USMLE Questions Summarized

Pulmonary How do you calculate the A-a gradient? What causes an A-a gradient and how is it useful in differentiating causes of hypoxemia?

Difference in partial pressure of Oxygen, PO2, between the alveolar PO2 and arterial PO2 PAO2=FiO2(713) - arterial PCO2/0.8 A-a gradient is caused by a mismatch between ventilation and perfusion. Hypoxemia of pulmonary origin causes an increased A-a gradient (>30). Hypoxemia of extrapulmonary origin has a normal A-a gradient.

What are some causes of ventilation defects? What are some causes of perfusion defects?

Impaired O2 delivery to the alveoli for gas exchange, e.g. from airway collapse due to respiratory distress syndrome or atelectasis. Decreased or absent blood flow to the alveoli, e.g. pulmonary embolus

What are some causes of diffusion defects?

O2 cannot diffuse across alveolar-capillary interface, e.g. pulmonary fibrosis or pulmonary edema. Causes decreased DLCO

What are some causes of shunting?

A shunt is technically blood going from right to left because of heart issues, e.g. right to left shunting from tetralogy of fallot. Depression of the respiratory center in the medulla (barbiturates, brain injury); upper airway obstruction (epiglottitis, croup); Chest bellows dysfunction (paralyzed diaphragm, ALS with degeneration of anterior horn cells).

What are some causes of hypoxemia with a normal Aa gradient? Define Functional Residual Capacity, FRC (Refer to Pulmonary attachment 1). Define Total Lung Capacity, TLC Define Residual Volume, RV

Total amount of air in the lungs at the end of normal expiration Total amount of air in a fully expanded lung Volume of air left over in the lung after maximal expiration: FRCERV

Define Tidal Volume, TV Define Forced Vital Capacity, FVC Define Forced Expiratory Volume, 1 second, FEV1 What is the normal FEV1/FVC? Define Expiratory Reserve Volume, ERV

Volume of air that enters/exits the lungs during normal respiration Total amount of air expelled after maximal inspiration Amount of air expelled from the lungs in 1 second after maximal inspiration 70-80% Amount of air forcibly expelled at the end of normal expiration

Describe spirometry in restrictive lung disease

TLC decreased, RV decreased, FEV1 decreased, FVC decreased, FEV1/FVC normal to increased, PaO2 decreased, A-a gradient increased (if disease of lungs, not just restriction of chest wall

Describe spirometry in obstructive lung disease

TLC increased, RV increased, FEV1 decreased, FVC decreased, FEV1/FVC decreased, PaO2 decreased, A-a gradient increased

Define Dyspnea and list some causes. Where are cough receptors located? What is the most common cause of cough with a normal CXR? What causes nocturnal cough?

Difficulty breathing. Can be due to stimulation of J receptors causing decrease in full inspiration. Also decreased compliance, e.g. interstitial fibrosis; increased airway resistance, e.g. chronic bronchiti; chest bellows disease, e.g. obesity; kyphoscoliosis, interstitial inflammation or fluid accumulation, e.g. left sided heart failure. They're at the bifurcation of airways, larynx and distal esophagus

Postnasal discharge GERD from acid refluxing into the bronchial tree at night. Bronchial asthma due to airway constriction

What causes productive cough?

What are some causes of hemoptysis?

Chronic bronchitis, usually associated with smoking cigarettes. Typical bacterial pneumonia. Bronchiectasis ACE inhibitors-inhibit degradation of bradykinin which causes mucosal swelling and irritation in the tracheobronchial tree. Aspirin causes increases in Leukotriene C, D and E4 which are all bronchoconstrictors Coughing up blood-tinged sputum. Caused by parenchymal necrosis and/or bronchial/pulmonary vessel damage. Chronic bronchitis (most common), pneumonia, bronchogenic carcinoma, tuberculosis, bronchiectasis, aspergilloma (fungus in a cavitary lesion)

Define tachypnea and list the causes.

Rapid, shallow breathing, more than 20 breaths/minute. Causes are restrictive lung disease, pleuritic chest pain, pulmonary embolus with infarction (tachypnea is the key finding)

What drugs cause cough? Define hemoptysis and the mechanisms.

