Clinical Microbiology Made Ridiculously Simple

In addition to being a good USMLE review book, Clinical Microbiology could replace the syllabus, especially for bacteria. Its easy to read and has enough supporting details to give a clear understanding of the pathogens. The virus, fungi, and parasite sections are very basic, and they hit the main topics of each pathogen. The medicine chapters are also very basic. Each chapter has a good summary table of pathogens or medicines. A pathology textbook would be good for associated color pictures and diagrams.

MedicalMnemonics.com | Browse | Browse by Category

MedicalMnemonics.com | Browse | Browse by Category

Contains contributions from around the world. Also available for download onto a PDA.

BRS Physiology

Organized by organ systems, this 322 page book can be finished in four days with relative ease. It does not require any other supplementary books. Although the questions at the end of each chapter are good review questions of concepts, they seem to be a lot easier than board type questions. Related pathology and pharmacology are integrated well into the text. It's a good book to have during first year while taking physiology, and it would be a good idea to review of the physiology of an organ system before learning about its pathology. Important concepts can be found on pages 92-93, 142, 196, 200, 252, 256, 265, 270, and 283.

BRS Pathology

At 450 pages, this book can be finished in 5 days, spending about 8 hours a day, and finishing 90 pages per day. It is organized by organ systems. This book lacks color pictures, so its a good idea to use this book with a pathology textbook like Rubin's Pathology Fourth Edition. In addition to good microscopic, gross, and radiologic pictures, Rubin's has diagrams explaining diseases. Unlike a textbook, the main distinguishing factors of a disease are emphasized. The details are usually left out since they could cause confusion when covering several diseases in one organ system. This BRS book is purely a review book, and it would be difficult to understand unless you learned about the diseases while in class. This book is good to have while you take the course. In the second edition, important tables can be found on pages 6, 24, 62, 66, 75, 284, 320, and 384. The comprehensive examination at the end of book is a good, challenging review of the entire book.

USF USMLE 1

Contains several documents for Step 1 studying with hundreds of flashcards in Word documents for anatomy and biochemistry. Smaller documents on specific topics like metabolic diseases are available.
http://www.med.usf.edu/2003/usmlesmack.html

The New York Times > Technology > Circuits > State of the Art: A New Spin on a Palmtop (or Inside It)

The New York Times > Technology > Circuits > State of the Art: A New Spin on a Palmtop (or Inside It)

Great PDA, have to wait till the problems are worked out before it could be really useful in the field.

http://www.palmone.com/us/products/mobilemanagers/lifedrive/

High Yield Neuroanatomy

133 pages may seem like a lot to get through in one day for board review. The preface does a good job of highlighting important topics in each chapter for the USMLE Step 1. The clinical correlations at the end of each chapter are excellent. Pick and choose which chapters to review since a chapter like autonomics can be found in other review books. It's a good book to have while taking the course.

BRS Histology

Although this large book is too much for board review, it would probably help while taking the class, even in undergraduate. The first five chapters are sufficient for USMLE Step 1 Review, and it contains detailed review of the basic concepts of histology. The chapter on blood may overlap with immunology review.

Gosling - Atlas of Human Anatomy

It has good gross pictures of anatomy with simple drawings accompanying them. The captions are concise.

Step 1 Released Questions

http://www.usmle.org/Orientation/Step1MCQ.zip

This is the software link for the 150 questions released by USMLE.org. It can be taken in a test format or untimed. Kaplan provides detailed explanations for this series of questions.

High Yield Anatomy

This USMLE step 1 book is a lot more dense than the title implies. With over 180 pages, it does provide a good basis for anatomy based pathology. The MRI pictures are great. Key chapters would be heart, lung, upper extremity, spine, and lower extremity. Anatomy of the upper limb is extremely high yield review. A good understanding of the nerves and muscle enervation of the hands and arms will help answering several questions. An other priority is to understand fractures and their related deficiencies.

Student Loan Consolidation

Recently, loan companies have decided to allow students to consolidate their student loans while they are still attending college. Currently, interest rates are at a historic low around 2.77% for Stafford loans. The interest rate could be lower for people who pay their loans on time. By June 30, 2005, the rates will rise to 4%, and they will probably not decrease after this time. Students are eligible to consolidate loans accrued up to this time; loans for next year are not eligible. Although a student could save up to fifty percent on their loan repayments, the payment period could be extended from 10 years to 30 years. Currently, THE, Wells Fargo, and several other lending companies are offering consolidation.

