolyarteritis Nodosa (PAN)Young and Middle aged males Blood vessels of Skin/ muscles/ joints/ intestines/ kidney/ nerves commonly involvedfever/weakness/wt losspainful nodules/ ulceration/ gangrenous skin lesions/livedo reticularis / purpuraPeripheral neuritisHypertensionPresence of p-ANCA (may or may not be present)Never in childPolyarteritis nodosa: Livido reticularis/wrist drop when we rode the kawasaki we ate strawberries and rode it fast so got desquam with lymn in neckA 6yrs Japanese Child is brought with fever and a rash. o/e you notice red eyes, a strawberry tongue, diffuse erythematous skin rash with desquamation and cervical lymphadenopathy. her younger sister was also affected with the same problem few weeks ago.What is the diagnosis KAWASAKI (kinda like measles) after fluWhat is the dreaded complication Coronary artery aneurysmCommon in JapaneseChildhood disease, can affect young Multiple members of family affectedViral/immunological etiologyClinical featuresFeverConjunctivitisOral lesions strawberry tonguePapular skin rashCervical lymphadenopathyDesquamation of skinLethal complication is coronary artery aneurysm, thrombosis and ruptureCase scenario8 yrs old boy is brought to a pediatrician with h/o recent URTI, colicy abdominal pain, and haematuria. o/e you detect palpable reddish purple skin lesions on his legs and stools are positive for occult bloodWhat is your diagnosisWhat deposits will be seen in kidney/skin vessels (IGA)HSP, follow URI, bleed in urine/stools Henoch Schonlein Purpura = IgA- top notch A grade + URTI+ nephritis[font class="Apple-style-span" face="monospace"] [/font] Case:40 yrs male with recent onset of asthma presents with wheezing. O/E purpura, eosinophilia and p-ANCA antibodies in serum = chugh loves p-anca and he has EOSINs coz of all the asthma
Wegener’s Granulomatosis = weg sat on the saddle so he got a lot of granulomasPulmonary: nodules /fulminant alveolar hemorrhageSinuses-Sinusitis deformities: saddle nose Renal disease-progressive glomerulonephritisPresence of c-ANCAGranulomatous arteritisChurg Strauss syndrome Pulmonary infiltrates Purpura Eosinophilic infiltrate small arteries Igg antibodies against glomerular basement membrane- the chug uhad canca -- hemoptysis in churg Behcet’s DiseaseRare USACommonly seen in men of Middle eastern/AsianCharacterized byOral ulcers painful Genital ulcersEye inflammationAcne like lesions Treatment of VasculitisGlucocorticoidsImmunosupressants: azathioprineCyclophosphamide is used in life threatening disease Vascular surgery: Stenosis or aneurysmBone diseasesosteoporosis = neck of femur = external rotation Q: what metabolic bone disease is she likely to have?Osteoporosis, decrease bone mass, increase oseoclastic activity. Defined as reduced bone mineral density>2.5 standard deviation below normal bone mass in young women.Risk factors White/asian race/genetic/petite frame/Old age /Post Menopause- no estrogen/sec to steroid useResults in brittle bones easily fracture even without traumaPresents with loss of height/fractures wrist /Femur /compression fracture of the vertebrae /dowager humpDXA testnormal serum and calciumeosinophil-- rank receptors will be really low..rank ligand and rank receptor interaction to make the osteroclastsconfirm with dexa scantreat with bisphosphonates- risidronate and elandronate- COMP - reduceyour osteoclastic activity Cause is vitamin D deficiency (dietary or lack of sun exposure)Kidney failure and liver disorders affect vit D metabolismActive form (1,25 dihydroxyl vit D) is required for calcium absorption in the gut Calcium and phosphorus are required for bone mineralizationIn the absence of adequate calcium absorption bone cannot be mineralized and remains weak and softPresents with bony pain, deformity and fractures, muscle weaknessXray:“Looser zone”(pseudo fractures)WEAK BONE, NOT REAL FRACTURE, have BOWEL LEGS, genu varum. case45 yrs old male presents with bony pain, diminished hearing and says his hat size has recently increased. O/e you detect a sensorineural acoustic nerve damage and Xray skull shows mosaic pattern, serum alkaline phosphatase is raisedWhat is the diagnosis? Pagets disease of boneWhat is the mechanism of action of the drug used to treat this disorder?What genetic mutation is this condition associated with? Osteroclastic activityPaget’s Disease of Bone (Osteitis deformans)Etiology: slow reaction to paramyxo virus infection Exuberant osteoblastic activity mosaic pattern Asymptomatic, bone pain, skeletal deformity (bossing of skull, bow legs), fractures, nerve entrapment, hearing loss Xray: mosaic pattern (sclerotic and lytic lesions)Entrapement neuropathy, foramina in skull gets closeTreatment: Bisphosphonates & calcitonin reduce osteoclastic activitycaseA 45 yrs man presents with bony pain, severe fatigue and blind spells. He says every few days for a few secs everything goes black. MRI shows markedly increased density of skullisOsteopetrosis: Marble bone diseaseRare inherited diseaseDecreased functioning of osteoclastsAbnormal thickening of boneMultiple fractures case