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58 Cards in this Set
- Front
- Back
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Serum bilirubin rarely exceeds what in hemolysis?
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3 mg/dL
won't see sublingual icterus, if you see it think hepatic and biliary |
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Causes of jaundice
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hemoylsis, defiecny og glucornysl transferase (gilbert, crigler-Najar), defect in transport from hepatocyte to duct (ROtor, Dubin-Johnson), obstruction of biliary system
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Bilirubin formation
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RBCs die -> release of Hb, heme oxxidase converts to biliverdin, bilverdin reductase converts to unconjugated binds to albumin and is delivered to liver, conjugated by uridine diphosphate glucosoronysl transferase
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Congenital causes of juandice, compare Gilbert, Crigler Najjar, Rotor and Dubin Johnson
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Gilbert and Crigler Najar- glucoronsyl transferase, gilbert is decreased expression (mild), CN type 2 AD is decreased, CN type 1 AR and absent UGT
Rotor- impaired hepatocelular secretion, elevated direct bilirubin (different) Dubin jhnson- impaired hepatocellu secretion elevated direct |
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Hep B antigens indictes an especeillly infective state?
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HBeAg, Hbs-Ag indicates current or chronic infection
DNA virus, 10% beccome chronic |
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Hep D
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requires either previous or coinfection with Hep B, requires HBV antigen to coat for repilcation, increases mortality of Hep B infection
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Incubation times and nucleic acid type for hepatitis
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Hep A- 2-6 weeks, RNA
Hep B - 2-6 months, DNA Hep C- 1-2 months, RNA most become chronic |
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HBsAg means...
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current hepatitis presence, HBeAg indicates extreme infectiousness
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Anti-HBs significance
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indicates immunty
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Patinet is postive for anti-HBs and anti Hbc, what is the difference between this and a person with only Anti-HBs?
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1st patient had a resolution in hep B infection
2nd patient had immunization |
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Major medication causes of toxic hepatitis?
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inflammaiton of lvier d/t toxin
methotrexate, chloamphenicol, halothane, isonizazid |
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Pathophys of cirrhosis
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hepatic injury leads to refeneration that is disorganzed and do not function as well, scar tissue impair blood flow leading to portal HTN
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Alcoholic cirrhosis histology
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fatty change initially -> focal liver necrosis w/ neutrophil infilytates, intracytoplasmic eospinophillic inclsions (Mallory bodies), continue inflammation leads to cirrhosis by causing heatocyte destruction
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Alcoholic cirrhosis complicztions
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toxicity to testes leads to atrophy
high estrogen leads to spider angiomata, gynecommastia and palmar erythema impaired blood flow thorugh liver d/t fibrotic nbands, portal HTN, ascites varices |
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Female patient 40-60 presents w/ pruritis at night and has elevated alk phos. Dx?
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primary biliary cirhosis, micronodular liver dz, anti-mitochondrial antibodies
would see macronodular if d/t biruses or toxins |
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Patient presents with psychosis, cirrhosis, orange ring around cornea, inhertiance pattern and defect
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AR decrased ceruloplasmin leads to ielevated copper and deposition in brain, kidney, corena and lvier
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Common causes for a patient presenting with severe epigastric pain radiating to back, elevated amylase and lipase?
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pancreatitis, alcoholism, gallsotnses and increased TGs all cause
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Most common site of intussusseption?
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ileocecal junction, risk is adenoviirus infection, palpable RUQ mass, vancant LRQ, currant jelly stool
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Vomiting, bloody diarrhea in neonate, DDX?
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w/ abd distetion- midgut volvulus
w/ lethargy and temp instability, nectrotzing enterocolitis |
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Osteoarthritis vs. RA
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slow, progressive, DIP in hands and weight bearing = OA, loss of cartilage
RA = abrubpt multiple joints, PIPs and MCPS, stiggness over 1 hour, synovial proliferation |
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Major medication causes of toxic hepatitis?
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inflammaiton of lvier d/t toxin
methotrexate, chloamphenicol, halothane, isonizazid |
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Pathophys of cirrhosis
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hepatic injury leads to refeneration that is disorganzed and do not function as well, scar tissue impair blood flow leading to portal HTN
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Alcoholic cirrhosis histology
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fatty change initially -> focal liver necrosis w/ neutrophil infilytates, intracytoplasmic eospinophillic inclsions (Mallory bodies), continue inflammation leads to cirrhosis by causing heatocyte destruction
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Alcoholic cirrhosis complicztions
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toxicity to testes leads to atrophy
high estrogen leads to spider angiomata, gynecommastia and palmar erythema impaired blood flow thorugh liver d/t fibrotic nbands, portal HTN, ascites varices |
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Female patient 40-60 presents w/ pruritis at night and has elevated alk phos. Dx?
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primary biliary cirhosis, micronodular liver dz, anti-mitochondrial antibodies
would see macronodular if d/t biruses or toxins |
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Major medication causes of toxic hepatitis?
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inflammaiton of lvier d/t toxin
methotrexate, chloamphenicol, halothane, isonizazid |
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Patient presents with psychosis, cirrhosis, orange ring around cornea, inhertiance pattern and defect
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AR decrased ceruloplasmin leads to ielevated copper and deposition in brain, kidney, corena and lvier
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Pathophys of cirrhosis
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hepatic injury leads to refeneration that is disorganzed and do not function as well, scar tissue impair blood flow leading to portal HTN
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Common causes for a patient presenting with severe epigastric pain radiating to back, elevated amylase and lipase?
