Bio

Dr. Farhana Rob is a board-certified, fellowship-trained family medicine doctor with Stanford Health Care. She is also a clinical assistant professor in the Department of Medicine, Primary Care and Population Health at Stanford University School of Medicine.

Dr. Rob provides personalized and compassionate primary care for people ranging from newborns to older adults. She specializes in women’s health and maternity care, managing conditions such as heavy menstrual bleeding, pregnancy-induced hypertension, and gestational diabetes. She also has expertise in birth control, discussing and providing options particularly for adolescents and postpartum mothers. Dr. Rob also specializes in minor injuries and musculoskeletal problems, providing therapies such as laceration repair, tendon and joint injections, and trigger point injections.

Dr. Rob emphasizes preventive care and early diagnosis through routine and diagnostic screenings. She strives to empower them to become active participants in their health care. She is open to discussing alternative and natural treatments to support holistic healing. Dr. Rob also enjoys teaching and has mentored medical students and residents throughout her career.

Dr. Rob has published research on heart failure in peer-reviewed journals including the Journal of Cardiovascular Electrophysiology. She shared her findings on using ultrasound to estimate birthweight at the American Academy of Family Physicians Family-Centered Pregnancy Care Conference. She has also written about heavy menstrual bleeding for The 5-Minute Clinical Consult, a physician guidebook that focuses on evidence-based medicine.

Dr. Rob is a member of the American Academy of Family Physicians, the American Board of Family Medicine, and the American Medical Association.

Clinical Focus

  • Family Medicine

Academic Appointments

Honors & Awards

  • Resident Teacher Award, Society of Teachers of Family Medicine

Boards, Advisory Committees, Professional Organizations

  • Member, American Medical Association (2008 - Present)
  • Member, American Board of Family Medicine (2012 - Present)
  • Member, American Academy of Family Physicians (2012 - Present)

Professional Education

  • Board Certification: American Board of Family Medicine, Family Medicine (2015)
  • Residency: Memorial Family Medicine Residency (2015) TX
  • Medical Education: University of Northern Texas College of Osteopathic Medicine (2012) TX

Contact

  • Academic
    farhanar@stanford.edu
    University - Academic staff Department: Med/Primary Care and Population Health Position: Clinical Assistant Professor
  • Clinical (Primary)  Stanford LifeConnection at Cisco 3571 N 1st St San Jose, CA 95134 (408) 688-9608 (fax)

Additional Clinical Info

Additional Info

  • Mail Code: 5702

All Publications

  • Menorrhagia 5-Minute Clinical Consult Rob, F., Locus , P. 2016
  • Diminished cardiac fibrosis in heart failure is associated with altered ventricular arrhythmia phenotype. Journal of cardiovascular electrophysiology Massare, J., Berry, J. M., Luo, X., Rob, F., Johnstone, J. L., Shelton, J. M., Bassel-Duby, R., Hill, J. A., Naseem, R. H. 2010; 21 (9): 1031-7

    Abstract

    We sought to define the role of interstitial fibrosis in the proarrhythmic phenotype of failing ventricular myocardium.Multiple cellular events that occur during pathological remodeling of the failing ventricle are implicated in the genesis of ventricular tachycardia (VT), including interstitial fibrosis. Recent studies suggest that ventricular fibrosis is reversible, and current anti-remodeling therapies attenuate ventricular fibrosis. However, the role of interstitial fibrosis in the proarrhythmic phenotype of failing ventricular myocardium is currently not well defined.Class II histone deacetylases (HDACs) have been implicated in promoting collagen biosynthesis. As these enzymes are inhibited by protein kinase D1 (PKD1), we studied mice with cardiomyocyte-specific transgenic over-expression of a constitutively active mutant of PKD1 (caPKD). caPKD mice were compared with animals in which cardiomyopathy was induced by severe thoracic aortic banding (sTAB). Hearts were analyzed by echocardiographic and electrocardiographic means. Interstitial fibrosis was assessed by histology and quantified biochemically. Ventricular arrhythmias were induced by closed-chest, intracardiac pacing.Similar degrees of hypertrophic growth, systolic dysfunction and mortality were observed in the two models. In sTAB mice, robust ventricular fibrosis was readily detected, but myocardial collagen content was significantly reduced in caPKD mice. As expected, VT was readily inducible by programmed stimulation in sTAB mice and VT was less inducible in caPKD mice. Surprisingly, episodes of VT manifested longer cycle lengths and longer duration in caPKD mice.Attenuated ventricular fibrosis is associated with reduced VT inducibility, increased VT duration, and significantly longer arrhythmia cycle length.

    View details for DOI 10.1111/j.1540-8167.2010.01736.x

    View details for PubMedID 20233273

    View details for PubMedCentralID PMC3703442

  • Remodeling of outward K+ currents in pressure-overload heart failure. Journal of cardiovascular electrophysiology Wang, Y., Cheng, J., Chen, G., Rob, F., Naseem, R. H., Nguyen, L., Johnstone, J. L., Hill, J. A. 2007; 18 (8): 869-75

    Abstract

    Outward K+ currents are critical determinants of action potential repolarization and the site of action of a number of electrophysiologically active drugs. Further, expression and processing of the channels underlying these currents is altered in heart disease. Here, we investigated the native transmural gradient of outward K+ currents in murine left ventricle (LV) and delineated disease-related remodeling of these currents in heart failure (HF).Pressure-overload heart failure was induced in mice by thoracic aortic constriction. Outward K+ currents were recorded using the whole-cell patch clamp technique in acutely dissociated ventricular myocytes.Unambiguous gradients of outward K+ current density and Kv4.2 protein abundance were observed across the wall of the LV, with significantly larger current density and protein levels in subepicardial (SEP) myocytes, compared with subendocardial (SEN) myocytes. Voltage dependences of current activation and inactivation were similar in SEP and SEN myocytes. In failing LV, however, outward K+ current density was significantly decreased in SEP but not in SEN cells leading to elimination of the native transmural gradient. In failing LV, the voltage dependences of K+ current activation and inactivation were not altered. However, current inactivation (decay) was significantly accelerated and recovery from inactivation was significantly slowed. Consistent with this, Western blot analysis revealed a decrease in KChIP2 protein abundance in failing LV.This is the first report of HF-related remodeling of outward K+ currents in murine LV. Similar to humans, disease-related remodeling occurs differentially across the murine ventricular wall, leading to loss of the native gradient of repolarization. Together with slowed recovery from inactivation, these alterations likely promote abnormal impulse conduction, a major proarrhythmic mechanism.

    View details for DOI 10.1111/j.1540-8167.2007.00864.x

    View details for PubMedID 17537202