Osteitis Fibrosa cystica & Renal Osteodystrophy Renal failure Metastatic calcificationBone pain/fracturesRenal stones ON COMP SHELF***[font class="Apple-style-span" face="monospace"] [/font][font class="Apple-style-span" face="monospace"] [/font] Secondary:Cancer prostate (osteoblastic), Lungs, breast and kidney (osteolytic lesions)Breast both Site for metastatsis – vertebra, proximal femur, pelvis. Symptoms: Dia ganosis: x ray affects children and young people, involves metaphysis of long bones results in fracturesHappens in knee Xray sunburst appearance and codman’s triangle h/p spindle shaped cells Affects diaphysis of long bonesCommon in childrenXray shows onion peel appearance central nidus surrounded by sclerotic bone Multiple Myelomas [font class="Apple-style-span" face="monospace"] [/font] Vertbae, ribs!! NOT KNEE Can be from benign tumorOLDER PEOPLEEdited by cxcr5 on Mar 28, 2010 - 9:48 PM
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
ecver chest pain fatigue malaise, sw SLE 1. photosensitivity 2. multisystem disorder 3. skin is involved and serosal fcavity is involved 4. jkoints and arhtritis 5. leiukopenia and thrombocytopenia multisystem disorder systemic - constritutional sundromes = fever weight loss and fatigue arthritis other organ involvements renal inolvement veryoftenpresent diag autoantibodies - sensitive which are specific for SLE DVT-w hat is the cause of the SVT pregnant = 120x more common in women young ladies- child brearing age very likely to be pregnant etiology ladies in 20s and 30s and black woemn multifactorial etiology- hormonal and immuneproblems many antibodies photosensitivity to sun flared up in areas with a lot of sunlight autoimmunity drug induced category
myocarditis- raynauds phenomenon- white blue and then red due to vasospasm - sever or mild arthritis lupus - CNS symtposm with psychosis and
Clinical SIca yndrome -- dry mouth and eye zeropsis xerotpthomia- dry mouth
38 yea r old woman - of cold and painful tip
poly = many - inflmamtion of cartilage0 in the nose+ ears and trachea+ saddel shaped node ears peel off develop laryngotracheal deformity and cant speak of eat Multiple areas- poly chondritis
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
drug eruptions- Pennicilin allergic reaction IgE mediated mast cell histamien release sometimes induced by cold- cold induced artricaria red itchy and iitchy and elevated and has dermal edema- sometimes can occur due to cold exposure-- cold induced artericaria erythyma multiform - antibiotic reasction- generalized not in a particular aread- it is called toxic epidermal necrosis. - get steven hohnson-- very high mortality dart like contact dermatitis - has to come in cometact with the substance nigericans- acantohosis - white velverty groin skin folds and axilla hyerperpigmented skin leision hallmark of a GI malignant erythyma nodosum - crohns - sarchoidosis - crampy abdominal pain and bloody disatrha and nmutliple fistulas - bumpy leisions on her skin- - 50 year od- schromnbic cough and red ness of hilar lymphadenopathy ertyhyma migrans lyme borrileiea dburdogeria bitten while camping byut the tick that causes that organis> buls eye rash causes arthritis and severe confusuion and problems with cns and impaired cognition= severe headache _+ arthritidis + epidermal includsion scyyst - swelling in the ear lobulkes keratinocytes form horn like stucture in dermis thin squamous latyers with keratin deep down in the skin due to trauma nail fold infection - painful - psudomonoas- green ungulunum- yellow and crumble into powder ingrawoing toe nails - cutt off after surgeyr- nail plate growing underst the skin spliter hemorahage - bacterial nail pitting- psoriasis0- crumbling ogf the nail koinikolysis - hair leisions hirsusim- pocd Edited by cxcr5 on Mar 28, 2010 - 7:42 AM
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
CNS LA - bupivacaine GA- halothane Opioids - routes of admin - morphine uses - Contraindications - detoxification Methadone -uses Antidepressants – uses & adverse effects Antipsychotics - adv effects Dopamine pathways & their functions Antiepileptics – drug for myoclonic & absence cocaine - MOA amphetamines - MOA benzodiazepines – adv effects & overdose barbiturates – poisoning dependenca Parkinsonism - uses & MOA Blood folic acid – uses & deficiency vit b12 - metabolism warfarin – adverse effects & lab test Heparin – adverse effects & overdose growth factors- GCSF & GMCSF iron - oral & parenteral iron preps indications Antiplatelets uses & MOA Fibrinolytics uses Git antiemetics – prokinetics – adv effects - 5HT 3 antagonists uses Antiulcer agents – H2 blockers, PG analogs cimetidine – interactions H pylori treatment antidiarhreals - loperamide & lactulose Endocrines GNRH analogs uses oral antidiabetic drugs – PPAR agonists Oxytocin uses HRT Osteoporosis – raloxifene & bisphsop Insulin – Rx of diabetic ketoacidosis - goals of therapy Antiandrogens – 5 a reductase inhibitors Contraceptives post coital Corticosteroids - adv effects - dexamthasone test Antithyroid drugs – propylthiouracil Addisonian crisis
