MKSAP 2 Flashcards
Why tx outpatient PE with apixaban and not dabigatran
Dabigatran (direct thrombin inhibitor) requires bridging w/ parenteral therapy (5 days of heparin gtt vs. lovenox)
While apixaban doesn’t require bridge
Cryo helpful in hemophilia A, B, or both?
Cryo has factor VIII (deficient in hemophilia A), XIII, fibrinogen, and von willebrand factor
So cryo can be used in hemophilia A if individual recombinant factor unavailable
Main indications for cryo transfusion
DIC- cryo replaces fibrinogen, DIC is a state of hypofibrinogenemia (consuming clotting factors)
Other indications for hydroxyurea aside from sickle cell disease
Hydroxyurea = antimetabolite, can be used to reduce number of platelets in essential thrombocytopenia and RBCs in polycythemia vera
Describe type of disorders where you expect to see dense/hyperchromic RBCs vs. hypochromic RBCs on peripheral smear
Dense/hyperchromic RBCs = spherocytes in hereditary spherocytosis and autoimmune hemolytic anemia
Hypochromic (central pallor) RBCs from microcytic anemias like iron deficiency, thalassemias, sideoblastic anemia
Define
(a) Anistocytosis
(b) Poikilocytosis
(a) Anistocytosis = general term for RBCs of different sizes (high RDW)
(b) Poikilocytosis = term for RBCs of abnormal shape
Differentiate schistocytes and tear dropped shaped RBCs
Shistocytes (or helmet cells) = fragmented RBCs in intravascular hemolysis
Tear dropped cells from extramedullary hematopoesis seen in primary myelofibrosis or thalassemias
Tear drop shaped cells vs. bite cells
Tear drop RBCS are a marker of extramedullary hematopoesis seen in primary myelofibrosis or thalassemias
Bite cells- seen in hemolysis event in pt w/ G6PD deficiency
Why not test for G6PD deficiency during acute hemolysis reaction?
B/c G6PD enzyme is present at normal levels in new RBCs, then reduces by up to 75% as RBC lifespan proceeds. The older, more deficient, RBCS are destroyed first in a hemolysis event so if G6PD level measured then it will be falsely normal
74 y/oM w/ night sweats, found to have Hb 8.1. Normal Cr and calcium. Exam w/ splenomegaly, further bloodwork with IgM spike.
Most likely dx?
Anemia, B-symptoms, M-spike without kidney involvement. Get bone marrow biopsy to dx Waldenstroms macroglobulinemia = indolent B-cell lymphoma (lymphomatous infiltration causes lymphadenopathy and organomegaly)
Clonal bone marrow infiltrate that secretes IgM into blood
Best first diagnostic test for hereditary hemochromatosis
Serum ferritin and transferin sat (over 45% is typically the diagnostic cutoff) to dx iron overload
What is a DAAT for?
DAAT = direct antiglobulin antibody test, looks for IgG against RBC surface
test for warm autoimmune hemolytic anemia
What is warm agglutinin AIHA?
Warm agglutinin AIHA = autoimmune acquired hemolytic anemia where IgGs develop against RBC surface antigens that agluttinate at body temp (hence warm) causing RBC destruction
Why are spherocytes seen in AIHA?
B/c the IgG doesn’t allow it to be fully phagocytosed => reduced surface to volume ratio = spherocyte which then gets destroyed in the spleen
So igG medicated AIHA (warm AIHA) produces spherocytes
List some common causes of warm AIHA
Infection- viral (HIV, mono)
Drugs
lymphoid malignancies (seen in CLL)
Other autoimmune disorders (SLE, AI)
First line tx for stages I-III anorectal CA `
Both chemo and radiation, surgery only used as salvage therapy b/c need to remove sphincter
Chemo + rad is superior to radiation alone
Different than rectal (higher up, can often spare the sphincter) where options are surgery alone (stage I) vs. surgery/chemo/radiation (all three for full thickness stage II and lymph nodes stage III)
Typical clinical features of paroxysmal noctural hemoglubinuria (PNH)
Otherwise unexplained intermittent hemolytic anemia that presents w/ fatigue, jaundice, and intermittent red urine
Fatigue and abdominal pain often worse at times of higher hemolysis (urine more red)
How to diagnose/test for PNH
PNH = CD55/59 deficiency on RBC surface => test by flow cytometry for CD 55/59
Absence of CD55/59 (which normal prevents complement activation) => overdestruction/hemolysis of RBCs prematurely
24 y/oM p/w fatigue and intermittent dark urine, labs w/ pancytopenia
Dx?
