Lecture 25

1. Be able to demonstrate the proper technique for examination of the breasts.
Not on exam

2. Given the clinical examination of any patient presenting with a breast mass, be able to:
a. Identify the features that suggest that the mass is "probably benign" or "probably malignant"
Probably benign – a lesion that is smooth, rounded or lobulated, mobile, discrete (well-circumscribed border), soft to rubbery firm consistency
DDx – fibroadenoma, cyst, intraductal papilloma, cystoscarcoma phyllodes (benign/malignant), sebaceous cyst, lipoma, metastatic cancer, primary breast cancer.
Probably malignant – a lesion that is irregular in shape; immobile with respect to adjacent breast tissue, skin, or chest wall; ill-defined margins; and firm to rock hard, +/-- skin changes.
DDx – cancer, fibrocystic changes, infection, fat necrosis.

b. Describe the appropriate evaluation to disclose the definitive diagnosis
(So for some reason I can't imbed an image, so I'm just going to email you the flowchart I made based on notes/slides)

c. Describe the clinical presentation of "fat necrosis" of the breast.
Can mimic breast cancer on physical exam and mammogram (see above).
History of trauma/prior surgery, remembered in 50%
Superficial mass, associated with skin retraction
Stellate mass w/ calcifications on mammography
Often requires surgical biopsy to get the diagnosis

3. Given any patient with a normal clinical examination found to have a suspicious lesion on screening mammography, be able to:
a. Choose the best of the three options for management and
Early mammographic follow up and physical exam in 4-6 months
• ACR category 3 – probably benign
• If stereotactic technique has shown a negative result
Needle localized surgical excisional breast biopsy
• Suspicious abnormality, or highly suggestive of malignancy
Stereotactic or sonographic guided core needle biopsy or FNA – core needle biopsy is more commonly done that FNA because FNA has more inadequate sampling and requires an experienced cytopathologist. Rationale for either is to reduce surgeries for benign findings. Most commonly done.
• Indications for stereotactic breast biopsy – Low to intermediate suspicion lesion
• Sample other abnormalities when patient is having surgical biopsy for a more suspicious lesion
• Patient is not a candidate for breast conservation if cancer diagnosed
• Significant co-morbid medical conditions that make surgery undesirable
• Lesion identified in one mammographic view only

b. List the indications for referral to a surgeon.
For ACR categories 4 and 5 (Mammography – BIRADS – Nomenclature)
4 – Suspicious abnormality; biopsy should be considered
5 – Highly suggestive of malignancy; appropriate action should be taken
*Note that ACR 0 = assessment is incomplete, and it requires additional imaging studies*

4. Given any clinical examination of a patient with a nipple discharge, be able to:
a. Identify which symptoms suggest an increased likelihood of cancer
Serous, serosanguinous, sanguinous or water in nature
Associated with a mass
Unilateral
Uniductal
Spontaneous
Associated with abnormal cytology or abnormal mammogram
Occurring in a patient >50 years old
b. Recognize when the likely diagnosis is fibrocystic disease
Multi-ductal
Multi-colored
Bilateral
Usually elicited with manual comrpession
c. The differential diagnosis of galactorrhea
Oral contraceptives
Thyroid disease
Chest wall trauma or stimulation
Pituitary adenomas
Medications – phenothiazines, reserpine, methyldopa
d. Describe the appropriate evaluation.
P/E – characterize color, location, multiple/single ducts, amount, ease of flow.
Spontaneous non-lactational galactorrhea – check prolactin and thyroid function tests
Dark or bloody discharges – hemoccult tested. Cytologic examination. Biopsy (whether cytology is positive/negative)
Manage worrisome discharges by cannulation and excision of the involved duct and its arborization. Do ductogram first only if it will influence the decision for surgical excision (may help to localize better the intraductal lesion to facilitate excision).