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
Q: A 12yo patient was treated for a reaction to a bee sting, what drug provides the best coverage of sympathomimetic receptors? A: Epinephirine(Alpha1,2 and Beta 1,2)- when we go to epi we get everything all the alphas and the betas Q: A 57 yo heart failure pt develops cardiac decompensation, what drug will give you adequate perfusion of his kidneys as well as tx for his Hypotension A: Dopamine Q: A fellow passenger on a Carnival cruise ship looks pale and diaphoretic, what antimuscarinic agent would you give them? A: scopolamine Q: A group of pts are rushed into the ER complaining of excessive sweating, tearing, salivation, HA, N and V, muscle twitching, difficulty breathing and diarrhea. What drug would be the most effective immediate tx A: Atropine pts are suffering from Cholinestrase inhibitor poisining(Nerve gas/Organophosphate poisining) Q: As an Anes you want to use a depolarizing neuromuscular blocking drug on your pt, what do you use A: Succinylcholine Q: By what mechanism does this drug help A: Prevents the release of Ca from SR of skeletal muscle Q: Clonidine is the preferred sym pathomimetic tx of HTN in pts with renal disease, why?? A: Centrally acting alpha agonist, thus causing a decrease in central adrenergic outflow, spairing renal blood flow Q: Cocaine casues vasoconstriction and local anesthesia by what mechanism A: Indirect agonist, uptake inhibitor Q: Cocaine shares is mechanism of action with what antidepressant A: TCA Q: Dobutamine used for the tx of shock acts on which receptors A: Beta1 more than B2 Q: Guanethidine enhances the release of Norepi? A: No, it inhibits the release of Nor Epi Q: How does angiotensin II affect NE release? A: It acts presynaptically to increase NE release. Q: How does botulinum toxin result in respiratory arrest? A: Prevents the release of ACh, which results in muscle paralysis. Q: How does dantrolene work? A: Prevents the release of calcium from the sarcoplasmic reticulum of skeletal muscle. Q: How does NE modulate its own release? What other neurotransmitter has this same effect? A: NE acts presynaptically on alpha-2 receptors to inhibit its own release. A: ACh also acts presynaptically through M1 receptors to inhibit NE release. Q: How would hemicholinium treatment affect cholinergic neurons? A: Hemicholinium inhibits the transport of choline into the nerve, thus inhibiting formation of ACh. Q: How would you reverse the effect of a neuromuscular blocking agent? A: Give an antichloinesterase - neostigmine, edrophonium, etc Q: If a patient is given hexamethonium, what would happen to his/her heart rate? A: It would increase to ~ 100 beats/min. Both sympathetic and vagal stimulation would be knocked out, but the SA node has an intrinsic pace of 100 beats/min, which is normally checked by vagal stimulation. Q: Isopoterenol was given to a patient with a developing AV block, why? A: Stimulates beta adrenergic receptors Q: Norepi feedbacks and inhibits the presynaptic receptor by what mechanism A: Binding to the presynaptic alpha 2 release modulating receptors Q: Reserpine will block the syntheis of this drug and but not its precursor. A: Blocks Norepi, but not Dopamine Q: These drugs acts indirectly by releasing strored catecholamines in the presynaptic terminal A: Amphetamine and Ephedrine Q: What anticholinesterase crosses the blood-brain-barrier? A: physostigmine Q: What antimuscarinic agent is used in asthma and COPD? A: Ipratropium Q: What antimuscarinic drug is useful for the tx of asthma A: Ipratropium Q: What are the classic symptoms of cholinesterase inhibitor poisoning (parathion or other organophosphates)? A: Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation = DUMBBELS; also abdominal cramping Q: What are the clinical indications for bethanechol? A: Activates cholinergic receptors on bladder and bowel smooth muscle, alleviating post-op and neurogenic ileus and urinary retention. Q: What are the clinical indications for neostigmine? A: Post-op and neurogenic ileus and urinary retention, myasthenia gravis, and reversal of neuromuscular junction blockade (post-op) through anticholinesterase activity. Q: What are the indications for using amphetamine? A: narcolepsy, obesity, and attention deficit disorder (I wouldn't recommend this) Q: What are the nondepolarizing neuromuscular blocking drugs? A: Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium Q: What are the phases of succinylcholine neuromuscular blockade? A: Phase 1 = prolonged depolarization, no antidote, effect potentiated by anticholinesterase; Phase 2 = repolarized but blocked, an anticholinesterase is the antidote for this phase. Q: What are two indirect acting adrenergic agonists? A: amphetamine and ephedrine Q: What beta 2 agonist will help your 21yo Astma pt? A: Albuterol, tertbutaline Q: What cholinergic inhibitor acts by directly inhibiting Ach release at the presynaptic terminal A: Botulinum Q: What cholinomimetic is useful in the diagnosis of Myasthenia Gravis A: Edrophonium Q: What cholinomimetics