Quiz (3rd midterm) Flashcards
1
Q
I. Breast disease
A. Common symptoms (not specific for cancer, fibrotic growths, cysts; however, the older the patient, the greater the likelihood that it is malignant)
A
- Pain
- Palbable masses
- Nipple discharge
2
Q
B. Mammography
A
• Start screening at ~40 yrs because younger women have denser breast tissue making it difficult to identify a mass
- It detects density
- Can show architectural distortions
- Identifies calcification
- Changes over time and these changes can indication pathologies such as cancers
- ~10% of breast cancers that are not detected by mammography, can be detected by palpitation
- Can use imaging to help guide biopsy needle in order to sample a growth.
- 85-90% predictive
3
Q
II. Acute mastitis
A
- Can cause breast abscesses and necrosis
- Typically associated with women who are breast feeding.
- Can be caused by plugged ducts
- Can be infectious or non-infectious
4
Q
III. Fat necrosis
A
• Usually associated with trauma (from a seat belt during an accident)
5
Q
IV. Breast cysts
A
- Fibrolytic changes
- Higher risk of breast cancer
- Occurs 20-40 years old
- Doesn’t typically occur after menopause
- Can calcify
- Can look like cancer on mammogram
6
Q
V. Benign neoplasm
A
- Fibroadenomas are the most common
- Mostly connective tissue
- Well circumscribed
- Don’t typically remove unless uncomfortable.
7
Q
VI. Breast carcinoma
A
• Rarely occurs
8
Q
Breast cancer symptoms, prognosis
A
A. Symptoms:
• Pain
• Masses (assessed by palpitation, mammography, ultrasound, MRI, or tissue biopsied)
B. Prognosis
• Based on size, axillary node status, and distant metastasis
• 5 year Survival rate of stage 0 (early stage)=92%, stage IV (late)= 13%
• If tumor expresses estrogen/progesterone receptors, it often responds to hormonal treatment
9
Q
C. Types of breast cancer
A
- Invasive carcinoma: 75-85%
- Most are ductal and the incidence increases with age & have invasive and non-invasive types
- Can do lumpectomies to remove smaller masses.
10
Q
D. Benign epithelial lesions
A
-typically fibrocytic changes (e.g.,60% of women have microscopic cysts associated with epithelial tissue.
11
Q
VII. Cervical Cancers
A
• HPV (human papillomavirus)- associated squamous cell neoplasm represents most cervical cancers -use pap smear to detect early • Risk factors -multiple sex partners -Immunosuppression -early age of first sexual contact -oral contraception for >5 years -nicotine use
12
Q
VIII. Endometrium
A. Polyps
A
- Causes:
• Hypertension
• Obesity
• Late menopause
13
Q
B. Endometrial cancer (adenocarcinoma)
A
- Risks
• Obesity
• Diabetes
• Hypertension
14
Q
B. Endometrial cancer (adenocarcinoma) tx
A
- Treatment
• Hysterectomy-treatment of choice
• Radiation/chemotherapy adjunctive
15
Q
C. Endometritis (infections)
A
-cause is often IUDs (intrauterine devices)
16
Q
D. Endometrial hyperplasia—can progress to a cancer
A
- Exaggerated responses due to excessive estrogen (e.g., excessive ovarian activity)
- Treatment:
- Progesterone
- Hysterectomy
17
Q
IX. Ovarian masses (ovary cancer is amass )
A. Types:
A
• Non-neoplastic cysts (e.g., follicular)
• Neoplastic: e.g., endometroioid
• Most are sporadic
• Contraceptives can decrease risk
• Treatment:
-total hysterectomy + removal of surrounding tissue + chemotherapy
18
Q
IX. Ovarian masses (ovary cancer is amass )
A. symtoms:
A
• Pelvic pain
• Pelvic mass
• Abdominal bleeding
C. Unlike cervical cancer, there is no effective screening for ovarian cancer
19
Q
A. Estrogens and Progestins
A
- Natural estrogens are steroid hormones—synthesized estrogens may be non-steroidal
- They cross cell membranes and activate estrogen receptors inside cell—modulate expression of genes
20
Q
. The menstrual cycle:
A
- Menstrual stage—menses
- Follicular stage—proliferative
- Luteal stage—secretory
21
Q
- As populations age, they …
A
- As populations age, they spend more time in menopause (females) or andropause (males
22
Q
- Estrogens:
a. Natural
A
- Estrone (predominant during menopause)- E1
- Estradiol (predominant during productive years)—E2
- Estratriol (predominant during pregnancy)—E3
23
Q
- Estrogens:
a. synthetic
A
- Steroidal: ethinyl estradiol
* Non-steroidal: diethylstilbesterol
24
Q
c. Physiological functions of estrogen
A
- Sexual maturity
- Increased CNS excitability (seizure inducing?)