PNH = paroxysmal nocturnal hemoglobinuria- CD55/59 deficiency (RBC surface protein that prevents complement activation)
Intermittent hemolysis- often p/w fatigue, abdominal pain, intermittent hematuria
Target Hb for sickle cell pt undergoing minor surgery
Simple transfusion to 10 improves surgical outcomes in sickle cell patients
(not exchange transfusion). Only use exchange transfusion for acute stroke, acute chest, retinal artery occlusion
Well’s score vs PERC criteria
Well’s score gives a pre-test probability of PE to help you decide d-dimer vs. CT PE
vs. PERC criteria is used as a rule out tool for low risk patients, if all criteria are NO, then no further testing (including d-dimer) is required
‘PERC out’
Coags (lab) finding most common in lupus anticoagulant
(a) Prone to bleeding or clots?
Lupus anticoagulant = acquired antibody to phospholipids.
Prolonged PTT that doesn’t improve with mixing w/ regular plasma (b/c Abs present still)
(a) Despite prolonged PTT in vitro, is associated w/ clots (not bleeding) in vivo
What is factor V leiden?
Factor V leiden = mutated factor V that is immune to the anticoagulant properties of protein C
=> higher risk of VTE
Explain how antithrombin deficiency (either genetic or acquired) can lead to heparin resistance
Heparin binds to antithrombin to inactivate thrombin, Xa, and other clotting factors => without antithrombin pt will be refractory to heparin (aka won’t see PTT prolong despite high dose of gtt)
Pt w/ transfusion-dependent MDS develops worsening fatigue, Hb stable but ferritin 1850.
Next step in tx?
Once ferritin is over 1,000 an iron chelator is indicated
Deferasirox (PO)
Deforoxamine (IV)
F w/ newly diagnosed metastatic lung adenocarcinoma- next steps to determine tx?
Mutation testing for non-small cell lung cancers to determine first line tx.
Specifically for EGFR mutations, ROS1 mutations, and ALK translocation
EGFR mutation- first line Erlotinib
ALK/ROS- first line Crizotinib
Erlotinib vs. crizotinib for non-squamous cell lung cancer
Erlotinib- use for NSCLC with EGFR mutations
-also first line for pancreatic cancer
Crizotinib- oral med for ROS-1 and ALK mutation positive NSCLC
Pt on R-CHOP develops neutropenic fever, what to do during next chemo cycle to reduce risk of recurrence
G-CSF 2 days into next cycle, to prevent neutropenia which is at highest risk 5-15 days after cycle
(answer is not to dose reduce the chemo)
For AIHA w/ symptomatic Hb 5, but cross-match incompatible, best strategy for transfusion?
Just use same type but cross-match incompatible b/c RBCs won’t last as long but will hopefully last long enough for immunsuppressants (steroids) to kick in
- not plasma exchange b/c it doesn’t remove IgG
- don’t withhold transfusion until find a compatible one b/c may never find a compatible one and need to tx symptoms
Genetic condition that increases risk of warfarin-induced skin necrosis
Protein C/S deficiency
Transient hypercoagulable state during initial 50% reduction of protein C activity when warfarin is initiated => when baseline deficiency increases risk of transient hypercoagulability => arterial clots => retiform purpura seen in warfarin-induced necrosis
What level of fibrinogen is an indication for transfusion?
(a) Transfusion of what?