5. Given the clinical presentation of any patient with breast pain, be able to:
a. List the six most common etiologies
Diffuse fibrocystic changes – waxes and wanes in severity related to hormonal cycling. More severe if patient, especially a postmenopausal patient, is on hormone replacement therapy; and regress if hormone is stopped.
Sudden enlargement of a gross cyst – cyst is found on P/E, which should be aspirated
Breast infection – has other signs of inflammation
Physiologic hormonal cycling or exogenous hormone therapy
Costochondritis
Cancer – consider especially in older women not on hormone replacement therapy. May have other ssx of breast cancer
b. Describe the appropriate further evaluation
Physical examination – rule out mass lesion or inflammatory condition
Mammography – women >40 + women 30-40 depending on history, P/E, and prior available mammograms
c. Diagnose which of the above etiologies is present
See above

6. Given the clinical presentation of any patient with an inflammatory condition of the breast, be able to:
a. List the six most common etiologies and
Mastitis – inflammation of the mammary gland
Abscess – may have a fluctuant (moveable, compressible) area, which should be aspirated to confirm abscess and get material for culture
Recurring subareolar abscess – spontaneous drainage of pus from around the nipple areolar complex
Skin infections such as folliculitis or an infected sebaceous cyst
Superficial thrombophlebitis
Cancer – consider in patient w/ erythematous, edematous, firm breast w/o fever or other systemic signs of infection, and who fail to respond to antibiotic therapy

b. Recognize which is most likely to be present.
See above. Also, look at history and physical.

7. Given a woman of any age, be able to list the breast cancer screening techniques as recommended by the American Cancer Society.
After age 20 Monthly breast self-examination
20-40 +Physical exam by health professional q3 yrs
40+ +Physical exam by health professional annually + Mammogram annually

Lecture 11

Lecture 11. Basic principles of diabetes
1. Describe the diagnostic criteria for diabetes mellitus.
Fasting plasma glucose >126 mg/dl, on ≥2 occasions – Gold standard
Glucose tolerance test (administer 75 g glucose and get 2hr plasma glucose ≥200 mg/dl) – Research only, not used clinically
Hemoglobin A1c increased – Used to assess effectiveness of treatment, not diagnosis

2. List the three acute-phase and six late-phase risks from diabetes and how the risks can be minimized.
Acute - Poor control can cause diabetic ketoacidosis (type 1) or non-ketotic hyperosmolar coma (type 2). Too tight control can cause hypoglycemia.
Late - Microvascular (retinopathy, nephropathy, neuropathy). Macrovascular (coronary artery disease, cerebrovascular disease, peripheral vascular disease)

3. Given a clinical presentation, be able to diagnose:
a. Type 1, insulin dependent diabetes mellitus
Hyperglycemia (see above)
Hx – Polyuria, polydipsia, polyphagia
Weight loss, thin patient
Young patient
Labs – Loss of insulin and C-peptide
Positive anti-islet antibodies
May present in DKA

b. Type 2, non-insulin dependent diabetes mellitus
Hyperglycemia
Hx – Polyuria, polydipsia, polyphagia
Mild weight loss if any, obese patient
Older patient
Labs – Normal/increased insulin and C-peptide
Possible proteinuria
May present in hyperosmolar coma – massive glucose

4. Describe the pathophysiology of types 1 and 2 diabetes mellitus in terms of causes for abnormal beta cell activity, autoimmunity, and hormone levels.
Type 1 – is due to autoimmune destruction of pancreatic beta cells, thought to occur after a precipitating environmental event (viral infection). Beta cell mass, insulin secretion, and C-peptide (a marker) all decrease. The patient goes from clinically silent to abnormal glucose tolerance to non-ketoacidotic diabetes to ketoacidotic diabetes.
Some patients can briefly return to normoglycemia even after presenting in ketoacidosis – the honeymoon period – because they still have enough insulin to prevent hyperglycemia. Then there is another precipitating event (e.g., infection, surgery), which increases epinephrine and norepinephrine release, which diminish insulin secretion (in normal and prediabetic people). After this stress is over there can be another honeymoon period in which the remaining beta cells are able to control blood glucose for an additional (short) period.