- Increased endometrial and uterine growth
- Maintain skin elasticity
- Reduce bone adsorption
- Increase blood coagulability
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d. Clinical uses of estrogen
• Primary hypogonadism
• Postmenopausal
(1) Guidelines for use
• Always use the smallest dose for the shortest period of time possible
• Sometimes local creams are preferred to minimize exposure
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e. Adverse effects of estrogen
* Postmenopausal bleeding
* Nausea, breast tenderness
* Migraines
* Hypertension
* Hyperpigmentation (especially around eyes)
* Increases some cancers (e.g.. breast and endometrial)
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f. contraindicated: for estrogen
* Liver disease (slows metabolism)
* Breast/endometrial cancers
* Thrombolytic disorders
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Progestin
• Made from cholesterol
• Present in males, but less than females
a. Progesterone (natural)—most important progestin in human
• Precursor to estrogen, androgen and adrenalcortical steroids (e.g., cortisol)
• Also precursor to testosterone and estradiol
b. Synthetic progestins
c. Half life= 5 min. (very short acting)
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Progestin effects
d. Effects:
• Increase fat deposition
• Decrease CNS excitability (e.g., antiseizure—opposite of estrogen)
• Increase aldosterone---increase Na+ retention—increase BP—increase water retention and blood volume
• Increase body temperature
30
Clinical uses of progestin
| and contraindications
* Replacement therapy
* Oral contraception
* Long-term ovarian suppression (e.g., dysmenorrhea or endometriosis)—in contrast to estrogens, no problem with bleeding or clotting
* Contraindications:
* Breast cancer is a risk
* Severe hypertension or heart disease is risk
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Combination contraception :
| progesterone+ estrogen
* Decreases ovulation (approaching 100%)
| * Decreases conception and implantation
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Progestin only effects
. Progestin only (less effective, ~80-90%)
• Decreases ovulation 50-80%
• Thickens mucus and reduces sperm penetration
• Impairs implantation
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Delivery forms
* Combinations:
* Monophasics- constant doses of both estrogen and progesterone
* Biphasic- dosage of one or both change one time during cycle
* Triphasic-dosages change 2 times
* Progestin only—referred to as the “minipill” (no estrogen); fewer side effects, but less effective
* Implantable
* Injections (i.m., sustained effects)
* Intravaginal rings
* IUDs with and without estrogen/progestin
* Transdermal combinations
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Side effects of combination
Side effects of combinations
• Reduced ovarian functions and size
• Increased breast size and tenderness
• Increased thrombolytic events
• Increased heart rate and BP
• Hyperpigmentation, especially around the eye
• Mild nausea, breakthrough bleeding, headaches
• May interact with antibiotics that disrupt G.I. normal flora (e.g., wide spectrum antibiotics such as amoxicillin)—normal absorption of contraceptives from GI system is dependent on these flora
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Contraception uses
* Oral contraception
* Menstrual disorders, irregularity, heavy discharge
* Acne
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Tamoxifen
• Tamoxifen—blocks actions of estrogen in breast-used to treat breast cancers
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Mifepristone
• Mifepristone- morning after contraceptive: blocks progesterone and glucocorticoid receptors
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Danazol
• Danazol—suppresses ovarian function (has a masculinizing effect)
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Clomiphene
. Ovulation-inducing; for promoting fertilization and pregnancy (increased risk of multiple births—e.g., twins)
• Clomiphene (Clomid)
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Androgen-testosterone effects
1. testosterone—causes male puberty
• Converts to estradiol
• Replacement therapy for males
• Gynecological disorders—reduces breast size (gynecomastia)
• Has protein anabolic effects—helps replace muscle loss
