Boards Book Flashcards
Answer these questions about the following BENIGN ovarian neoplasms
- Serous cystadenoma: what type of epithelium
- Mucinous cystadenoma: what type of epithelium
- Mature cystic teratoma: what presentation
- Brenner tumor: what histology
- Fibromas: what histology and presentation
- Thecoma: what presentation
- Serous cystadenoma: fallopian-like epithelium
- Mucinous cystadenoma: mucus-secreting epithelium
- Mature cystic teratoma (dermoid cyst): can present with pain secondary to ovarian enlargement or torsion. Can also contain functional thyroid tissue and present as hyperthyroidism (struma ovarii)
- Brenner tumor: looks like bladder; pale yellow-tan in color and appears encapsulated. “Coffee bean” nuclei.
- Fibroma: bundles of spindle-shaped fibroblasts. Meigs syndrome - triad of ovarian fibroma, ascites, and hydrothorax (pleural effusion). Pulling sensation in groin.
- Thecoma: like granulosa cell tumors, may produce estrogen; abnormal uterine bleeding in postmenopause.
Answer the following questions about MALIGNANT ovarian neoplasms
- Immature teratoma: most likely to contain what
- Granulosa cell tumor: what histology
- Serous cystadenocarcinoma: what histology
- Mucinous cystadenocarcinoma: what association
- Dysgerminoma: What histology and tumor markers
- Choriocarcinoma: what presentation
- Yolk sac (endodermal sinus) tumor: What histology and tumor markers
- Krukenberg: what histology and location
- <u>Immature teratoma</u>: neuroectoderm
- <u>Granulosa cell tumor</u>: can produce estrogen/progesterone; abnormal uterine bleeding, sexual precocity, breast tenderness.<strong>Call-Exner bodies</strong>(resemble follicles)
- <u>Serous cystadenocarcinoma</u>: <strong>psammoma</strong>
- <u>Mucinous cystadenocarcinoma</u>:<strong>pseudomyxoma peritonei</strong>= intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor
- <u>Dysgerminoma</u>:<strong>“fried egg</strong>” cells; tumor markers = hCG and LDH
- <u>Choriocarcinoma</u>: trophoblastic tissue; no chorionic vili present; increased frequency of TL cyst. Abnormal hCG, SOB, hemoptysis. Hematogenous spread to lungs.
- <u>Yolk sac (endodermal sinus) tumor</u>: yellow, friable (hemorrhagic) solid mass with<strong>Schiller-Duval bodies </strong>(resemble glomeruli). <strong>AFP</strong> = tumor marker
- <u>Krukenberg</u>: GI malignancy (diffuse gastric adenocarcinoma) that metastasizes to ovaries, causing a mucin-secreting <strong>signet-cell</strong>adenocarcinoma
Describe the histology and features of the various testicular germ cell tumors including: seminoma, yolk sac (endodermal sinus) tumor, choriocarcinoma, teratoma, embryonal carcinoma
- <u>Seminoma</u>: 30 y/opainless testicular enlargement. Large cells in lobules with watery cytoplasm and<strong>“fried egg”</strong>appereance. Increase<strong>ALP</strong>.
- <u>Yolk Sac (Endodermal Sinus)</u>: < 3 y/o withyellow, mucinous tumor;<strong>Schiller-Duval bodies</strong>
- <u>Choriocarcinoma</u>: <strong>hCG.</strong>hematogenous mets to lungs (may present wtih “hemorrhagic stroke” d/t bleeding into mets). Gynecomastia or hyperthryoidism (hCG is an LH and TSH analog)
- <u>Teratoma</u>: mature teratomas CAN be malignant. increased hCG and AFP.
- <u>Embryonal carcinoma</u>: malignant, <strong>hemorrhagic mass with necrosis</strong>; <strong>painful scrotal mass</strong>. Often <strong>glandular/pappilary morphology</strong>. increasd hCG (and AFP if mixed tumor)
Describe the testicular non-germ tumors, specifically Leydig type
- Leydig: Reinke crystals; androgen producing, gynecomastia in men, precocoious puberty in boys. Golden brown color.
What breast pathology is associated with serous or bloddy nipple discharge?
Intraductal papilloma: small tumor that grows in lactiferous ducts; typically beneath teh areola. Slight (1.5-2X) increase risk for carcinoma
Describe the 3 types of noninvasive breast carcinomas including: DCIS, Comedocarcinoma, and Paget Disease
DCIS: fills ductal lumen and arises from ductal atypia. Often seen as microcalcifications on mammo. No BM penetration.