Type 2 – is due to insulin resistence. Obesity leads to insulin resistance; most patients with NIDDM are obese. This causes the beta cell to have to increase glucose secretion; however, over time the beta cell fails and can no longer produce the levels of insulin necessary to control blood glucose. This failure is due to either genetic reasons or because of toxicity of elevated glucose and free fatty acids. When the beta cells are unable to compensate is when the patient presents with overt diabetes. However, this form of diabetes is not associated with DKA because there is enough insulin to prevent that; instead they are at risk of hyperosmolar coma.
Caloric excess leads to hyperinsulinemia leads to increased SREBP1c leads to increased lipogenesis leads to increased adiposity (obesity) leads to ectopic fat deposition leads to insulin resistance leads to beta cell lipotoxicity leads to hyperglycemia (diabetes)

Lecture 17

1. Obtain a targeted but thorough gynecologic and obstetrical history.
Observation
Chief complaint
Gynecologic history
•Menstrual history – menarche, last menstrual period, cycle length and characteristics (color, amount, assoc sx)
• Pregnancy history
• Vaginal or pelvic infections – type of infection, treatment, any complications, risk factors
• Gynecologic surgical procedures
• Urologic history – incl. bladder dysfunction, acute or chronic bladder or kidney infections, hematuria, stones
• Pelvic pain – Sx, relation to menstrual cycle or assoc w/ other events
• Vaginal bleeding
• Sexual and contraceptive status – sexually active?, types of relationshps, individual(s) involved, satisfaction/orgasmic, dyspareunia, sexual dysfunction (patient/partner), onset of sexual activity, number of partners
Significant medical history
Medications, allergies, habits
Preventative measures
• Immunizations, incl. HPV vaccine
• Cancer screening – breast, pap smear
• Vitamins, calcium
• Diet, exercise
Family history
• Illness, cause of death – esp. cancers
• Congenital malformation, mental retardation, reproductive wastage
Occupational and vocational history
Social history
Review of systems
• Remember psychiatric – depression, physical abuse, sexual abuse

2. Demonstrate a proper breast and pelvic examination (ICM Pelvic Workshop).
Not on exam.

3. Plot the relative levels of estrogen, progesterone, FSH, and LH during a menstrual cycle.
[Hmm...I can't figure out how to upload this image, but it's on page 17-5 fo the syllabus]
Day 1 is the first day of menses, which typically lasts 4-5 days.
Cycles can last from 25-30 days, w/ the luteal phase 14 days, and the follicular phase of varying length.
Follicular phase = proliferative phase. Luteal phase = secretory phases.

4. Counsel a patient about condom effectiveness with regard to sexually transmitted infections.
• Barrier and spermicidal methods provide protection against STIs, but even 100% condom use does not eliminate the risk of any ST.
• Protection against STIs has a beneficial impact on the risk of tubal infertility, ectopic pregnancy, and cervical cancer.
• Types –
• Latex – may cause allergy
• Polyurethane – 4-6 times greater risk of breakage and slippage as compared to latex condoms
• Silicone rubber
• “Natural skin” (lamb’s intestine) condoms do not offer STI protection.
• The typical use failure rate (12%, 18% for adolescents) is much higher than the perfect use failure rate (3%).
• Incorrect and inconsistent use contributes to condom failures, so it’s important to use condoms correctly and consistently.
• Use with a spermicide decreases the failure rate and increases protection against STIs.
• 100% condom use, in actuality, is so uncommon that it is almost a theoretical concept.
• It is important to consistently use condoms to reduce risk and to
• Condoms reduce the risk of infections, and never by 100%.
• No risk reduction for HPV or trichonomas vaginalis
• 29-50% risk reduction for syphilis transmission w/ 100% condom use.
• 50% risk reduction for gonorrhea and Chlamydia w/ 100% condom use.
• W/ 100% condom use there remains a 60% relative risk of herpes, and a 15% relative risk of HIV.