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pancreatitis, alcoholism, gallsotnses and increased TGs all cause
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Alcoholic cirrhosis histology
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fatty change initially -> focal liver necrosis w/ neutrophil infilytates, intracytoplasmic eospinophillic inclsions (Mallory bodies), continue inflammation leads to cirrhosis by causing heatocyte destruction
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Most common site of intussusseption?
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ileocecal junction, risk is adenoviirus infection, palpable RUQ mass, vancant LRQ, currant jelly stool
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Alcoholic cirrhosis complicztions
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toxicity to testes leads to atrophy
high estrogen leads to spider angiomata, gynecommastia and palmar erythema impaired blood flow thorugh liver d/t fibrotic nbands, portal HTN, ascites varices |
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Vomiting, bloody diarrhea in neonate, DDX?
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w/ abd distetion- midgut volvulus
w/ lethargy and temp instability, nectrotzing enterocolitis |
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Female patient 40-60 presents w/ pruritis at night and has elevated alk phos. Dx?
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primary biliary cirhosis, micronodular liver dz, anti-mitochondrial antibodies
would see macronodular if d/t biruses or toxins |
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Osteoarthritis vs. RA
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slow, progressive, DIP in hands and weight bearing = OA, loss of cartilage
RA = abrubpt multiple joints, PIPs and MCPS, stiggness over 1 hour, synovial proliferation |
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Patient presents with psychosis, cirrhosis, orange ring around cornea, inhertiance pattern and defect
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AR decrased ceruloplasmin leads to ielevated copper and deposition in brain, kidney, corena and lvier
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Common causes for a patient presenting with severe epigastric pain radiating to back, elevated amylase and lipase?
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pancreatitis, alcoholism, gallsotnses and increased TGs all cause
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Most common site of intussusseption?
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ileocecal junction, risk is adenoviirus infection, palpable RUQ mass, vancant LRQ, currant jelly stool
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Vomiting, bloody diarrhea in neonate, DDX?
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w/ abd distetion- midgut volvulus
w/ lethargy and temp instability, nectrotzing enterocolitis |
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Osteoarthritis vs. RA
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slow, progressive, DIP in hands and weight bearing = OA, loss of cartilage
RA = abrubpt multiple joints, PIPs and MCPS, stiggness over 1 hour, synovial proliferation |
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Heberden's nodes, Bouchards nodes vs,. rheumatoid nodules
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Heberden;s and bouchards- palpable osteophytes at interphalgenal joints in OA
Rheumotoid nodues are palpable soft tissue nodules on extensor surfaces |
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7 criter for RA
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need 4:
morning stiffness over 1 hour atrthitis in 3 or more joints at same time arthtitis in hands symmetrical rheumatoid nodules Rheumatoid factor + Erosions or bondy decalcification on X-ray |
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Felty's syndrome
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polyarticular RA w/ splenomegally, leukopenia, ulcers and increased infections, severe variant of RA
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ASeptic necrosis of bone
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Osood-Schlater- tibial tuberosity, Legg-Calve-Perthes disease (aseptic necorsis of femoral head w/o trauma Hx
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Findings pon x-ray in osteoporosis
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thinned cotical bone and enlarged medullary cavity, diffuse radiolucency
associated w/ decreased estrogen, inactivity, hypercoltrisolism, hyperthyroidism, subclinical calcium deficits |
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Optimal calciium intake
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1000-1500 mg/day
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Osteomalacia
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inadequate bone mineralization, low Ca, low PO4, high alk phos
diffuse radiolucency w/ occasional bands perpendivualr to periosteal surface d/t pseudofractures |
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Causes of osteomalacia
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Vit D deficit, severe liver disease (prevents convertion of Vit D to form that can be activated in kidneys), anticonvulsants, renal pronbs, Fanconi syndrome, malnutrition
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Findings in Paget Dz
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very high alk phos, occasional hypercalcemia, causes deagness, bony pain, chalkstic fractures, high output cardiac failure, frontal bossing
enlarged theickend bones with coarse thickened cortices |
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Common sacral somatic dysunction in post=partum
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bilateral sacral flexion, back pain worsens with backward bending
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Most common type of sacra shear
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unilateral sacral flexion, surprise step into a hole, lumbar dysfunction
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Forward sacral torsions an lumbar rotation
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lumbar rotation occurs in opposite diretion of sacrum
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backward sacral torsions, rotation of lumbar spine relative to sacrum
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L5 rotated contralateral to the sacrum
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Nonseelective beta blockers that also block a1
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carvedilol, labetalol
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ADRs of BBs
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fatigue, insomnia, impotence, decreased HDL, increased TGs, nonsletive not for COPD or asthma
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Which CCB is preferential blocking for heart?
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diltiazem, verapamil is about equal
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DOC for angina or MI patients for management of HTN
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fisrt line BB, plus ACE or ARBm can add thiazide or CCB if not under 130/80
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Ergots and triptans MOA
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ergots- act on 5HT1 stimulate and block 5HT2 to cause vasoconstriciton, have more peripheral side effects
Triptans- 5HT1 agonsit, more powerful anti-migraine dtug, still aboid with PVD, uncontrolled HTN and prinzmetals angina and SSRIs |