Fibrinogen under 100 w/ active bleeding- transfuse (a) cryoprecipitate to replace fibrinogen (has higher fibrinogen than FFP)
What factor level may be conceptually helpful in differentiating coagulopathy of liver disease and DIC
They can look the same- low fibrinogen (under 100 necessitating cryo transfusion)
Prolonged PT/PTTs
but factor VIII actually is ironically elevated in liver disease b/c required liver-synthesized factor to clear it
Differentiate electrophoresis patterns for alpha-thal trait and beta-thal minor
4 alpha globin genes (alpha-thal due to deletions), 2 beta globin genes (beta thal due to mutation or deletion) Alpha trait (a-,a- or aa,--): normal HbA, A2, and F (normal Hb electrophoresis)
while beta-thal minor (BB+ or B0) has low HbA (a2b2), more HbA2 (a2d2) b/c of defective beta-gene
CBC factor that can differentiate iron deficiency anemia from thalassemia
Both are microcytic anemias- but RDW (anisopoiliolocytosis) higher/abnormal in iron deficiency, while RDW is normal in thalassemias b/c all are uniformly small/dense/nucleated RBCs
Chronic management (supplement) for alpha and beta thalassemias
Folate supplementation, but no iron! and no transfusions (unless 7 or bleedgin). Avoid supplemental iron b/c side effects of overload
Components of a hemoglobin molecule
HbA vs. A2 vs. F
HbA = alpha2beta2 HbA2 = alpha2delta2 HbF = alpha2gamma2
4 alpha genes, 2 betagenes
What is hemoglobin H?
Hemoglobin H = tetramers of beta-globin
in pts w/ only one copy of alpha globin gene (while normal is 4)
Copies of alpha globin gene: 4- normal 3- asymptomatic carrier 2- alpha thal trait 1- hemoglobin H disease 0- intrauterine demise
Can you be asymptomatic from just one deleted copy of alpha-globin gene for hemoglobin?
Yes! aa, aa- will have normal HbA (alpha2beta2)
What does HELLP syndrome stand for?
Hemolysis, elevated liver enzymes, and low platelets
What is hemoglobin E disease?
Hemoglobin E disease = point mutation in beta-globin gene, makes its own hemoglobin (alpha2, beta-mutated globin gene)
migrates separately on electrophoresis
Differentiate hemoglobin electrophoresis for sickle cell disease vs. sick cell trait
Sickle cell disease: both beta globin genes are mutated => over 90% HbS, tiny percent HbF in adults potentially
Sickle cell trait: only one beta globin gene has mutation => about 30% HbS (variable), lots of HbA still
First line antiepileptic after benzos for status epilepticus
Status epilepticus: immediately give benzos (ativan if have IV access, versed if need IM)
Then first line antiepileptic is choice of: keppra (levetiracetam) or fosphenytoin/phenytoin (fosphenytoin is the prodrug)
Medication adjust for tx of vascular dementia
Vascular dementia- treat reversible risk factors like obesity, HTN, AFib etc
Then donepazil used off label (acetylcholinesterase inhibitor)
What malignancy is associated with NMDA encephalitis?
50% of females over 18 yoa w/ NMDA encephalitis found to have ovarian teratoma => get CT A/P and transvaginal ultrasound
How long after onset of headache for subarachnoid hemorrhage is lumbar puncture helpful for diagnosis?
RBCs rapidly lyse upon entering the CSF- present in ~2-4 hrs after SAH starts
Then 12+ hours after- highest yield for xanthrochromia (yellow CSF) b/c RBCS break down into bilirubin
Pathogenesis of Parkinsons disease
Progressive loss of dopamine-producing neurons in the substantia nigra
What is the pull back test for Parkinsons and what does it indicate?
Pull back test- pull back on patient’s shoulders. Considered positive if they fall back onto you or take 2 or more corrective steps.
Best predictive factor for falls in Parkinsons
First line treatment for Parkinsons
(a) Age under 65
(b) Age over 65
Parkinsons treatment- disease is caused by loss of dopamine producing neurons on substantia nigra => want to replace dopamine
(a) Under 65: use dopamine agonists = carbegoline, ropinirole
(b) Over 65 or for younger once agonists stop being effective- use dopamine precursor = levodopa
To reduce overall dose-exposure to levodopa and delay levodopa-related complications
Mechanism of carbidopa/levodopa
Levodopa = dopamine precursor
Carbidopa = peripheral decarboxylase inhibitor to inhibit peripheral levodopa breakdown into active form => more active form available to cross BBB into CNS
Key clinical feature of multiple system atrophy that differentiates it from Parkinsons
Multiple system atrophy is a Parkinsons “plus” diagnosis- most notable is dysautonoma
ALS- two most common clinical presentations
ALS = amyotrophic lateral sclerosis = progressive motor neuro disease
80% of pts initial presentation is unilateral limb weakness
20% have presenting bulbar features (dysphagia, dysarthria)
Pathogenesis of ALS
ALS = progressive demyelinating disease of motor neurons => have UMN and LMN symtpoms without sensory deficits
What does POEMS stand for?