5. Given any pertinent clinical presentation, be able to recognize when a woman is peri-menopausal and describe the pathophysiology of the anatomic and physiologic effects on the bones, heart, breasts, vaginal mucosa, and endometrium.
Menopause = no menstrual period for 12 months in the setting of ovarian failure that comes with age.
Perimenopause = no menstrual period for less than 12 months.
SSX
• Age, 45-52 y/o (average age = 52)
• Low estrogen and inhibiin production leads to FSH and LH >40 miU/ml
• Irregular bleeding patterns secondary to anovulation leading to amenorrhea
• Osteoporosis
• Hot flashes/fushes (vasomotor instability)
• Dryness and atrophy of the urogenital epithelium and vagina
• Sleep disturbances – insomnia
• Mood changes, irritability nervousness
Pathophysiology
• Loss of ova and associated follicles (mainly by atresia) leads to decreased ovarian estrogen secretion
• After menopause, extraglandular (in adipose tissue, bone, muscle, skin, brain) formation of estrone becomes the dominant pathway
• Hot flush – sensation of warmth and heat followed by profuse sweating
• Pathogenesis is unclear – related to pulses of LH secretion
• Estrogen replacement alleviates symptoms
• Triggered in central nervous centers (e.g. the hypothalamus)
• Urogenital atrophy – thinning of vaginal epitheliu, atrophy of the vagina, and symptoms of atrophic vaginitis [burning, dyspareunia (painful sex), vaginal bleeding, loss of uterine support w/ subsequent uterine descensus (slipping/falling out of place)]
• Due to estrogen deficiency. Symptoms relieved by estrogen treatment
• Other – depression, anxiety, fatigue, and irritability
• Relieved w/ estrogen therapy, either directly or by preventing hot flashes (which disrupt sleep)
• Osteoporosis – loss of structural support in trabecular bone, predominantly of the axial skeleton
• Due to estrogen deficiency, which causes increased bone resorption and mobilization of Ca w/ increased urinary or intestinal excretion of Ca.
• Estrogen deficiency may lead to increased sensitivity to PTH in bone.
• Estrogen decreases bone turnover by acting on osteoblasts.
• Cardiovascular effects
• Estrogen in the vasculature leads to decreased binding to inflammatory cells and LDL, increased production of endothelial NO
• Loss of ovarian function leads to decreased HDL cholesterol and increased LDL cholesterol

6. Given any pertinent clinical presentation, be able to recognize when estrogen, alone and in combination with progesterone, is indicated in the management of menopause.
Indications for estrogen treatment
• Osteoporosis (lower the risk of spine and hip fractures esp.)
• Caucasian or Asian race
• Low body weight
• Hypoestrogenism
• Early menopause
• FHx
• Diet low in Ca and vitamin D
• Diet high in caffeine, phosphate, alcohol, and protein
• Cigarette smoking
• Sedentary life style
• Reduced risk of colon cancer
• Indications for estrogen + progesterone treatment – If a woman still has her uterus, she needs to receive progesterone to prevent endometrial hyperplasia and endometrial cancer
Contraindications for estrogen +/— progesterone treatment
• Increased risk of breast cancer, heart attacks, strokes, blood clots w/ E + P therapy
• Estrogen alone, or w/ progesterone, does not prevent cardiovascular disease

Lecture 18

1-2. Physical Exam


3. Descrie the pathophysiology of erectile dysfunction that is due to vascular, endocrinological, psychological, and idiopathic etiologies.


Erectile Dysfunction-the consistent inability to acheive and/or maintain an erection sufficient for sexual activity.