might your pt be taking for his glaucoma A: Carbachol, pilocarpine, physostigmine, echothiophate Q: What class of drug is echothiophate? What is its indication? A: anticholinesterase A: glaucoma Q: What conditions would you use dantrolene? A: In treatment of malignant hyperthermia, due to concomitant use of halothane and succinylcholine. Also in neuroleptic malignant syndrome, a toxicity of antipsychotic drugs. Q: What drug is used to diagnose myasthenia gravis? A: edrophonium (extremely short acting anticholinesterase) Q: What drugs target this enzyme A: Neostigmine, pyridostigmine edrophonium physostigmine echothiophate Q: What effect would atropine have on a patient with peptic ulcer disease? A: Theoretically it could be used to block the cephalic phase of acid secretion (vagal stimulation). Q: What effect would atropine have on the preganglionic sympathetic activation of sweat glands? Would this person sweat? A: None. No, because atropine would block the postganglionic muscarinic receptors involved in sweat gland stimulation. Q: What enzyme is responsible for the breakdown of ACh in the synaptic cleft? A: Acetylcholinesterase; ACh is broken down into choline and acetate. Q: What enzyme is responsible for the degredation of Ach A: Acetylcholine esterase Q: What enzyme is responsible for the production of Ach from Acetyl CoA and Choline A: Choline acetyltransferase Q: What is the clinical utility of clonidine? A: Treatment of hypertension, especially with renal disease (lowers bp centrally, so flow is maintained to kidney). Q: What is the clinical utility of cocaine? A: The only local anesthetic with vasoconstrictive properties. Q: What is the difference between the affinity for beta receptors between albuterol/terbutaline and dantroline? A: Dobutamine has more of an affintiy for beta-1 than beta-2, and is used for treating heart failure and shock. Albuterol and terbutaline is the reverse, and is used in treatment of acute asthma. Q: What is the difference in receptor affinity of epinephrine at low doses? High doses? A: Prefers beta's at low doses, but at higher doses alpha agonist effects are predominantly seen. Q: What is the effect of epinephrine infusion on bp and pulse pressure? A: Increased systolic and pulse pressure, decreased diastolic pressure, and little change in mean pressure. Q: What is the effect of guanethidine on adrenergic NE release? A: It inhibits release of NE. Q: What is the effect of norepinephrine on bp and pulse pressure? A: Increases mean, systolic, and diastolic bp, while there is little change in pulse pressure. Q: What is the effect of TCA's on the adrenergic nerve? A: They inhibit reuptake of NE at the nerve terminal (as does cocaine). Q: What is the only depolarizing neuromuscular blocking agent? A: Succinylcholine Q: What is the receptor affinity and clinical use of isoproterenol? A: It affects beta receptors equally and is used in AV heart block (rare). Q: What makes this drug effective A: It antagonizes Ach M receptors and decreases parasym (GI) rxn Q: What nondepolorizing agents could you have used A: Tubocurarine, atra-, miv-, pan-,ve-, rapacuronium Q: What other substances regulate the Norepi nerve ending A: Ach, AngiotensinII Q: What other syndrome can this drug tx A: Neuroleptic malignant syndrome Q: What physiological effects was the Anes using Atropine to tx A: SLUD (salivation, Lacrimation, urination, Defecation)as well as airway secretion, GI motility, acid secretions Q: What reversal agent could a Anes give to reverse the effects of Atropine A: Bethanechol, Neostigmine, physostigmine Q: What side effect of using atropine to induce pupillary dilation would you expect? A: Atropine would also block the receptors in the ciliary muscle, causing an impairment in accommodation (cycloplegia). Q: What sympathomimetic would you not prescribe for hypotension in a pt with renal artery sclerosis. A: Norepinephrine (Alpha1,2 and beta 1) Q: What type of neurological blockade would hexamethonium create? A: Hexamethonium is a nicotinic antagonist, and thus is a ganglionic blocker. Q: What would be the effect on blood pressure with infusion of the alpha -2 agonist clonidine? A: Initially vasoconstriction would increase bp, but then it acts on central alpha-2 receptors to decrease adrenergic outflow resulting in decreased bp. Q: What would be the next drug that you would give and why A: Pralidoxime, regenerates active cholinestrase Q: Which antimuscarinic agents are used in producing mydriasis and cycloplegia? A: atropine, homatropine, tropicamide Q: Which drug increases Sys BP w/o affecting Pulse Pressure A: Epinephrine Q: Which of epi, norepi, or isoproterenol results in bradycardia? A: Norepinephrine Q: Which of the following would atropine administration cause? Hypothermia, bradycardia, excess salivation, dry flushed skin, or diarrhea A: Dry flushed skin, due to inhibition of sympathetic post-ganglionic blockade on muscarinic receptors of sweat glands. All others are opposite of what would be expected. Q: Which of these three drugs will cause a reflex bradycardia in your