POEMS = polyneuropathy, organomegaly (ex: splenomegaly), endocrinopathy, monoclonal gammopathy (ex: serum immunofixation + for alpha light chain monoclonal protein), skin manifestations (ex: telangiectasias, hyperpigmentation)
Clinical features of POEMS syndrome
Most prevalent is polyneuropathy (ex: impaired sensation, weakness) with monoclonal gammopathy
ex: middle aged M w/ a year of progressive weakness, found to have +Romberg test, lots of falls, sensation deficits. then serum immunofixation + for alpha light chain monoclonal protein
First line med for secondary prophylaxis of cluster headaches
Verapamil- CCB
Acute management of cluster headaches = subQ triptan and supplemental oxygen.
Prevent recurrence- quit smoking (big risk factor) and verapamil
Best acute medical management for cardioembolic stroke presenting 12 hours after symptom onset
ASA
ASA superior to heparin in acute management of cardioembolic stroke, proven to reduce recurrence of stroke within first 2 weeks
(12 hrs so out of tPA window)
UMN vs. LMN features
UMN (in the brain)- weakness, hyperreflexia, spasticity
LMN (brainstem and spinal cord)- weakness, areflexia, atrophy, fasiculations
Link btwn testosterone and Hb abnormality
Testosterone stimulates EPO production => secondary polycythemia
hold testosterone if Hct > 54%
Two indications for eculizumab (IgG against C5, terminal complement protein)
Eculizumab = mAb against terminal complement protein => inhibits end of complement cascade
- PNH where absence of CD55/59 inhibits inhibition (lol) of complement => premature RBC hemolysis
- Atypical HUS (atypical b/c not associated w/ diarrheal illness/ shiga toxin)- more congenital hyper-complement disease where it’s overactivated causing thrombotic microangiopathy
50% of Budd-Chiari syndromes are associated w/ what underlying disease process?
50% of Budd-Chiaris (hepatic vein thrombosis) and 25% portal vein thromboses are associated w/ underlying myelodyplastic syndrome
Ex: Budd-Chiari and JAK2+ polycythemia vera
DAT results for cold vs. warm AIHA
Direct antiglobulin tests classically (can have overlap):
Cold: C3 positive (RBCs coated in complement => get destroyed by Kuppfer cells in liver)
Warm: IgG positive (RBCs coated in IgG => incompletely hemolyze and cause schistocytes on peripheral smear, get taken out in spleen)
Infections highly associated with cold AIHA
Cold AIHA: EBV and mycoplasma
Tx for warm vs. cold AIHA
Cold AIHA (C3 binds to RBC surface causing phagocytosis by Kuppfer cells in liver): tx with warm infusions (avoiding cold temps) and Rituximab
vs.
Warm AIHA (IgG binds to Rh factor on RBC surface => removed in spleen and in circulation): intravascular hemolysis reduced by steroids and IVIG. Then splenetomy 70% effective
Location of phagocytosis of RBCs in warm vs. cold AIHA
Warm- IgG against Rh antigen on RBC surface
IgG incompetely phagocytosed => spherocytes
IgG coated gets phagocytosed in spleen (hence why splenectomy is helpful tx in warm AIHA)
Cold AIHA- C3 against RBC surface antigen: gets phagocytosed by Kuppfer cells (liver macrophages)
Underlying disease process associated with
(a) Warm AIHA
(b) Cold AIHA
(a) Warm AIHA: idiopathic, drugs, CLL, SLE
(b) Cold AIHA: mycoplasma, HBV
Spherocytes associated w/ warm or cold AIHA?