Comedocarcinoma: ductal, caseous necrosis. Subtype of DCIS.
Paget Disease: suggests underlying malignancy, as it results from underlying DCIS! Eczematous patches on nipple (red, itchy, swollen, rash on areola and nipple). Paget cells = large cells in epidermis with clear halo.
Describe the 4 types of invasive breast carcinoma: invasive ductal, invasive lobular, medullary, inflammatory
- <u>Invasive Ductal:</u><strong>“rock-hard”fixed and immobile</strong>. Small, glandular, duct-like cells. Grossly see “stellate” infiltration. Worstand most invasive AND most common.
- <u>Invasive Lobular:</u>orderly row of cells <strong>(“Indian File”)</strong>; signet-ring cells. Often bilateral, ER/PR+
- <u>Medullary:</u>fleshy, cellular, lymphocytic infiltrate with good prognosis
- <u>Inflammatory</u>: dermal lymphatic invasion. <strong>Peau d’orange </strong>(orange peel); neoplastic cells block lymphatic drainage. Focal dimpling d/t involvment of suspensory ligament with nipple retraction.
Describe teh different types of proliferative breast disease
MCC of “breast lumps” in 25-menopausal women.Present with premenstural breast pain and multiple lesions, often bilateral. Fluctuation in size of mass with hormone levels.
- <u>Fibrosis</u>: hyperplasia of breast stroma
- <u>Cystic</u>: fluid filled, <strong>blue dome</strong>. Ductal dilation.
- <u>Sclerosing adenosis</u>: <strong>increased acini and intralobular fibrosis</strong>. Associated with <strong>calcifications</strong>. <em>Increased risk </em>(1.5-2X) of developing cancer.
- <u>Epithelial hyperplasia</u>: <strong>increase in number of epithelial cell layers</strong> in terminal duct lobule. <em>Increased risk</em> of carcinoma with atypical cells.
What is acute mastitis vs. fat necrosis
Acute mastitis: breast abscess (redness, pain, fever); during breast-feeding. Increased risk of bacterial infection through cracks in nipple; S. aureus is MC pathogen. Treat with dicloxacilin and continued breast-feeding.
Fat necrosis: benign, usually painless lump; forms d/t trauma. Abnormal clacification on mammo; biopsy shows necrotic fat, giant cells.
What is the MOA of each of the following:
- Leuprolide
- Clomiphene
- Tamoxifen + Raloxifene
- Anastrozole/Exemestane
- Mifepristone
- Terbutaline
- Danazol
- Finasteride
- Flutamide
- <u>Leuprolide</u>: GnRH analog with agonist properties when used in pulsatile fashion (tx infertility) or antagonist in continuous fashion (tx prostate cancer, uterine fibrioids, precocious puberty)
- <u>Clomiphene</u>: antagonist at estrogen receptors in hypothalamus; prevents normal feedback inhibiton and increases release of LH and FSH, which stimulates ovulation (tx infertility d/t anovulation e.g. PCOS). Can cause multiple simulltaenous prgenancies
- <u>Tamoxifen</u>: antagonist on breast; agonist on uterus, bone (tx ER+ BC)
- <u>Raloxifene</u>: agonist on bone; antagonist at uterus (tx osteoporosis)
- Anastrozole/Exemestane: aromatase inhibitors (tx BC in postmenopausal women)
- <u>Mifepristone</u>: competitive inhibitor of progestins at progesterone receptor; used with misoprostol (PGE1) to terminate pregnancy.
- <u>Terbutaline</u>: b2 agonist that relaxes uterus; usd to decrease contractions in labor (other tocolytics include magnesium sulfate, nifedipine, indomethacin)
- Danazol: synthetic androgen that acts as partial agonist at andorgen receptors (tx endometriosis and hereditary angioedema)
- Finasteride: 5a-reductase inhibitor; BPH and promotes hair growth
- Flutamide: competitive inhibitor of andorgens at testosterone receptor; tx prostate cancer
What is the MOA of Theophylline, Ipratropium, and Bosentan
- Theophylline: methylxanthine that causes bronchodilation by inhibiting phosphodiesterase, leading to increased cAMP levels. Narrow TI (cardiotoxicity, neurotoxic). Blocks actions of adenosine. Antidote: BB
- Ipratropium: competitive block of muscarinic receptors; prevents bronchoconstriction. Used in COPD (as well as tiotropium)
- Bosentan: used to treat PAH; antagonizes endothelin-1 receptors to decrease pulmonary vascular resistance.