Mechanism of Erection
-Corpora Cavernosa are surrounded by tunica albugiea, and contain a lattice of blood sinusoids surrounded by trabeculae of smooth muscle
-Blood in the sinusoids exit through the tunica albuginea as emissary veins to form the deep dorsal vein.
-Parasympathetic nerves from S2-s4(S2,3,4 keep the dick off the floor) are for erection
-Sympathetic nerves from T11-L2 are for ejaculation and detumescence.
-Neuroendocrine messages from the brain due to audiovisual stimuli or fanasy(with or without tactile stimulation) activates the erectile response
-When flaccid the arterioles and sinusoids are contracted and the venous blood exits freely through emissary veins
-During erection the muscles of the sinsoid wallas and arterioles relax which increases blood inflow. This causes the sinusoids to expand and compress the venules, while the emissary veins are compressed under the tunica albuginea. The compression prevents venous outflow and erection occurs.
-Increased sympathetic vasoconstictor activity and break down of cGMP by PDE5 causes detumescence. This is mediated through alpha 1 adrenergic receptors
-The most improtant neuro transmitter is Nitric Oxide. NO activates GTP conversion to cGMP. cGMP causes smooth muscle relaxation and erection. VIP and PGE1 also support erection.


Psychogenic Anxiety; loss of attraction; stress; relationsship problems
Psychiatric Depression
Neurogenic Trauma; myelodysplasia; MS; diabetes; EtOH, pelvis surgery
Endocrine Primary or secondary hypogonadism; hyperprolactinemia
Arteriogenic Hypertension;smoking;diabetes;hypercholesterolemia; peripheral vascular dz
Venous Impariment of veno-occlusive mechanisms(venous leak)
Drug Induced Antihypertensives; antidepressants;hormones

4. Given the clinical presentation of any patient with eD, be abkle to:
a.) Recognize when a questionnaire, physiologic testing, and further lab tests are indicated
b.)when the most likely etiology is vascular, neurological, endocrinologica,psychological, or idiopathic
Using the history in diagnosis
-Psychogenic ED is characterized by sudden onest, situational, relationship issues, and normal nocturanl erections
-Organic ED is usually gradual in onset, progressive, absent nocturnal and morning erections.
- A quantitative structured questionnaire may be helpful to obtain a benchmark of the severity.
-Talk about current medications that could cause ED

Lab Tests
-used on an individual basis and based on goal oriented treatment plan
-Serum Glucose for diabetes
-Serum testosterone
-Serum prolaction
-thyroid hormone panel
-lipid profile
-serum PSA
-Nocturnal penile tumescence testing can help to evaluate psychogenic ED
-Selected cases can have cavernosography, cavernosometry, arteriography to check for normal anatomy, blood flow, and pressure response to erectile stimuli

psychogenic ED should be treated in cooperation with psychologist or psychiatrist and a physician .

Lecture 12

1. List three microvascular and three macrovascular complications of diabetes mellitus.
Microvascular

Diabetic Retinopathy
-Types: Non-proliferative, Pre-proliferative, Proliferative
-Leading cause of blindness in adults
-Increases the relative risk of cataracts and glaucoma by 2-3X


Diabetic Nephropathy
-occurs in 35% of patients with type 1 diabetes and 20% of patients with type 2 diabetes
-Accounts for 50% of all ESRD patients

Diabetic Neuropathy
-Common in both forms of diabetes mellitus
-One of the common causes of mortality in diabetes
-Cause of ulcers which lead to amputation


Macrovasular


Coronary Heart Disease
-2X increased risk in men 4X increased risk in women


Cerebrovascular disease
-increases stroke risk 4X

Peripheral Vascular Disease
-8% have this at diagnosis
-40-50% of non-traumatic amputations
-50% three year suurvival after amputation



2. List four risk favtors for the development of diabetic complictions
-Hyperglycemia
-Duration of Disease
-Dyslipidemia
-Blood Pressure
-tobacco
-Genetics

3. Retinopathy:
a) Given a picture of a retina, be able to recognize non-proliferative and proliferative retinopathy.

Non-proliferative
Microaneurysms
-These are red dots on exam approx 20-200microns, these are the earliest findings
-Often times they leak lipoproteins and form hard exudates