Metabolic Bone Diseases

Condition	Thin Trabeculae	Numerous Osteoclasts	Excessive Osteoid	Fibroblast/ Collagen
Osteoporosis	X
Osteomalacia			X
Primary Hyperparathyroidism		X		X
Renal Osteodystrophy		X	X	X

Source: Rubin's Pathology 4th Edition

Dermatopathology II

Disease	Pathogenesis	Pathology	Clinical Features/ Treatment
Erythema nodosum	trigger: drugs, microorganisms, systemic diseases drugs: sulfonamides	fibrous septa of subcutaneous tissue - neutrophil inflammation, extravasation of erythrocytes chronic - septa widened, giant cell macrophages, altered collagen	dome-shaped, tender, nodules on extensor surface of legs 3rd decade, 3xF:M
Erythema induratum	Mycobacterium tuberculosis	initially lobular panniculitis, vasculitis - ischemic necrosis of fat lobules dense, chronic inflammatory infiltrate in fat lobules extensive ischemic necrosis - ulceration of overlying epidermis	chronic, recurrent, subcutaneous plaques or nodules on legs, women T - systemic steroids
Scleroderma		pathcy lymphocytic infiltrate, loss of peri-eccrine fat, plugging of sweat glands, obliteration of hair follicles, subcutaneous fat turns into collagen	fibrosis and tightening of skin mask face 4xF:M, 30-50y non-pitting edema of hands or fingers
Granulomatous dermatitis	localized collection of epitheliod macrophages around insoluble antigen
Allergic Contact dermatitis	sensitization - haptens: oleoresins, Langerhans Cells - CD4+ T cells Elicitation - activated T cells, IFN-gamma - Fas ligand on keritanocytes - apoptosis	spongiotic dermatitis - edema in epidermis spongiotic vasculitis - vacuoles filled with lymphocytes and macrophages	immune rxn to poison ivy, poison oak, poison sumac

Source: Rubin's Pathology 4th Edition

Dermatopathology I

Disease	Pathogenesis	Pathology	Clinical Features/ Treatment
Pemphigus Vulgaris	antibodies to keratinocytes, autoimmune IgG to desmoglein 3	seperation of stratum spinosum and outer epidermal layers from basal layer blister - moderate lymphocytes, macrophages, eosinophils, neutrophils	blistering skin large, scalp, mucous membranes, periumbilical and intertriginous areas
Diseases of the Basement Membrane Zone
Epidermolysis Bullosa	hereditary	splitting of epidermis at or near basement membrane	blisters
Epidermolytic EB	disruption of basal keratinocytes	vacuoles filled with abnormal keratin 5 and 14	blisters from minor trauma - no scarring
Junctional EB	AR benign - mutation in gene encoding for type XVII collagen severe- laminin and integrin genes	lamina lucida blister roof - intact epidermis base - lamina densa	blisters
Dermolytic EB	defect in anchoring fibrils, defective collagen type VII	roof - normal epidermis, lamina lucida, lamina densa floor - outer part of papillary dermis	atrophic scarring
Bullous Pemphigoid	complement fixing IgG antibodies to BPAG1 and BPAG2	subepidermal blisters roof - intact epidermis base - lamina densa cytology - numerous eosinophils, arranged along BMZ seperation at lamina lucida	large, tense blisters erythematous base +/- T - corticosteroids

Source: Rubin's Pathology 4th Edition

Psoriasis

Disease	Psoriasis
Pathogenesis	Genetic factors - HLA-B13,HLA-B17, HLA-Bw57, HLA-Cw6 increased Environmental factors - physical injury, infection, drugs Abnormal cellular proliferation of keratinocytes microcirculatory changes - "bridged" fenestrations, neutrophils at tipsof dermal papillae, dec cAMP Immunologic factors - T cell infiltration
Pathology	thickened epidermis -hyperkeratosis + parakeratosis uniformally elongated rete ridges and dermal papillae dilated and tortuous capillaries of papillae epidermal hyperplasia Munro microabscesses - dense collection of neutrophils
ClinicalFeatures/Treatment	large, erythematous, scalyplaques dorsal extensor cutaneous surfaces 7% - seronegative arthritis, mild neutrophilic pustules T - coal tar or wood tar, anthralin, corticosteroids, methotrexate,vitamin A, vitamin D