Spherocytes seen in warm AIHA b/c IgG coated get incompletely phagocytosed causing increased surface to volume raito
Mechanism of pseudothrombocytopenia when plt result low and see platelet clumping on peripheral smear
(a) Repeat in what tube for accurate results?
Pseudothrombocytopenia 2/2 antibodies against EDTA in purple tubes- see clumping on peripheral smear
(a) Repeat in heparinzed tube and should be normal
Differentiating factor btwn HUS and atypical HUS
HUS- shiga toxin binds directly to epithelium (intravascular RBC destruction) and renal tubulal/mesangial cells (AKI), diarrhea
Atypical HUS- no preceding diarrheal illness, congenital predisposition to over-complement activation
-Eculizumab (anti-CD5 mAb) helpful in tx
Why is it clinically relevant to distinguish atypical HUS from TTP?
B/c atypical HUS will respond to eculizumab (anti-CD5 terminal complement protein mAb), while TTP wont
Coag study results of acquired hemophilia A
Hemophilia A = deficiency in factor VIII (X-linked recessive)
Acquired hemophilia A = Ab production against factor VIII
Expect prolonged PTT (extrinsic pathway) that doesn’t completely resolve w/ mixing study (b/c antibodies present so replacing factor doesn’t fully fix)
Which lung CA is
(a) More typically peripherally located
(b) Associated w/ smokers
Lung cancer
(a) Peripherally- non-small cell. Expect small cell centrally
(b) Small cell is solely associated w/ smoking
When to use chemo/radiation combo vs. just chemo alone for small cell lung CA
Small cell lung CA: superior outcomes if use combined chemo/radiation for localized disease
vs. extensive disease- chemo alone w/o radiation
Why is tamoxifen not first line for post-menopausal breast cancer
Tamoxifen (SERM) associated w/ higher risk of endometrial cancer in F over 55, also w/ stroke and VTE
Hence why aromatase inhibitors are preferred
Why is anastrazole not first line for pre-menopausal breast cancer
Aromatase inhibitors (anastrazole, letrozole) inhibits adrenal androgen conversion, but doesn’t inhibit estrogen production in ovaries => ineffective in premenopause to reduce estrogen androgen exposure
In order to use aromatase inhibitor effectively in premenopausal, need to use leuprolide (GnRH agonist) for ovarian suppression
Optimal duration of hormone therapy for ER/PR+ breast cancers
10 years: often start w/ 5 and then reassess if any side effects, but for both SERM and aromatase inhibitor 10 showed reduction in cancer over 5
Difference in tx for partial vs. full thickness rectal adenocarcinoma
Rectal (not anal- in anal want to avoid surgery if possible to spare the sphincter)
Partial thickness- first line is surgery alone
full thickness w/ or w/o lymph nodes- all 3 chemo/radiation/surgery
S/p stage II lung adeno tumor resection w/ clear margins- any further therapy recommended?
Yes- cisplatin (not carboplatin) based chemo regimens improve survival when used adjuvantly in stage II and III lung adeno
No increased benefit w/ radiation given negative margins
32 y/oF w/ high-risk hormone-receptor positive breast cancer- best hormone therapy
a
Two mechanisms by which renal cell carcinoma can cause hypercalcemia in 15% of advanced RCC pts
aa
2 malignancies associated w/ exogenous secretion of EPO (paraneoplastic)
HCC (hepatocellular carcinoma)
RCC (renal cell carcinoma)
Indications for olaparib (PARP inhibitor)
Metastatic breast CA with positive BRCA 1/2 mutation
Metastatic ovarian CA w/ positive BRCA 1/2 mutation refractory to multiple lines of chemo
38 y/oF premenopausal with +BRCA2 already s/p b/l ppx mastectomy- best way to reduce risk of ovarian cancer?
(a) how different if +BRCA1?
FOr BRCA2 (lower risk of ovarian ca at earlier age): recommend ppx b/l sapingooophorectomy (BSO) at age 40-45
(a) For BRCA1 recommend BSO at 35-40 since risk is higher at younger age
Peripheral smear findings characteristic of CLL
CLL- characteristic smudge cells- as a result of smearing the blood on the glass slide, the very fragile WBCs ‘smudge’ given their lack of cytoplasmic membrane and nuclear structure
Smudge cells = basket cells
After TURBT what is the management of early stage, noninvasive high grade bladder cancer?