Hard Exudates
-yellow and sharply demarcated structures on fundoscopic exam
-they lead to edema



Macular Edema
-thickening of the retina less than 500 microns from te macula
-hard exudates less than 500 microns from the macula
-Macular edema causes a loss in visual acuity, and can lead to retinal ischemia

Retinal Ischemia
-cotton wool spots(soft exudates which are whitish gray areas)
-venous beading
-Intra-retinal micovascular abnormalities (IRMA), these are dilated capillaries due to retinal hypoxia
-Intra retinal hemorrhages


Pre-proliferative Retinopathy
-when the constellation of symptoms from retinal ischemia is seen together it is called pre-proliferative retinopahty
-This includes IRMA, Intra-retinal hemorrhages, Cotton wool spots, and venous beading

Proliferative Retinopathy


Neovascularization
-appearance of abnormal retinal blood vessls, usually on or near the optic nerve head or in the vicinity of other normal retinal vessels

Vitreous Hemorrhage
-as a consequence of abnormal neovasularization, vessels can often rupture into the vitreous

Fibrous Tissue

-Fibrous tissue is associated with the deelopment of new vessels.

-late in the course the blood vessels regress and the fibrous tissue may be the only sign

Traction Retinal Detachment

-When the fibrous tissue contracts it can drag the retina and cause a traction retinal detachment

b) Given a patient who has just been diagnosed with diabetes mellitus, be able to recognize whether, how often, and why that patient needs to be scheduled for an eye exam
Initially
Type 1 Diabetes patients within 3 t0 5 years after diagnosis
Type 2 Diabetes always at the time of diagnosis
Follow-up
Annually
-children and adolescents
-Adults without retinopathy
Semi-annually
-Non-proliferative retinopathy
Quarterly
-Pre-proliferative retinopathy
Individualized
-Proliferative retinopathy
-Pregnancy during each trimeseter

c) List four modifiable risk factors other than glucose control that predispose the development of diabetic retinopathy.
-Blood Pressure
-Smoking
-Pregnancy
-Nephropathy

4. Nephropathy: Given a patient with diabetes mellitus, be able to recognize diabetic nephropathy iin its early stages and recommend treatment aimed to slow its progression
Early Diagnostic findings
-Genetics
-Blood pressure elevation
-Creatinine Clearance above the upper limit of normal
-Alterations in glomerular structure
-Microalbuminuria
--measured by24 hour collection or morning urine test
--Normal less than 20micrograms/min dipstick negative
--microablbuminuria 20-200 micrograms/min (30-300mg/24hr) dipstick negative
--Overt proteinuria >200micrograms/min (>300mg/24hr) dipstick positive
--Diagnosis is made if microalbuminuria is foundin 2/3 urine samples in less than 6 months
Treatment
-Aggressive blood glucose control
-Aggressive blood pressure control
-ACE Inhibitor is the first line of therapy if they have hypertension and/or albuminuria. Ocassionally considered if there are cardiovascular problems, because of the cardiovascular benefit from ACE inhibitors
-low protein diet

5. Neuropathy
a) Given the clinical presentation of any patient with diabetes mellitus, be able to recognize the complications of distal symmetrical polyneuropathy and neuropathic ulcers.
Distal Symmetrical Polyneuropathy
-paresthesias(tingling and numbness)
-pain(dull ache, burning, lancinating)
-Impaired Sensation(vibratory, pain)
-Nocturnal exacerbation
-absent knee and ankle reflex
-motor involvemnt
Neuropathic Ulcer
-Major source of morbidity
-caused by the loss of protective sensation and repetetive trauma (i.e. walking)
-Over Areas of increased pressure( i.e. metatarsal heads or under calluses)
-Hammer-claw toe deformity of foot causes increased pressure on metatarsal heads
b) List Five risk factors for the development of diabetic neuopathy.
-Genetics
-Males
-Height
-Alcohol
-Hyperglycemia