Source: Rubin's Pathology 4th Edition

Ichthyosis

Disease	Pathogenesis	Pathology	ClinicalFeatures/Treatment
Ichthyoses	increasesed cohesiveness,abnormal keratinization, increased basal cell proliferation	abnormally thickened stratumcornerum, hyperkeratosis, thin nucleated epidermis	coarse, fish-like scales
Ichthyosis Vulgaris	Autosomal Dominant - reduced or absent keratohyaline granules in epidermis attenuated stratum granulosum - reduced profilaggrin	loose stratum corneum,basket-weave appearance	most common, begins earlychildhood, small white scales on extensor surfaces of extremities andon trunk and face, lifelong disease abnormalities in lipid metabolism from drugs or other diseases
X- linked ichthyosis	deficiency of sterioid sulfatase steroid sulfatase degrades cholesterol sulfate	persistent cohesion of stratumcorneum
Lamellar ichthyosis	autosomal recessive - disorderof cornification, defect in lamellar body secretion	increased cohesivenss of stratumcorneum, numerous keratinosomes, abnormally large amount ofintercellular substance	severe and generalized ichthyosis
Epidermolytic hyperkeratosis	autosomal dominant, mutation inkeratin genes in suprabasal epidermis	faulty assembly of keratintonofilaments, impaired insertion into desmosomes, prevents normaldevelopment of cytoskeleton -> epidermal lysis and vesicles	generalized erythroderma,blistering, ichthyosiform skin

Source: Rubin's Pathology 4th Edition

Skin Layers and Diseases

Layer of Skin	Associated Disease
Basement Membrane	Bullous pemphigoid - antibodies to BPAG1 and BPAG2 - Type XVII colagen
Papillary dermis	psoriasis, lichen planus
Recticular dermis	scleroderma, erythema nodosum

Source: Rubin's Pathology 4th Edition

Skin Cell Types

Cell Type	Function	Structures
Melanocytes	color of the skin	melanosome - melaninsynthesis
Langerhan cells	antigen presenting cells	Birbeck granules, MHC I, MHC II,receptors for Fc IgG and Fc IgE
Merkel Cell	neurosecretory, tactilemechanoreceptor	form desmosomes with keratinocytes, basal aspect apposed to a small nerve plate
Keratinocytes	produce keratin filaments	Keratohyaline granules, Odlandbodies - keratinosomes

Source: Rubin's Pathology 4th Edition

Gynecological Pathology Endometrium

Condition	Cause	Pathology/Histology	Clinical Features	Other Features
Proliferative Enodmetrium		· Straight glands · Narrow lumens · Pallisading nuclei · Ovoid nuclei · Mitoses
Early Secretory Endometrium	First manifestation of effect of ovulation on endometrium	· Glands remain straight · Lumens remain narrow · Subnuclear vacuoles appear		24-36 hours after ovulation
Mid Secretory Endometrium		· Glands become coiled · Vacuoles no longer present in glands · Secretory product appears in lumen		Postovulatory days 5-9
Late Secretory Endometrium		· Intralumenal secretions are spent · Stromal predecidua appears · First predecidua around spiral arteries · Later predecidua beneath surface		Postovulatory days 10-14
Menstrual Endometrium		· Stromal collapse · Fribrin thrombi and blood · Glands are broken apart · Glands have no secretions
Hyper-secretory Endometrium of Pregnancy		· Arias-Stella reaction · large, hyperchromatic nuclei · prominent cytoplasmic vacuolization
Atrophic endometrium		· short glands · glandular cells – flat, without significant mitotic activity
Dysfunctional Uterine Bleeding		· anovulatory bleeding · luteal phase defect
Unopposed Estrogen		· proliferative glands · stromal breakdown · fibrin thrombi · wreathing of stroma by glandular cells
Contraceptives	Combined oral agents	· mix of proliferative and secretory changes · long use · atrophic glands · stromal predecidual pattern dominates
	Depoprovera	· unopposed progesterone
Tamoxifen		· inc risk of carcinoma · inc incidence of polyps · large, mucinous metaplasia, fibrotic
Endometrial Hyperplasia	· unopposed estrogen stimulation – exogenous, endogenous · no progestational stimulation	· simple or complex architecture · typical or atypical nuclei	Vaginal bleeding, 60s Risk factors – obesity, diabetes, nulliparity, early menarche, late menopause	Complex atypical hyperplasia progresses to carcinoma – 1/3 T – hysterectomy, hormonal manipulation
Endometrial Carcinoma Type 1 Endometrioid	· PTEN gene mutation à cell growth and apoptosis	· squamous or mucinous		Grade determines prognosis T – hysterectomy, good survival Low grade – hormonal
Endometrial Carcinoma Type 2 Unfavorable Histology	· serous-p53 mutations	· clear cell		Early spread outside uterus long term survival uncertain