Define tracheal shift and list the mechanism. What is vocal tactile fremitus? What causes decreased tactile fremitus? What causes increased tactile fremitus? What causes absent tactile fremitus? What causes dull and hyperresonant percussion?

shift of trachea from large changes in pleural fluid volume. Causes are pressure in contralateral lung, large tension pneumothorax, large pleural effusion; decreased volume in ipsalateral lung, large spontaneous pneumothorax, resorption atelectasis. Palpable thrill (vibration) transmitted through the chest when the patient says "99," or "E" Emphysema or asthma with increased AP diameter from increased total lung capacity. Sound travels better through fluid/solid so any type of lung consolidation, pneumonia, etc. Atelectasis/collapse of airways, fluid/effusion, air in pleural space (pneumothorax) Dull percussion comes from pleural effusions, lung consolidations, atelectasis. Hyperresonant percussion comes from pneumothorax, asthma or emphysema

What is the origin and mechanism of normal breath sounds? Where does laminar air flow start?

Normal breath sounds come from the trachea and are caused by air velocity and turbulence inducing vibrations in airway walls Terminal bronchioles where the increased surface area converts turbulent to laminar flow

What are vesicular breath sounds?

Sound like air blowing through a tube-this is normal over the trachea but is always abnormal over the bronchi. Causes a loud, high pitched sound with a tubular or hollow quality. Expiration is longer than inspiration. Means that there is consolidation or patent but partially collapsed bronchi Tracheal sounds that are modified in the alveoli. Inspiratory to expiratory ratio is 3:1. Diminished in emphysema and asthma due to increased AP diameter. Absent in pneumothorax, atelectasis or effusion

What are bronchovesicular breath sounds?

Normal breath sounds over the main bronchi with an equal inspiratory and expiratory ratio.

What are crackles and how are they caused?

Extra sounds, usually inspiratory, that sound like (you guessed it), crackles! Early and midinspiratory crackles are due to secretions in proximal large to medium sized airways. These clear with coughing. Late inspiratory crackles are due to reopening of distal airways partially occluded by increased interstitial pressure (fluid, transudate, pus). These do not clear with coughing and vary from fine to course

What are tubular breath sounds?

What is inspiratory stridor and how is it caused?

High pitched musical sound usually in expiration. Caused by inflammation of segmental bronchi and small airways by asthma or chronic bronchitis; pulmonary edema constricting airway (cardiac asthma); pulmonary infarction (release of TXA from platelets in the embolus causes bronchoconstriction Low pitched snoring sounds during inspiration or expiration. Due to secretions in large airways (bronchus or trachea). Usually clear with coughing, common in chronic bronchitis High pitched inspiratory sound. Indicates upper airway obstruction. Caused by epiglottitis (H. Influenzae), croup (parainfluenza)

What is a pleural friction rub and how is it caused? What does grunting in a newborn mean?

Two inflamed surfaces (pleural and parietal) rubbing against each other. Usually happens at the end of inspiration and beginning of expirations when things are changing direction. Caused by pleuritis due to cancer, infarction, pneumonia, serositis (SLE). Disappears with alrge effusion bc separates layers and stays with holding breath. Newborns should not grunt after 24 hours. It's a sign of respiratory distress syndrome.

What is wheezing and how is it caused? What are Rhonchi and how are they caused?

What is bronchophony and egophony? What is a flow volume loop?

Caused by alveolar consolidations. Spoken numbers, syllables are heard more distinctly through stethoscope. Egophany is when the patient says E and you hear an A through the stethoscope. Plot of inspiratory and expiratory flow rate(L/sec) versus lung volume(L)

Where is maximal inspiration on the diagram? (see Pulmonary attachment 2 for following)

Define Peak Expiratory Flow (PEF) What is the volume between points B and C? Describe the flow-volume loop in obstructive lung disease. Describe the flow-volume loop in restrictive lung disease.

What is Choanal Atresia?

What is a Nasal Polyp? Define Obstructive Sleep Apnea

Begins at point A, RV and goes to point B, TLC Begins at point B, TLC, and goes to point C, PEF. Occurs early in expiratory phase of loop due to elastic recoil of the lungs with low resistance and large caliber. Slope decreases to point A as resistance increases and airways get smaller. Vital Capacity TLC is increased and RV is increased. AKA left shifted curve. Decreased PEF. Can have concavity at C from mucus plugs or collapsed airways.

TLC is decreased, RV is decreased. AKA right shifted curve. Unilateral or bilateral bony septum between the nose and pharynx. Newborn urns cyanotic on breast feeding but crying causes them to pink up again Non-neoplastic tumefactions which develop as a response to chronic inflammation. Allergic polyps are the most common and are most often seen in asults with IgE mediated allergies. Also associated with aspirin and other NSAIDs b/c Cyclooxegenase block increases Leukotrienes whcih results in bronchoconstriction. Oten associated with CF Excessive snoring with intervals of breath cessation (apnea)

What causes obstructive sleep apnea?

Most commonly a result of obesity causing the pharyngeal muscles to collapse under the weight of the tissue. Can also result from tonsilar hypertrophy or nasal septum deviation.