Noninvasive means you can TURBT it out- then if high grade or recurrent low grade you follow it by intravesicular chemo (BCG or mitomycin directly into the bladder)
Turbt, then intravesicular chemo x6 rounds, then q3-6 months cystoscopy given high rate of recurrence
Which colon cancers benefit from post-surgical adjuvant chemo?
All stage III colon CA (lymph nodes involved) should get post-surgical FOLFOX or CAPOX (chemo)
Stage II w/ high risk features should be considered for post-adjuvant chemo, but stage III definitely increases rate of cure
Recommended post-treatment surveillance for colon cancer
- Serum CEA q6 months
- Annual CT C/A/P x5 years (want to find mets early b/c surgical metastectomy can still result in cure)
- Colonoscopy at 1 year out, then in 3 years, then q5 years
Management of testicular mass found on ultrasound- steps to take before removal
Testicular mass- cancer is dx of exclusion (biopsy contraindicated given risk of seeding tract- scrotum or inguinal nodes)
First- measure tumor markers (beta-hCG and AFP) b/c need to track post-op markers (if markers don’t fall appropriately, correlates w/ recurrence)
Then can remove surgically (w/o biopsy) for both diagnosis and treatment
Prognostic factors for testicular cancer
-CXR, CT A/P for distant sites/lymphadenopathy
-response of serum markers after surgery (appropriate decline in beta-hCG and AFP)
-
Which lung cancer pts should receive prophylactic CNS radiation?
Pts w/ limited and extensive-stage SCLC (small cell, the 10% smoking one that is neuroendocrine) who respond to chemotherapy
-only if responsive to chemo, then ppx carnial irradiation improves survival
Which NSCLC
(a) chemo alone
(b) chemo + radiation
(c) surgery alone
NSCLC If early (stage I/II) try surgery, then
(a) Chemo alone- not for any NSCLC.
For metastatic SCLC (10% of lung cancers are small cell neuroendorine tumor)- if (and only if) good functional status can do chemo alone
(b) Combo chemo/radiation for non-surgically locally advanced NSCLC (superior to sequential tx)
(c) surgery alone (no adjuvant radiation) if early (stage I/II) with negative surgical margins
Which lung cancer is treated with
(a) Erlotinib
(b) Crizotinib
Tx of NSCLC
(a) Erlotinib for metastatic NSCLC with +EGRF mutation
(b) Crizotinib for metastatic NSCLC with translocations of ALK or ROS1
Which lung cancer is treated with
(c) Pembrolizumab
(d) Carboplatin/paclitaxel + bevacizumab
(c) Pembrolizumab- first line for NSCLC (both squamous and nonsquamous) with PD-L1 expression > 50%.
(d) Metastatic NSCLC with good functional status (chemo not proven to help if poor functional status): chemo doublet + bevacizumab (mAb against VEG-F)
Which NSCLC gets tx with
(a) Surgery alone
(b) Surgery + chemo
(c) Surgery + radiation
(d) Surgery + chemo/radiation
(e) Radiation alone
NSCLC treatment
(a) Surgery alone if early (I/II) disease with amenable anatomy and negative margins
(b) Stage II/III- surgery if anatomy allows then adjuvant chemo improves survival
(c) Surgery with radiation for early (I/II) with positive margins in surgery
(d) All 3- not indicated for any, do chemo/rads together if not surgically resectable for stage III
(e) Radiation alone for early (I/II) who are not surgical candidates
When to add docetaxel to androgen deprivation therapy in prostate cancer
Add chemo with docetaxel to metastatic prostate cancer that is responsive to initial androgen therapy treatment
ex: 65 y/oM w/ met prostate CA initially tx with bicalutamide (androgen receptor blocker) and leuprolide (GnRH agonist) x4 weeks then leuprolide alone x2 months- w/ excellent symptomatic bone pain relief and PSA from 122 to 20.