Gynecological Pathology I

Condition	Cause	Pathology/Histology	Surface Features	Other Features
Vulvar Malgnancies
Vulvar Intraepithelial Neoplasia	HPV	Varying degrees of loss of maturation of squamous cells	Single or multiple plaques or papules	Co-exists with cervical dysplasia
Invasive squamous cell carcinoma		Keratinizing squamous cell histology	Ulcerated exophytic lesions	Most common vulvar malignancy
Verrucous carcinoma		Well differentiated, locally invasive	Giant condyloma	Unlikely to metastasize, subset of invasive squamous cell carcinoma
Extramammary Paget’s Disease		Intraepithelial adenocarcinoma in the vulva	Red, moist plaque
Malignant Melanoma		Same as skin melanoma		Second most common malignant tumor in vulva
Benign Disorders of Vulva
Lichen Sclerosis		Atrophic epidermis, hyalinized epidermis	White plaques
Squamous hyperplasia		Thickened epidermis	White plaques
Hidradenoma	Benign tumor	Sweat gland origin – apocrine
Syringoma	Benign tumor	Sweat gland origin – eccrine
Hemangioma	Benign tumor	Mesenchymal
Vagina
Failure of squamous cell maturation	Absence of estrogen
Adenosis	DES exposure, sporadic	Abnormal retention of embryologic glandular epithelium
Benign disorder
Squamous cell carcinoma	Vaginala intraepithelial neoplasia			Most common vaginal neoplasm, assoc w cervical and vulvar SSC, 80% spread from cervix
Clear Cell Adenocarcinoma	Prior DES exposure			Peak age 17-22, very uncommon
Embryonal Rhabdomyosarcoma		Sarcoma of primitive skeletal muscle	Sarcoma botryoides – grape like	Seen in young children
Cervix
Cervical Intraepithelial Neoplasia	HPV esp types 16,18, 31, 33, 35 à Inactivation of suppressor gene products p53 and Rb	Occurs in transition zone Degree of loss of maturation in squamous cells
Invasive Carcinoma of Cervix		Microinvasion, non-keratinizing squamous cel,l Advancing disease can obstruct ureters, invade locally		Adenocarcinoma – less common, more aggressive 2nd most common cause of death WW