• Growth stimulation—can prematurely close growth plates in growing adolescents
• Counter some age-related loss of muscle mass
• Adverse effects in women especially—masculinization
• Testosterone analogs abused for muscle and strength building—can cause acne, aggressiveness and “roid rage”, although this I controversial
41
Bone and Joint Intro
* 99% Calcium stored in bones
* In adult, the bones are the primary site of hematopoeises
* Constantly remodeling
* Medullary bone resists compression forces, Cortical bone is thick and resists bending forces
* Periosteum is tough fibrous membrane—covers bone surfaces except at joints—well innervated
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B. Abnormal bone matrix
| 1. Osteogenesis imperfecta
a. Deficient or defective type 1 collagen—too little bone
b. Generalized osteopenia
• Multiple fractures and bone deformities
• Malformed teeth (dentin deficiency)
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C. Acquired diseases of the bone
| • Nutritional, endocrine and systemic disorders
1. Vitamin deficiencies : scurvy (vit. C), rickets (vit. D)
| 2. Endocrine factors—hyperparathyroidism
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3. Types: of acquired diseases of bone
* Osteoporosis—common in elderly women, after menopause
* Osteomalacia—vitamin D deficiency
* Hyperparathyroidism
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4. Osteoporosis:
| causes
a. Causes
Genetic: age, low estrogen, fair hair and skin, tall and thin
Behavior: inactivity, smoking/alcohol, malnutrition, medication (chronic corticosteroids)
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burden of osteoporosis
* 10 million have osteoporosis in US, mostly women
| * 1/3 women >50 years old have at least one osteoporitic fracture
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c. Disorders of bone instability
* Kyphosis—abnormal forward curvature of spine
| * Scoliosis—abnormal lateral curvature of spine
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d. Types of fractures
* Complete
* Closed (overlying tissue intact)
* Commuted—bone splintered
* Displaced
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3.Osteomyelitis (inflammation of bone/marrow)
a. blood-born or direct
b. trauma from compound fractures
c. pyogenic infections (e.g., staph aureus or salmonella)
d. granulomatous (TB or fungal)- called “Pott disease” when associated with TB
e. Diabetes—due to poor circulation in the extremities-if chronic can form a drainage site and can even become osteosarcoma
50
1. Osteoarthritis (OA)
a. Loss of articular cartilage with secondary changes in bone
b. Presents in some degree in most persons >65 years of age. Symptoms worsen with excessive use.
c. Due to wear and tear
d. No inflammatory changes
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2. Rheumatoid arthritis
a. Autoimmune- 1% prevalence
b. Most common in Caucasians/ uncommon in Asians
c. Onset age: 25-50 yrs.-75% female/ can have juvenile RA
d. Joint swelling, pain and tenderness—often cause extreme distortions of joints and surrounding bone—deforming and debilitating
e. Other areas also affected:
• Ulcers
• Pulmonary nodules and fibrosis
• Carditis and pericarditis
• Vasculitis
52
3. Other inflammatory arthritides
a. Psoriatic (psorias) arthritis
b. Other autoimmune diseases (e.g., lupus [erythematosus], scleroderma)
c. Postinfections (e.g., rheumatic fever)
d. Infectious—staph/strep, TB
e. Gout (crystallized uric acid)
f. Lyme disease, if not treated—arthritis and neurological consequences
53
4. Gout
a. Primary cause by reduced renal excretion of purine
b. A primary treatment is with allopurinol—decreases the synthesis of purines
c. Symptoms:
• Hot, swollen, pain in joints---progressive joint destruction—gouty tophi (crystalized aggregates of uric acid)
d. Pseudo-gout—crystal deposits of calcium pyrophosphate
54
5. Ganglion cysts
a cyst resulting from connective tissue around joints—often painful
55
Dermal path overview
* Skin provides important protection against infection
* Cell types include: squamous cells, basal cells, melanocytes
* Appendages include: apocrine (sweat milky with odors-located near hair follicles), eccrine (found widely distributed, and sweat is watery for thermo control), sebaceous (also located near hair follicles—secrets oily sebum for lubrication and to prevent water loss).