- Continue leuprolide and add docetaxel
Differentiate symptoms of etiologies of vaginosis
(a) Gardenerella
(b) Trichomoniasis
(c) Candidiasis
Vaginosis
(a) Gardenerella = BV- thin gray discharge w/ fishy odor
(b) Trichomoniasis-discolored thicker discharge
(c) Candida- chunky white discharge
Which etiology of vaginosis is associated with
(a) fishy discharge
(b) +whiff test
(c) pseudohyphae on wet mount
(d) strawberry cervix on exam
Vaginosis
(a) Fishy discharge = BV (gardenerella)
(b) +whiff test = BV
(c) pseudohyphae = candidiasis
(d) strawberry cervix = punctate hemorrhages on cervix = trichomoniasis
Which etiology of vaginosis is associated with
(a) clue cells
(b) +NAAT
Vaginosis
(a) Clue epithelial cells = BV (bacterial vaginosis) = gardenerella
(b) +NAAT = trichomoniasis
Treatment by etiology for vaginosis
(a) gardnerella
(b) candidiasis
(c) trichomoniasis
Vaginosis treatment
(a) Gardeneralla = BV- flagyl or clindamycin oral orvaginal gel
(b) candidiasis- ‘azole’ so fluconazole single oral dose or miconazole vaginal cream
(c) trichomoniasis- flagyl
Outcome in RCT used to reduce lead time bias
Reduce lead time bias (increased measured survival, but not overall survival b/c detecting something sooner) by using disease specific mortality rather than survival time
Differentiate lead time bias and length time bias
Both types of selection bias
-Lead time bias speaks to the difference in time btwn when an early dx is made w/ screening and when the dx would be made w/o screening
(speaks to effectiveness of a test)
-While length time bias is when screening overestimates survival by finding early/asymptomatic/indolent cases
Weber vs. Rinne test for hearing loss
Weber test for sensorineural hearing loss
Hold tuning fork in middle of head, sound will lateralize to unaffected ear
ex: Sensorineural hearing loss c/f R ear, then Weber test (tuning fork louder) lateralize to L
Rinne test for conductive hearing loss- hold at mastoid process then bring forward, should hear still b/c air conduction is typically faster than bone (positive rinne test when can still hear it)
C/f conductive hearing loss in R ear- when tuning fork moved off mastoid process don’t hear it b/c bone conduction is greater than air conduction
Describe Weber/Rinne test results seen in sensorineural hearing loss of L ear
Sensorineural hearing loss of L ear
- Weber test (hold tuning fork in middle above head) will be heard louder in unaffected ear (R. ear)
- Normal/positive Rinne test (saying no conductive hearing loss) of both ears. So when hold tuning fork to mastoid process then move in front of ear will still hear both sides
Describe Weber/Rinne test results seen in conductive hearing loss of R ear
Conductive hearing loss of R ear-
-Weber test inconclusive (test for sensorineural hearing loss): tuning fork in middle of head, hear equally on both sides
-Negative Rinne test of R ear: hold tuning fork to mastoid process on R ear, will NOT still hear sound when move in front of ear (b/c air conduction is less than bone conduction)
Morton neuroma
(a) Pathophys
(b) Clinical features
Morton neuroma
(a) compression of interdigital nerve of the toes from overpronation (high heels) or tight shoes
(b) pain btwn 3rd and 4th metatarsal head, sensation of walking on a pebble
What is superior to standard gauze for management of pressure wounds?
Hydrocolloid or foam dressing superior to standard gauze for pressure wound
-has adhesive polymer and absorbant agent
Where do we stand of self breast exams?
Nope- nada, no benefit and actually lead to more biopsies
So don’t teach them anymore, pt age 40 can be shared decision making for mammo vs. no mammo, but NOT self breast exam
Duration of prophylactic anticoagulation after knee arthroplasty
35 days!! Long time, lovenox for 35 days after high VTE risk ortho procedures (knee/hip arthroplasty and hip fracture) if no prior elevated risk of bleeding
10-14 days insufficient, VTE risk remains elevated past that
In addition to gabapentinoids, what other class of drugs is first line for tx of diabetic neuropathy
SNRIs also FDA approved as first line for diabetic neuropathy
= duloxetine, venlafaxine
When to use trimethorprin-polymyxin B vs. levofloxacin opthalmic drops for tx of bacterial conjunctivitis
Diabetic with bacterial conjunctivitis- trimethoprin-polymyxin B,
Levaquin is expensive andnot good resistance profile, so only use when high risk for pseudomonas (aka contact wearers)
Differentiate absolute from relative risk reduction
Ex: Drug A reduces exacerbation from 50 to 25%, while drug B reduces exacerbation from 5 to 2.5%
Both have same relative risk reduction (50%), while drug A has absolute risk reduction of 25% while drug B has absolute risk reduction of 2.5%
68 y/oM w/ LE/nitrites on UA and dysuria/boggy prostate 48 hrs after prostate biopsy- urine Cx growing GNRs.