Gynecological Pathology

Condition	Cause	Pathology/Histology	Clinical Features	Other Features
Proliferative Enodmetrium		· Straight glands · Narrow lumens · Pallisading nuclei · Ovoid nuclei · Mitoses
Early Secretory Endometrium	First manifestation of effect of ovulation on endometrium	· Glands remain straight · Lumens remain narrow · Subnuclear vacuoles appear		24-36 hours after ovulation
Mid Secretory Endometrium		· Glands become coiled · Vacuoles no longer present in glands · Secretory product appears in lumen		Postovulatory days 5-9
Late Secretory Endometrium		· Intralumenal secretions are spent · Stromal predecidua appears · First predecidua around spiral arteries · Later predecidua beneath surface		Postovulatory days 10-14
Menstrual Endometrium		· Stromal collapse · Fribrin thrombi and blood · Glands are broken apart · Glands have no secretions
Hyper-secretory Endometrium of Pregnancy		· Arias-Stella reaction · large, hyperchromatic nuclei · prominent cytoplasmic vacuolization
Atrophic endometrium		· short glands · glandular cells – flat, without significant mitotic activity
Dysfunctional Uterine Bleeding		· anovulatory bleeding · luteal phase defect
Unopposed Estrogen		· proliferative glands · stromal breakdown · fibrin thrombi · wreathing of stroma by glandular cells
Contraceptives	Combined oral agents	· mix of proliferative and secretory changes · long use à · atrophic glands · stromal predecidual pattern dominates
	Depoprovera	· unopposed progesterone
Tamoxifen		· inc risk of carcinoma · inc incidence of polyps · large, mucinous metaplasia, fibrotic
Endometrial Hyperplasia	· unopposed estrogen stimulation – exogenous, endogenous · no progestational stimulation	· simple or complex architecture · typical or atypical nuclei	Vaginal bleeding, 60s Risk factors – obesity, diabetes, nulliparity, early menarche, late menopause	Complex atypical hyperplasia progresses to carcinoma – 1/3 T – hysterectomy, hormonal manipulation
Endometrial Carcinoma Type 1 Endometrioid	· PTEN gene mutation à cell growth and apoptosis	· squamous or mucinous		Grade determines prognosis T – hysterectomy, good survival Low grade – hormonal
Endometrial Carcinoma Type 2 Unfavorable Histology	· serous-p53 mutations	· clear cell		Early spread outside uterus à long term survival uncertain
Uterine Mesenchymal Tumors
Leiomyoma	·	· smooth muscle · multiple nodules · no coagulative necrosis · mitotic rate is low		Extremely uncommon
Leiomyosarcoma	·	· increased mitotic rate (>10/10 hpf) · necrosis · cytologic atypia
Stromal Sarcoma	·	· vascular invasion · receptors for progesterone	Appearance of endometrial stroma	T- hormonal therapy
Uterine Mixed Tumors
Adenomyoma	·	· benign glands and stroma
Adenosarcoma	·	· benign glands and malignant stroma
Carcinosarcoma	·	· malignant epithelial and stromal elements
Fallopian Tube
Infection	· STD · Polymicrobial infection			Important cause of infertility
Ecotpic Pregnancy	· Possible result of salpingitis		Ruptured fallopian tube is life threatening	Most common site of ectopic pregnancy
Ovary and Placenta
Polycystic Ovary Syndrome (Stein-Levanthal)		- Increased ovarian androgen production - Arrested follicle development due to androgens	- Androgen excess, ovarian cysts - Common cause of infertility
Endometriosis	- Mestrual implantation - Surgical - Vascular spread - Coelomic metaplasia	- Benign endometrial glands and stroma present outside the uterus	- cyclic pain with menses - may cause infertility
Ovarian Tumors	-	-	-
Ovarian Epithelial Carcinomas	- c-erbB-2 42% - K-ras mucinous lesions - P53 mutation 50-60% - BRCA1 and BRCA2 -15X risk, 10% - Lynch Syndrome II, subtype of HNPCC	-	-	Highest mortality rate of female genital cancers Difficult to detect early, spread beyond ovaries Adults, first-degree relatives, industrialized Inc with age, dec with parity and oral contraceptive
Benign Ovarian Germ Cell Tumors	-	- mature adult type tissue - all three germ layers - “dermoid cysts” - adult type carcinoma arises from tissue elements	-	Wide age range
Malignant Ovarian Germ Cell Tumors	-	- Dysgerminoma – undifferentiated germ cells – best prognosis - Immature (malignant) teratoma – fetal type tissue - Choriocarcinoma – mimics placental trophoblast - Endodermal sinus tumor – embryonic yolk sack type tissue	-	Highly malignant course but responsive to chemotherapy or radiation Exclusively children, young adults
Sex Cord Stromal Tumors	- ovarian stroma or primitive sex cords	-	-	- Variable from benign ot low grade malignancy - most hormonally active ovarian tumors
fibroma	-	-	- hormonally inert	- most common,
Thecoma	-	- lipid laden theca cells	- produces estrogen	-
Granulosa cell tumor	-	-	- produces estrogen	- low grade malignancy
Sertoli-Leydig cell tumor	-	-	- produces androgens	- rare
Metastatic Tumors to the Ovary (Krukenberg)	-	-	- can stimulate stroma to cause hormone production	- 3% of ovarian carcinoma - colon and upper GI
Placenta	-	-	-	-
Chorioamnionitis	- ascending infection through the birth canal - coliforms, vaginal bacteria	-	-	- preterm labor - neonatal infections
Villitis	- blood borne source of infection - viral, parasitic, spirochetes	-	-	-
Sponataneous Abortion	- infections - mechanical - endocrine - fetal abnormality - immunologic	-	-	- 15% of recognized pregnancy - 30% of unrecognized pregnancy
Septic Abortion	- uterine infection following induced abortion	- acute inflammatory cells and necrosis	-	- uncommon in hospital performed procedures
Toxemia of Pregnancy	- failure of spiral arterioles to fully dilate - placenta shows acute atherosis in maternal vessels - kidney: vacuolization of endothelial and mesangial cells, fibrin deposition	-	- hypertension - proteinuria - edema - convulsions - eclampsia	- more common in first pregnancy
Placental Abnormalities	-	-	-	-
Retroplacental Hematoma/ Abruption	- Hematoma separates placenta from uterine blood supply - Abruption: premature separation of placenta	-	-	-
Placenta Accreta	-	- abnormal adherence of placenta to myometrium - +/- invasion of myometrium	-	-
Gestational Trophoblastic Disease	-	-	-	-
Complete Hydatidiform Mole	- Fertilization of empty ovum - 23x paternal chromosome - divides to 46xx (diploid)	-	-	- Hydropic, avascular villi
Partial Hydatidiform Mole	- Fertilization of normal ovum by 2 sperm - Triploid karyotype	-	-	- some villi normal and others avascular
Choriocarcinoma	- malignant tumor derived from trophoblast	-	- vaginal bleeding - excessively high HCG levels	- good response to chemotherapy