56
• Macule-
flat, circumscribed less than 5mm
57
• Papule-
• Papule-elevated dome or flat topped ( less than 5mm
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• Nodule-
elevated dome ( greater than 5 mm)
59
• Plaque-
• Plaque-elevated flat-topped lesion ( greater than 5mm)
60
• Lichenfication-
thickened skin due to repeated rubbing
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• Pustule
-discrete, pus-filled raised lesion
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• Scale-
dry, plate-like excrescence, imperfect cornification
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• Vesicle
-fluid filled raised area, less than 5mm
64
• Acantholysis-
loss of intercellular adhesion keratinocytes (epidermis falls apart and sloughs off)
65
• Excoriation-
traumatic breakage of the skin (for example as a result of intense scratching)
66
• Bulla-
fluid-filled raised area, greater than 5 mm
67
• Dyskeratosis—
abnormal keratization, deeper in epidermis
68
• Hyperkeratosis—
hyperplasia of stratum cornum
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• Spongiosis-
intercellular edema of epidermis
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• Acute inflammatory:
| know the categories
• urticaria (hives), hypersensitivity mediated by antigens (e.g., pollen, food, drugs; mediated by IgE)
• eczematous dermatitis (e.g, contact dermatitis most common, delayed hypersensitivity reaction, can be pruritic, edematous or oozing plaques/vesicles),
• Allergic contact dermatitis—cellular memory of the reaction so that future contacts cause an increased dermatitis reaction
• Erythema multiforma (hypersensitivity to infections and drugs-dermal edema-can have blisters and necrosis)-wide range of expressions and severity
-can be severe life-threatening reaction known as Stevens-Johnson Syndrome—generalized all over the body—reaction to medicines (e.g., sulfonamides, salicylates)—can also be a reaction to infections such as herpes virus or fungal infections
71
Chronic inflamm
• psoriasis, inciting antigen—auto-rejection or environmentally induced
-1-2% in US
-can be accompanied by increased heart attacks and arthritis
-treatment includes NSAIDS and immunosuppressant drugs
-well-marked by pink to salmon colored plaques
-regular acanthosis in epidermis
• lichen planus;
-middle age
-extremities and oral cavity
-lace-like white markings.
-resolve after 1-2 years although often persists in oral cavity
Hyperkerotosis, and epidermal hyperplasia
-Unknown inciting mechanisms
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• Infectious dermatosis:
fungal
viral
- bacterial (e.g., impetigo: staph and strep infections superficial) on face and extremities, contagious through contact, --primarily kids; honey color crust-pustules
-fungal (tinea [ring worm] or candida); often infections in immunocompromised patients
-viral (wart pathology-human papillomavirus-HPV; verrucae); contagious by direct contact; can auto-innoculate and spread/epidermal hyperplasia, papillo mitosis
• Bulbous blistering prominent feature: pemphigus (painful flaccid blister like-deep erosions and crust after rupture-hypersensitivity reaction), dermatitis herpetiformis-use immunosuppressive treatment
-tend to be auto-immune responses
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• Herpes
```
Simplex/varicellular/Zoster
• Oral expression: HSV 1 (cold sores)
Genital: HSV 2
• Expressions:
-group vesicles—epidermal acantholysis—vesicles—sloughing
```
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• Zoster
-dermatomal distribution (can get trigeminal nerve involvement and can be very dangerous spreading to surrounding tissue such as eye or brain)
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- Varicella Zoster Virus (VZV)
can cause shingles usually later in life in those who experienced chicken pox (i.e., exposed to the VZV when young)
• Unilateral, dermatomal distribution
• Expresses as a band of rash that often itches, burns or throbs. It may persist for weeks to months. Usually is relieved by anti-inflammatories or opioid analgesics
• In extreme cases it becomes like an intense neuralgia and does not respond to traditional analgesics
• Not contagious, typically does not repeat, but can in some cases.
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Acne expressions
* Opened comodones (blackheads)
* Closed comodones (white heads)
* Cysts, pustules and abscesses
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Acne vulgaris
* Hormone changes (i.e., sex hormones)-increases testosterone influence
* Blocks hair follicle and sebaceous gland
* Hair follicle have proliferation of lining cells and cellular sloughing—forms a cellular plug and traps bacteria, cellular debris and sebum
* Gland ruptures and contents spreads to form cysts, abscesses and scarring—area is inflamed and swollen
78
Vulgaris tx
- antibiotics
- keratolytics
- drying agents
- vitamin A (topical and systemic-Accutane)
79
3. Perioral dermatitis
* Young women
* Long-term steroid use or cosmetic use
* Follicular papules, vesicles and pustules
80
2. Neoplastic benign
• Seborrhea keratosis (elderly, middle age-coin-like plaques;stuck-on appearance, tan to dark brown-granular surface)
81
Basal Cell, squamous cell malignant cancer
| 3. Malignant (most are UV-induced especially in fair skinned persons)-most common cancers
• Basal cell-most common, least aggressive/ most common malignancy worldwide. Slow growing.