First line tx?
Bactrim x6 weeks
first line treatment for acute bacterial prostatitis- bactrim, most likely culprit E. coli
Imaging for breast mass in pt under 40 years old
30 is the cutoff
Breast mass over 30- mammogram
Breast mass under 30- ultrasound b/c mammogram low sensitivity due to high density of breast tissue
Which BIRADS score for mammography necessitate biopsy?
Bi-RADS 4 (suspicious) or 5 (highly suspicious)
vs. 3 (likely benign)- no biopsy and 6-proven/known malignancy
29 y/oF s/p HPV vaccine, last pap smear 3 years ago- what type of cervical cancer screening is indicated?
For 21-30 (under 21- no benefit in screening this early, under 30- high incidence of transient HPV): cervical cytology alone (not cytology plus HPV testing)
For over 30- can add high risk HPV testing to cervical cytology to spread out to 5 years instead of 3 yrs
Safe during pregnancy
(a) Name 3 BP meds
(b) Oral diabetes med
Safe for pregnancy
(a) Labetalol, nifedipine, methyldopa
(b) Metformin- safe during pregnancy
Clinical features of complex regional pain syndrome
(a) Pain relief with what?
Complex regional pain syndrome- temperature fluctuations (skin feels hot then cold), parethesias, local edema (swollemn fingers)
(a) Pain relief with regional nerve block
Pt with high pre-test probability of PE and intermediate V/Q scan- how to interpret?
Intermediate V/Q scan is essentially non-diagnostic (doesn’t support diagnosis)
So if high pre-test probability and intermediate V/Q, consider further testing (ex: LE dopplers) if have high risk of bleeding that would increase risk of empiric AC
Clinical factor differentiating bulimia from binge-eating disorder
Binge-eating disorder is without any compensatory mechanisms (ex: excessive exercise, doesn’t just need to be purging)
If any compensatory measures considered bulimia
Which inhaler is associated w/ increase in mortality and asthma exacerbation?
LABA monotherapy (ex: salmeterol alone) is associated w/ increased mortality and asthma exacerbations
hence why combined with ICS
Illness script for acute rheumatic fever
Acute rheumatic fever- symptoms 2-4 weeks after strep throat (GAS), JONES criteria
-migratory Joint pains
-Cardiac abnormality (prolonged PR, murmur)
-Nodules (subcutaneous palpable)
-Erythema marginatum (rash)
-Sydenham chorea
Minor criteria- elevated serum markers (ESR/CRP), fever
When C-section is required to prevent vertical transmission
If viral load is above 1,000 copies- C-section (not vaginal delivery) and immediate ART for infant
Under 1,000 copies than vaginal delivery is ok
62M w/ PMH of HIV on ART, Tb s/p DOT tx now presents with massive hemoptysis. CT chest with bilateral upper lobe cavitation
Most likely dx
Massive hemoptysis w/ h/o of Tb- most likely aspergilloma (even though bilateral) due to aspergillus colonization of pre-existing cavities
Feared complication of acute rheumatic fever
Mitral valve regurg or stenosis
19F from Thailand w/ 1 week of migratory large joint pain. T 100.4F, holosystolic murmur, palpable subQ nodules on exam, ESR 100, BCx negative
(a) Dx
(b) Best diagnostic exam
(a) JONES criteria for acute rheumatic fever
- migratory joint pains
- <3 cardiac abnormalities
- nodules subcutaneously
- erythema marginatum (ringed rash)
- sydenhams chorrhea
(b) Diagnose with antistreptolysin O (ASO) titers