pt (Norepi, Epi, or Isoporterenol) A: Norepinephrine Q: Which receptors does phenylephrine act upon? A: alpha-1 > alpha-2; used as a pupil dilator, vasoconstrictor, and for nasal decongestion Q: While at a tail gait party, you bite into a sandwich that a yellow jacket is also enjoying. Knowing your allergy to this creature, what should you do? A: Epinephrine to treat anaphylaxis. Also useful if you have open angle glaucoma, asthma, or hypotension. Q: Why are albuterol and terbutaline effective in tx of acute asthmatic attacks? A: These B-2 agonists cause respiratory smooth muscle to relax. Q: Why does atropine dilate the pupil? A: Blocking muscarinic receptors in the circular fibers of the eye, results in unopposed action of radial muscles to dilate. Q: Why does NE result in bradycardia? A: NE increases bp, which stimulates baroreceptors in the carotid sinus and the aorta. The CNS signals through vagal stimulation to decrease heart rate. Q: Why is carbachol and pilocarpine useful in treatment of glaucoma? A: They activate the ciliary muscle of the eye (open angle) and pupillary sphincter (narrow angle). Q: Why is pyridostigmine effective in the treatment of myasthenia gravis? A: As an anticholinesterase it increases endogenous ACh and thus increases strength. Q: Why is reserpine effective in treating HTN? A: Reserpine inhibits dopamine transport into vesicles, attenuating its conversion to NE by dopamine beta-hydroxylase. Q: Why is there a drop in systolic, mean, and diastolic bp with infusion of isoproterenol? A: Stimulating beta receptors stimulates heart rate, but beta receptor induced vasodilation reduces peripheral resistance. Q: Why would a patient with cog-wheel rigidity and a shuffling gait be given benztropine? A: Parkinson patients benefit from antimuscarinic agents through its inhibitory action within the indirect pathway. Q: Why would dopamine be useful in treating shock? A: Receptors = D1=D2>beta>alpha, thus increasing heart rate (beta) and blood pressure (alpha vasoconstriction) while maintaining kidney perfusion (dopamine receptors) Q: Why would you give a drug like pancuronium or succinylcholine? A: Useful in muscle paralysis during surgery or mechanical ventilation. Q: Why would you use pralidoxime after exposure to an organophosphate? A: Pralidoxime regenerates active cholinesterase. Q: Will Hemicholinum affect the release of stored Ach during Cholinergic Stimulation A: No, hemicholinum block the uptake of Choline and thus Ach synthesis Q: Would blockade of muscarininc receptors in the bladder be useful in treating urinary retention? A: No. Atropine is used to reduce urgency in mild cystitis. So it would aggravate the urinary retention. Q: Would Hexamethonium be an effective substitute A: No, hexamethonium targets Nicotinc receptors and will block Parasym, Sym, as well as Somatic systems Q: You tx your pt with halothane as well and he has also developed malignant hypothermia, what drug can you give A: Dantrolene Q: Your patient develops a marked arrythmia due to a prolonged depolarization, can you tx this w/ Neostigmine A: No cholinesterase inhibitors will potentiate the stimulating action of Succinlycholine Q: Your patient has acute angle glaucoma, does this affect your tx A: Yes, Scopolamine would antagonize his glaucoma Q: Your patient wants an effective drug to treat his motion sickness, what would you prescribe A: Scopolamine Edited by cxcr5 on Apr 02, 2010 - 8:52 PM
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
parasternal heave- breathe out hold it-- RVH
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crazy_girl
| all steps DIED !  Topics: 17 Posts: 525
hi girl, what's up???  i can see that u are restless  i like those Q&A where are they from????? cool !!!!!!!!!!!keep gooooooing
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
Too much Hormone will inhibit Pitutary stimulation. hypothalamus--- pituatary--- endocrine gland release -- stimulate-- hormone--->too mcuh-- inhibit step 2 --- not step 1. estrogen protgesterone --> FSH LH decrease too much glucocorticoid?-- kill the acth too much TH? -- kill the tsh.
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
ant pit = flat pig anterior pit = ONE cell type --> 1 hormone in excess hypothalamus- MANY cell types--> more than 1 horomones in excess when would you produce a lot of prolactin?> PHYSIOLOGIC - if you are pregnant-- duh - if you are nursing early - stress? -- so say I am stressed about exams-- I ll start lacrimating? lol.. pathologic- - polactinoma = pit adenoma -- producing prolactin -- > drugs that block dopamine --> PIF what happen to prolactin when you block dopamine? normal prolactin = < 20 mg/ml modoerate = 30-300= preggo tumor - MRI- CT scan women - detect early == micoadenoma -- slight increase in prolactin gives galactorrhea -- irregular menses amenorrhea in men -- detected late - macoadenoma > 500 and loss of sex hormone and visual los + gynacomastea treatment - 80% = prolactinoma - responsd to odpamien agonist = bromocriptine+ perfoliede cabergoline > PIH --> prolactin inhibito hormone.