Describe kidney embryology
Pronephros: week 4; then degenerates
Mesonephros: interim kidney for 1st trimester; later contributes to male genital system
Metanephros: permanent; first apperas in 5th week of gestation; nephrogenesis continues to 32-36w
- Ureteric Bud: derived from caudal end of mesonephric duct; gives rise to ureter, pelvis, calyces, and collecting ducts; fully canalized by week 10
- Metanephric Mesenchyme: ureteric bud interacts with this tissue and induces differentiation/formation of glomerulus through DCT. Abnormal interaction causes multicystic dysplastic kidney (hypertrophy of contralateral kidney if unilateral; often diagnosed prenatally).
Ureteropelvic junction: last to canalize and is MC site of obstruction (hydronephrosis) in fetus.
What is the autonomic innervation of the male sexual response
Erection: PNS (pelvic nerve): NO causes increased cGMP, leading to smooth muscle relaxation, vasodilation, erection
Emission: SNS (hypogastric nerve)
Ejaculation: visceral and somatic nerves (pudendal nerve)
Describe the fluid compartments and how to calculate GFR, RPF, FF, Reabsorption and Secretion Rate
Total Body Weight= 60% TBW
- <strong>1/3 ECF</strong> (20%; measured by <strong>inulin</strong>):<strong>1/4 plasma volume </strong>(5%; measured by <strong>albumin</strong>) and <strong>3/4 interstital volume </strong>(15%)
- <strong>2/3 ICF</strong> (40%)
<strong>Inulin clearence</strong> can be used to calculate <strong>GFR</strong> because it is freely filtered and niether reabsorbed nor secreted. <strong>GFR = UV/P</strong>
- Cx < GFR = net tubular reabsorption of X; if Cx > GFR = net tubular secretion of X
<strong>PAH clearence </strong>can be used to calculate<strong>RPF</strong> because it is both filtered and actively secreted in proximal tubule. Note <strong>RBF = RPF / (1-HCT)</strong>
<strong>Filtration Fraction</strong> = GFR/RPF
<strong>Filtered load</strong> = GFR * Px
<strong>Excretion Rate</strong> = V * Ux
<strong>Reabsorption</strong> = filtered - excreted
<strong>Secretion</strong> = excreted - filtered
Describe AA clearence in the kidneys
Sodium-dependetn transporters in proximal tubule reabsorb amino acids.
Hartnup disease: AR; deficeincy of neutral amino acids (e.g., tryptophan) transporters in proximal renal tubular cells and on enterocytes. Leads to neutral aminoaciduria and decreaed absorption from teh gut; results in pellagra-like symptoms; treat with high-protein diet and nicotinic acid.
Describe what occurs in the collecting tubule
Reabsorbs Na+ in exchange for secreting K+ and H+ (regulated by aldosterone).
Aldosterone acts on mineralocorticoid receptor to cause insertion of Na+ channels on luminal side. ADH acts on V2 receptor to cause insertion of aquaporin H2O channels on luminal side.
Principal cells: reabsorb H20 and Na+, secrete K+
Intercalated cells: secrete either H+ or HCO3- and reabsorb K+. Alpha cells secrete H+ (A for Acid) and Beta cells secrete HCO3- (B for Base).
Describe the Renal Tubular Defects
“Kidneys put out FABulous Gliterring Liquid”
- Fanconi Syndrome: defect in PCT; metabolic acidosis. Can be d/t Wilsons disease, ischemia, and nephrotoxins/drugs
- Bartter Syndrome: NK2Cl cotransporter defect in TALH. Hypokalemia, metabolic alkalosis, hypercalciuria.
- Gitelman Syndrome: NaCl defect in DCT. Hypokalemia and metabolic alkalosis without hypercalciuria.
- Liddle Syndrome: increased activity of Na+ channel in distal and collecting tubules. HTN, hypokaemia, metabolic alkalosis, decreased aldosterone. Tx = amiloride.
What causes respiratory acidosis vs. alkalosis
Respiratory acidosis: HYPOVENTILATION; airway obstruction, acute lung disease, chronic lung disease, opioids/sedatives, weakening of respiratory muscles.