-remove with local incision—does not metastasize
• Squamous cell- next most common, intermediate aggression, no metastasis
-red scaling plaques—locally aggressive
82
• Melanoma-
least likely, typically aggressive and metastasizes
- warnings: rapid enlargement of nevus; new pigmented lesion-not from pre-existing nevi; irregular borders; irregular surface and colors
- caused by UV exposure and genetics
- prognosis: poor if metastasized (common sites are lungs, liver and brain)
• High mitotic rate, lack of immune response to slow spread especially once it hits lymph nodes
83
a. Chronic inflammation can lead to:
* Cancers
* Pulmonary diseases
* Cardiovascular diseases
* Diabetes
* Alzheimer’s disease
* Oral diseases (periodontal tissues)
* Neurological disease
* Arthritis
84
(1) NSAIDs
• Decrease pain and inflammation
• Cox I (GI, bleeding and kidney side effects) and Cox II (MI and stroke and hypertension side effects) inhibitors
• Aspirin, ibuprofen, naproxen are non-selective COX I & II inhibitors
• Celecoxib is COX II inhibiton
(a) CNS-tinnitis
(b) CVS-hypertension
(c) GI-nausea, ulcers or bleeding
(d) Hepatic-altered liver functions
(e) Pulmonary-asthma
(f) Skin-rashes
(g) Renal- insufficiency, in extreme can have failure
85
(2) Glucocorticoids
• Rapidly acting
• Dramatic effect on inflammation and slowing bone erosions in rheumatoid arthritis
• Side effect: loss of muscle mass, osteoporosis, diabetogenesis, peptic ulcers, round face, buffalo hump
• Drugs:
-dexamethasone: long-acting
-cortisone, prednisone: short- to medium-acting
86
DMARDS
(Disease modifying anti-rheumatic drugs) and other Immunosuppressants
• E.g., methotrexate, sulfasalazine
• Decrease inflammation and slow bone damage in rheumatoid arthritis
• Potentially more toxic than other options
-severe hepatotoxicity
-stomatitis
-immunosuppression
87
Acne vulgaris
| a. Cause:
inflammation/bacterial infection of plugged sebaceous glands: white heads, cysts, abscesses
88
Acne Vulgaris drugs
Drugs:
(1) Topical keratolytics-removes keratin layer and opens sebaceous glands (also used as wart removers)
• Salicylic acid
• Benzoyl peroxide
89
Acne vulgaris abx(2) Antibiotics:
(2) Antibiotics: erythromycin, tetracycline, clinidimycin and Dapson,-eliminate the bacteria that cause the infection and inflammation associated with acne. Can use either topical or systemic. Drugs concentrate in skin.
90
(3) Retinoids:
(3) Retinoids: vitamin A-derivatives; tretinoin (retin A: topical); isotretinoin (Accutane: systemic)
• Side effects: dry skin, sores, major birth defects with isotretinoin
91
c. Non-drug treatments
• UV phototherapy—acne-causing bacteria are UV sensitive
92
a. Acyclovir
D. Antivirals for Shingles and Herpes—use early in infection
(1. Viral thymidine kinase-dependent types—getting some resistant viruses)
Zovirax, Denavir ointments): most effective for herpes simples virsus (HSV-1 and HSV-2)-cold sores on mouth and nose; less potent on Varicella-zoster virus (VZV-chickenpox--shingles)
93
b. Famciclovir
D. Antivirals for Shingles and Herpes—use early in infection
(1. Viral thymidine kinase-dependent types—getting some resistant viruses)
effective against VZV virus and shingles and herpes viruses. Longer acting than acyclovir
94
2. Non-thymidine kinase dependent antiviral—less of a resistant problem
a. foscarnet