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
Q: ACE inhibitors- clinical use? A: hypertension -- CHF --diabetes--> which causes renal fuckkup because of the hypetension Q: ACE inhibitors- mechanism? = kill aii -- love brad--vasodialation--> decrese in my moms blood pressure when she sees brad it relaxes her. A: reduce levels of Angiotensin II, thereby preventing the inactivation of bradykinin (a potent vasodilator); renin level is increased- Aii hates brad. when brad is around evryoen feels relaxed. acei hates aii-- who hates brad-- so acei loves brad-- what is renin doing? Q: ACE inhibitors- toxicity? A: fetal renal damage, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL) too much brad pitt? not good--> K+++++ cough -- ang edema -- fat coz of the grief of losing brad pitt. cant get pregnant nemore. rash-- renin stalking her now-- rash from crying.adpoted kids damaged. no good taste nemoe. HYPOTENSION to my mom but adverse effects to angie. Q: Acetazolamide- clinical uses? - drug list A: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sicknes.- when you go on the high altitude and you have to pee really bad but you are drunk so your urine is alkaline-- and you are metabolizing alcohol but you are sick-- there is increas e in pressure on high altitude so you get a glaucoma but regardless you ace your exams drunk lolz. Q: Acetazolamide- mechanism? PCT+ CA+ A: acts at the proximal convoluted tubule to inhibit carbonic anhydrase. Causes self-limited sodium bicarb diuresis and reduction of total body bicarb stores. Q: acetazolamide- site of action? A: proximal convoluted tubule- you wanna sit in the proximal seats if you wanna ace your exams. bbut you also need to eat laminated tacos. Q: Acetazolamide- toxicity? A: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy- the taco has alot of cholorine in it and also a lot of sulfur and and ammoniaum in it. thats why you get hyperchrorimic-- whic causes metabolic acidosis and ammonium toxicitiy also sulfer allergy Q: Acetazolamide causesÉ? A: ACIDazolamide' causes acidosis Q: Adenosine- clinical use? A: DOC in diagnosing and abolishing AV nodal arrhythmias adeno-sin-e AVatar body is a sin of adeno Q: ADH antagonists- site of action? ADH = CD A: collecting ducts= Q: adverse effect of Nitroprusside? = pruss- CN A: cyanide toxicity (releases CN) Q: adverse effects of beta-blockers? A: impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations) cant have sex asthma sedated cant sleep chf brady asthma Q: adverse effects of Captopril? A: fetal renal toxicity, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL) Q: adverse effects of Clonidine? A: dry mouth, sedation, severe rebound hypertension Q: adverse effects of ganglionic blockers? A: severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction Q: adverse effects of Guanethidine? A: orthostatic and exercise hypotension, sexual dysfunction, diarrhea Q: adverse effects of Hydralazine? A: nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retention Q: adverse effects of Hydrochlorothiazide? A: hypokalemia, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia Q: adverse effects of Loop Diuretics? A: K+ wasting, metabolic alkalosis, hypotension, ototoxicity Q: adverse effects of Losartan? A: fetal renal toxicity, hyperkalemia Q: adverse effects of Methyldopa? A: sedation, positive Coombs' test Q: adverse effects of Minoxidil? A: hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention Q: adverse effects of Nifedipine, verapamil? A: dizziness, flushing, constipation (verapamil), nausea Q: adverse effects of Prazosin? A: first dose orthostatic hypotension, dizziness, headache Q: adverse effects of Reserpine? A: sedation, depression, nasal stuffiness, diarrhea Q: Amiodarone- toxicity? A: pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, consitpation, CV (bradycardia, heart block, CHF), and hypo- or hyperthyroidism. Q: antidote? A: slowly normalize K+, lidocaine, A: cardiac pacer, and anti-Dig Fab fragments Q: Beta Blockers- CNS toxicity? A: sedation, sleep alterations Q: Beta Blockers- CV toxicity? A: bradycardia, AV block, CHF Q: Beta Blockers- site of action? A: Beta adrenergic receptors and A: Ca2+ channels (stimulatory) Q: BP? A: decrease Q: BP? A: decrease Q: Bretyllium- toxicity? A: new arrhythmias, hypotension Q: Ca2+ channel blockers- clinical use? A: hypertension, angina, arrhythmias Q: Ca2+ channel blockers- mechanism? A: block voltage dependent L-type Ca2+ channels of cardiac and smooth muscle- decreasing contractility Q: Ca2+ channel blockers- site of action? A: Cell membrane Ca2+ channels of cardiac sarcomere Q: Ca2+ channel blockers- toxicity? A: cardiac depression, peripheral edema, flushing, dizziness, constipation Q: Ca2+ sensitizers'- site of action? A: troponin-tropomyosin system Q: Cautions when using Amiodarone? A: check PFTs, LFTs, and TFTs Q: class IA effects? A: increased AP duration, increased ERP increased QT interval. Atrial and ventricular. Q: class IB- clinical uses? A: post MI and digitalis induced arrhythmias Q: class IB- effects? A: decrease AP duration, affects ischemic or depolarized Purkinje and ventricular system Q: class IB- toxicity? A: local anesthetic. A: CNS stimulation or depression. A: CV depression. Q: class IC- effects? A: NO AP duration effect. A: useful in V-tach that progresses to V-fib A: and in intractable SVT A: LAST RESORT Q: class IC- toxicity? A: proarrhythmic Q: class II- effects? A: decrease the slope