Respiratory alkalosis: HYPERVENTILATION; hysteria, hypoxemia (e.g. high altitude), salicylates (early), tumor, pulmonary embolism
What causes metabolic alkalosis
With compensation (hypoventilation)
D/t loops, vomitting, antacid use, hyperaldosteronism
What are teh causes of normal anion vs. increased anion gap metabolic acidosis
Anion gap = Na - (Cl + HCO3)
Increased Anion Gap = MUDPILES = Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets or INH, Lactic acidosis, Ethylene glycol, Salicylates (late)
Normal Anion Gap = HARD-ASS = Hyperalimentation, Addison disease, RTA, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
Describes the type of RTAs
Non-anion gap hyperchloremic metabolic acidosis
Type 1 (distal, pH HIGH): defect in alpha intercalated cell to secrete H+. Thus, new HCO3- is not geenrated causing a metabolic acidosis. Associated wtih hypokalemia. Increased risk of calclium phopshate stones (d/t increase urine pH adn bone turnover). Causes: amphotericin B, analgesics, multiple myeloma
Type 2 (proximal, pH LOW): defect in proximal tuble HCO3- reabsorption result in increased excretion of HCO3- in urine and subsequent metabolic acidosis. Urine is acidified by alpha intercalated cells in CT. Associated with hypokalemia. Causes: Fanconi, chemicals toxic to proximal tubule (lead, aminoglycosides), and CA inhibitors.
Type 4 (hyperkalemia, pH LOW): Hypoaldosteronism, aldosterone resistance, or K+ sparing diuretics.
Benign epithelial cell tumor of the kidney
Renal oncocytoma: well-circumscribed with a central scar; large eosinophilic cells with abundant mitochondrial wihtout perinuclear clearning (vs. chormophobe RCC). Presents as painless hematuria, flank pain, and abdominal mass.
What is Wilms tumor (nephroblastoma) associated with?
MC renal malignancy of early childhood (ages 2-4). Presents with huge, palpable flank mass and/or hematuria. Involves LOF mutations of tumor suppressor genes WT1 or WT2.
May be part of Beckwith-Wiedemann syndrome or WAGR complex: Wilms tumor, Aniridia, Genitourinary malformation, and mental Retardation.
What shoudl you not confuse Wilms tumor with?
DO NOT confuse with neuroblastoma which is the MC tumro of adrenal medulla in children <4 y/o that originates from neural crest cells. Presents with abdominal distention and a firm, irregular mass that can cross midline (vs. Wilms tumor, which is smooth and unilateral). HVA in urine, Bombesin positive. Homer-Wright pseudorossettes (neuroblast around eosinophil neurophil).
What is associated with increased vs. decreased pulse pressure
Increased: hyperthyroidism, aortic regurgitation, arteriosclerosis, obstructive sleep apnea (increased sympathetic tone), excercise (transient)
Decreased: aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced heart failure.
What is SV affected by?
SV CAP: increased SV with increasedContractility, decreased Afterload, increased preload.
- <u>Contractility</u>: increased with catecholamines and digitalis. Decreased with b1 blockade, HF with systolic dysfunciton, acidosis, hypoxia/hypercapnea, and non-dihydropyridine CCBs
- <u>Preload</u>: depends on venous tone and circulating blood volume; approximated by ventricular EDV.vEnodilators (e.g. nitroglycerin) decrease prEload
- <u>Afterload</u>: approximated by MAP; chronic HTN (increased MAP) causes LV hypertrophy. vAsodilators (e.g. hydrAlazine) decrease Afterload.
- NOTE: ACE-I and ARBs decrease both preload and afterload
What are S3 and S4 heart sounds
S3: in early diastole durign rapid ventricular filling phase. Associated with increased filling pressures (e.g. mitral regurgitation, CHF) and more common in dilated ventricles (DCM)
S4 (“atrial kick”): in late diastole. High atrial pressure. Associated with ventricular hypertrophy. Seen with HCM, aortic stenosis, chronic HTN with LVH, and post-MI. LA must push against stiff LV wall.
When do you see wide splitting, fixed splitting, and paradoxical splitting?
<u>Wide splitting</u>: conditions that <strong>delay RV emptying (pulmonic stenosis, right bundle branch block)</strong>. Delay in RVemptying causes delayed pulmonic sound (regardless of breath). An exaggeration of normal splitting.
<u>Fixed splitting</u>: <strong>ASD</strong> causes L-R shunt with increased RA and RV volumes and increased flow thru pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed.
<u>Paradoxical splitting</u>: conditions that <strong>delay LV emptying (aortic stenosis, left bundle branch block).</strong>
Where is the location of synthesis for each of the following NTs: NE, Dopamine, 5-HT, ACh, GABA
NE: locus ceruleus (pons)
DA: ventral tegmentum and SNc (midbrain)
5-HT: Raphe nucleus (pons, medulla, midbrain)
ACH: basal nucleus of Meynert
GABA: nucleus accumbens