Pregnancy and Preeclampsia

	Normal Pregnancy	Preeclampsia
Blood Pressure	Fall in first 24 weeks, rises to baseline by term	140/90 after 20 weeks gestation severe - >160/100
Kidneys	GFR increases 50%, renal plasma flow increases serum urea and creatinine decrease; enhanced waste metabolite removal; glycosuria	Vasospasm and capillary endothelial swelling -> reduction in GFR Serum uric acid and creatinine increased Proteinuria > 300 mg in a 24 hour collection Severe – proteinuria > 5 g/24h, oliguria (<500cc/24h)
Edema	Normal	Presenting sign but 1/3 don’t have it
Hemostatic	Venous stasis from hypercoagulable state	Systemic vasospasm, coagulation system activation, abnormal hemostasis Cycle – endothelial injury, platelet activation, platelet consumption
Prostanoid Changes	Both prostacyclin (PGI) and Thromboxane A2 (TXA) elevated, PGI > TXA	TXA > PGI PGI – vasodilator and inhibitor of platelet aggregation TXA – vasoconstriction and platelet aggregation
Autonomic		Increased sympathetic state – vasoconstriction
Nitric Oxide		Reduced
Free radical oxidation products		Increased
Hematologic	Plasma vol inc, RBC mass inc à “physiologic anemia” of pregnancy Hgb 11.5 mg/dl WBC count increases Hypercoagulable state – inc fibrinogen, factor VII to X increase – venous stasis	- Thrombocytopenia - Severe - <100,000 - fibrinogen decreased - coagulation time increased (PT, PTT)
Hepatic	Signs of liver disease Spider angiomata and palmar erythema – elev estrogen Serum – dec albumin, elev alk phos, elev cholesterol Estrogen increased proteins – fibrinogen, thyroid hormone binding globulin, ceruloplasmin Hepatic enzymes – AST/ALT, PTT unchanged	10% - transaminase elevation severe – impaired liver function (AST/ALT >70)
Pulmonary		Severe – pulmonary edema
Cerebral or visual disturbances		Severe cases
Epigastric pain		Severe cases
Seizures		Severe cases -> Eclampsia

The New York Times > Business > Your Money > The Count: At These Prices, the Poor Get Poorer, the Rich Get College

The New York Times > Business > Your Money > The Count: At These Prices, the Poor Get Poorer, the Rich Get College

Medical school can also be applied to this article.