of phase 4, increase PR interval (the AV node is particularly sensitive) Q: class II- mechanism? A: blocking the beta adrenergic receptor leads to decreased cAMP, and decreased Ca2+ flux Q: class II- toxicity? A: impotence, exacerbation of asthma, CV effects, CNS effects, may mask hypoclycemia Q: Class III- effects? A: increase AP duration, A: increase ERP, A: increase QT interval, A: for use when other arrhythmics fail Q: class IV- clinical use? A: prevention of nodal arrhythmias (SVT) Q: class IV- effects? A: decrease conduction velocity, increase ERP, increase PR interval Q: class IV- primary site of action? A: AV nodal cells Q: class IV- toxicity? A: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression), and torsade de pointes (Bepridil) Q: classes of antihypertensive drugs? A: diuretics, sympathoplegics, vasodilators, ACE inhibitors, Angiotensin II receptor inhibitors Q: clinical use? A: angina, pulmonary edema (also, erection enhancer) A: (Nitroglycerine, Isosorbide Dinitrate) Q: clinical use? A: CHF, atrial fibrillation Q: contractility? A: increase (reflex response) Q: contractility? A: decrease Q: contraindications? A: renal failure, hypokalemia, pt on quinidine Q: decrease Digitoxin dose in renal failure? A: NO Q: decrease Digoxin dose in renal failure? A: YES Q: Digitalis- site of action? A: Na/K ATPase Q: Digoxin v. Digitoxin: bioavailability? A: Digitoxin>95% A: Digoxin 75% Q: Digoxin v. Digitoxin: excretion? A: Digoxin=urinary A: Digitoxin=biliary Q: Digoxin v. Digitoxin: half life? A: Digitoxin 168hrs A: Digoxin 40 hrs Q: Digoxin v. Digitoxin: protein binding? A: Digitoxin 70% A: Digoxin 20-40% Q: ejection time? A: decrease Q: ejection time? A: increase Q: EKG results? A: inc PR, dec QT, scooping of ST, and T wave inversion Q: end diastolic volume? A: decrease Q: end diastolic volume? A: increase Q: Esmolol- short or long acting? A: very short acting Q: Ethacrynic Acid- clinical use? A: Diuresis in pateints with sulfa allergy Q: Ethacrynic Acid- mechanism? A: not a sulfonamide, but action is the same as furosemide Q: Ethacrynic Acid- toxicity? A: NO HYPERURICEMIA, NO SULFA ALLERGY; same as furosemide otherwise Q: Furosemide- class and mechanism? A: Sulfonamide Loop Diuretic. Inhibits ion co-transport system of thick ascending loop. Abolishes hypertonicity of the medulla, thereby preventing concentration of the urine. Q: Furosemide- clinical use? A: edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hypercalcemia Q: Furosemide- toxicity? (OH DANG) A: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout Q: Furosemide increases the excretion of what ion? A: Ca2+ (Loops Lose calcium) Q: HDL effect? A: no effect Q: HDL effect? A: increase Q: HDL effect? A: moderate increase Q: HDL effect? A: increase Q: HDL effect? A: DECREASE Q: how do we stop angina? A: decrease myocardial O2 consumption by: A: 1-decreasing end diastolic volume A: 2- decreasing BP A: 3- decreasing HR A: 4-decreasing contractility A: 5-decreasing ejection time Q: HR? A: increase (reflex response) Q: HR? A: decrease Q: Hydralazine- class and mechanism? A: vasodilator- increases cGMP to induce smooth muscle relaxation (arterioles>veins; afterload reduction) Q: Hydralazine- clinical use? A: severe hypertension, CHF Q: Hydralazine- toxicity? A: compensatory tachycardia, fluid retention, lupus-like syndrome Q: Hydrochlorothiazide- clinical use? A: HTN, CHF, calcium stone formation, nephrogenic DI. Q: Hydrochlorothiazide- mechanism? A: Inhibits NaCl reabsorption in the early distal tubule. Decreases Ca2+ excretion. Q: Hydrochlorothiazide- toxicity? (hyperGLUC, plus others) A: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia, sulfa allergy. Q: Ibutilide- toxicity? A: torsade de pointes Q: K+- clinical use? A: depresses ectopic pacemakers, especially in digoxin toxicity Q: K+ sparing diuretics- clinical use? A: hyperaldosteronism, K+ depletion, CHF Q: K+ sparing diuretics- site of action? A: cortical collecting tubule Q: K+ sparing diuretics- toxicity? A: hyperkalemia, endocrine effects (gynecomastia, anti-androgen) Q: LDL effect? A: moderate decrease Q: LDL effect? A: large decrease Q: LDL effect? A: moderate decrease Q: LDL effect? A: decrease Q: LDL effect? A: decrease Q: loop diuretics (furosemide)- site of action? A: thick ascending limb Q: Mannitol- clinical use? A: ARF, shock, drug overdose, decrease intracranial/intraocular pressure Q: Mannitol- contraindications? A: anuria, CHF Q: Mannitol- mechanism? A: osmotic diuretic- increase tubular fluid osmolarity, thereby increasing urine flow Q: mannitol- site of action? A: proximal convoluted tubule, thin descending limb, and collecting duct Q: Mannitol- toxicity? A: pulmonary edema, dehydration Q: mechanism? A: vasodilate by releasing NO in smooth muscle, causing and increase in cGMP and smooth muscle relaxation (veins>>arteries) A: (Nitroglycerine, Isosorbide Dinitrate) Q: mechanism? A: inhibits the Na/K ATPase, A: increasing intracellular Na+ A: decreasing the function of the Na/Ca antiport A: causing an increase in intracellular Ca2+ Q: mechanism? A: Na+ channel blockers. Slow or block conduction. Decreased slope in phase 4 and increased threshold for firing in abnormal pacemaker cells. Q: Mg+- clinical use? A: effective in torsade de pointes and digoxin toxicity Q: MVO2? A: decrease Q: MVO2? A: decrease Q: name five in class II? A: propanolol, esmolol, metoprolol, atenolol, timolol Q: name four HMG-CoA reductase inhibitors. A: Lovastatin, Pravastatin, Simvastatin, Atorvastatin Q: name four in class IA. A: Quinidine, Amiodarone, Procainamide, Disopyramide Q: name four in class III. A: Sotalol, Ibutilide, Bretylium, Amiodarone Q: name three ACE inhibitors? A: Captopril, Enalapril, Lisinopril Q: name three calcium channel blockers? A: Nifedipine, Verapamil, Diltiazem Q: name three in class IB. A: Lidocaine, Mexiletine, Tocainide Q: name three in class IC. A: Flecainide, Encainide, Propafenone Q: name three in class IV. A: Verapamil, Diltiazem, Bepridil Q: name three K+ sparing diuretics? A: Spironolactone, Triamterene, Amiloride (the K+ STAys) Q: name two bile acid resins. A: cholestyramine, colestipol Q: name two LPL stimulators. A: Gemfibrozil, Clofibrate Q: Nifedipine has similar action to? A: Nitrates Q: preferential action of the Ca2+ channel blockers at cardiac muscle? A: cardiac muscle: Verapamil>Diltiazem>Nifedipine Q: preferential action of the Ca2+ channel blockers at vascular smooth muscle? A: vascular sm. Mus.: Nifedipine>Diltiazem>Verapamil Q: Procainamide- toxicity? A: reversible SLE-like syndrome Q: Quinidine- toxicity? A: cinchonism: HA, tinnitus, thrombocytopenia, torsade de pointes due to increased QT interval Q: Ryanodine- stie of action? A: blocks SR Ca2+ channels Q: selectivity? A: slectively depress tissue that is frequently depolarized (fast tachycardia) Q: side effects/problems? A: tastes bad and causes GI discomfort Q: side effects/problems? A: expensive, reversible increase in LFTs, and myositis Q: side effects/problems? A: red, flushed face which is decreased by ASA or long term use Q: side effects/problems? A: myositis, increased LFTs Q: side effects/problems? A: DECREASED HDL Q: Sotalol- toxicity? A: torsade de pointes, excessive Beta block Q: Spironolactone- mechanism? A: competitive inhibirot of aldosterone in the cortical collecting tubule Q: TG effect? A: slight increase Q: TG effect? A: decrease Q: TG effect? A: decrease Q: TG effect? A: large decrease Q: TG effect? A: no effect Q: thiazides- site of action? A: distal convoluted tubule (early) Q: toxicity? A: tachycardia, hypotension, headache - 'Monday disease' A: (Nitroglycerine, Isosorbide Dinitrate) Q: toxicity? A: nausea, vomiting, diarrhea, blurred vision, arrhythmia Q: Triamterene and amiloride- mechanism? A: block Na+ channels in the cortical collecting tubule Q: Verapamil has similar action to? A: Beta Blockers Q: what two vasodilators require simultaneous treatment with beta blockers to prevent reflex tachycardia and diuretics to prevent salt retention? A: Hydralazine and Minoxidil Q: which diuretics cause acidosis? A: carbonic anhydrase inhibitors, K+ sparing diuretics Q: which diuretics cause alkalosis? A: loop diuretics, thiazides Q: which diuretics decrease urine Ca2+? A: thiazides, amiloride Q: which diuretics increase urine Ca2+? A: loop diuretics, spironolactone Q: which diuretics increase urine K+? A: all except the K+ sparing diuretics Spironolactone, Triamterene, Amiloride Q: which diuretics increase urine NaCl? A: all of them Edited by cxcr5 on Apr 04, 2010 - 7:42 AM
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
eric causes hepatitis due to cholestasis nitro is furious and it therefore breaks down your rbc and causes hemolytic anemia when i had acne my mom had me take tetracycline thankgod i wasnt a child then ir it would cause me dental staining. when we were travelling in a van we couldnt hear a tihing because the van was sooo effing loud if I take opiods I will develop tolerance-- dang for the high and sedation. two things I will NOT develop a tolerance to are -- I will still feel constipated even though less sedated and my pupils will still be constricted. when I oversleep I get a migraine headache and so I should take valproic acid -- best cure ever + -------------- when my maid had TB she took ----- and thats why she couldnt differenitate between the red and the green of the gtraffic signals because she was taking= ETHAM-BUT-OL i am so sleepy and this site was down all day ughhhhhhhhhhhh digoxin--- digitoxin- hepatiically eliminated. diaz is a long laster midaz lasts for seconds only-- but both of them have a benz NE is reserved to dine but the gua diarrhea is previting him fom doing so before he even gets to the dining table cefuroxine and cefuclor ___ + MAOI = hypertensive crisis dipine is very relaxing-- lucky - gf...lol Edited by cxcr5 on Apr 05, 2010 - 11:25 AM
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
page 159
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cxcr5
| Forum Newbie Topics: 4 Posts: 83
toxicology - page 160 + nemonics in one note-> my notebook> micscellenous> page 4 To Do: next -> finish toxicology 2. Q and As 3. Anticancer drugs 4.Antimicrobial 5. Antiinflmmatory for now. Finish nemonics for all.
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crazy_girl
| all steps DIED ! Topics: 17 Posts: 525
my restless girl  what's up????? doing drugs?  keep it up !!!!
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crazy_girl
| all steps DIED ! Topics: 17 Posts: 525
 u had NBME today??????????cooooooool so u're in vacation now  until tomorrow....
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girl_doc
| Forum Elite  Topics: 1 Posts: 310
hey girl, How have u been ? It's hard to find ur current journal but i hope i have hit the right one . Are you done with nbme final ? How did it go ? Come back soon. see ya
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