What is the pathogenesis and clinical findings in sleep apnea?

Airway obstruction causes CO2 retention resulting in hypoxemia. Decreased PO2 and O2 saturation during apnea with increase in PCO2. See excessive snoring with apneic periods and excessive daytime somnolence. Can cause pulmonary arterial hypertension leading to Right Ventricular Hypertrophy and polycythemia secondary to hypoxemia.

What is a Nasopharyngeal Carcinoma?

Inflammation of the sinuses, most often maxillary or ethmoid sinuses. Caused by URI blocking drainage of sinuses into nasal cavity. Can be caused by a deviated nasal septum, allergic rhinitis, barotrauma, or cigarettes. Pathogens implicated are rhinovirus, strep pneumoniae, anaerobes (chronic sinusitis), systemic fungi (diabetics due to Mucor species). Most common malignant tumor of the nasopharynx, more common in males and increased incidence in the Chinese and African populations. Closely related to EBV. Often causes squamous cell carcinoma or undifferentiated cancers which can metastasize to cervical lymph nodes.

Define Laryngeal Carcinoma.

Carcinoma most commonly located on the true vocal cords. Mostly keratinizing squamous cell carcinomas, mostly in med. Related to cigarette smoking, alcohol (synergistic with cigarettes), HPV 6 and 11 and squamous papillomas and papillomatosis. Persistent hoarseness from cervical lymphadenopathy is common.

Define Sinusitis and describe its causes.

What is Atelectasis?

Loss of lung volume due to inadequate expansion of the airspaces (collapse). Collapse happens because of lack of air and distal resorption of air through pores of Kohn in the alveolar walls. May see ipsilateral elevation of the diaphragm and tracheal deviation. Treat with incentive spirometry, CPAP or PEEP.

What is resorption atelectasis? What is compression atelectasis?

Airway obstruction in bronchiols, segmental bronchi or bronchi, by thick secretions which prevents air from reaching the alveoli. Can be caused by mucus or mucopruluent plug after surgery, aspiration of foreign material or centrally located bronchogenic carcinoma. Air or fluid in the pleural cavity under increased pressure collapses small airways beneath the pleura.

What is atelectasis due to loss of surfactant?

What is Respiratory Distress Syndrome?

Synthesized by Type II pneumocytes starting in the 28th week of gestation. Stored in lamellar bodies. Major component is phosphatidylcholine (lecithin). Synthesis is increased by cortisol and thyroxine but decreased by insulin. Surfactant reduces surface tension so airways don't collapse. Without surfactant, airways can collapse causing atelectasis. Decreased surfactant in lungs results in atelectasis and respiratory distress from massive intrapulmonary shunting. Collapsed alveoli are lined by hyaline membranes (from protein leaking out of damaged alveoli). Causes respiratory difficulty, grunting, tachypnea, intercostal retractions and hypoxemia with respiratory acidosis.

What is Pulmonary Edema and what are the causes?

Superoxide radicals from O2 therapy can cause blindness (retinopathy of prematurity) and damage to small airways (bronchopulonary dysplasia). Can cause intraventricular hemorrhage, patent ductus arteriosus from hypoxemia, necrotizing enterocolitis from intestinal ischemia (allows entry of gut bacteria into intestinal walls) and hypoglycemia leading to seizures and neuronal damage. Collection of fluid. Can be due to Starling forces from left sided heart failure, volume overload or mitral stenosis. This produces transudate. Can be exudate from microvascular or alveolar injury resulting from infection. Can be from aspiration, drugs, high altitude or ARDS.

What is Acute Respiratory Distress Syndrome, ARDS?

Noncardiogenic pulmonary edema from acute alveolar-capillary damage. Caused by direct injury to the lungs or systemic disease. Risk factors are gram (-) sepsis, gastric aspiration, severe trauma and shock, diffuse pulmonary infections (SARS, hantavirus), Heroin, smoke inhalation, acute pancreatitis, cardiopulmonary bypass, DIC, amniotic fluid or fat embolism.

What is the pathogenesis of ARDS?

Acute damage to alveolar capillary walls and epithelial cells results in alveolar macrophages releasing cytokines. Capillary damage and chemotactic factors allow neutrophils and exudate to leak producing hyaline membranes. Neutrophils damage Type I and II pneumocytes, reducing surfactant and causing atelectasis.

What are clinical signs/symptoms of ARDS? What are the subtypes of Pneumonia?

Dyspnea/tachypnea, late inspiratory crackles, severe hypoxemia not responsive to 100% O2, increased pulmonary wedge pressure, increased A-a gradient, bilateral infiltrates and consolidations. Community acquired which can be typical or atypical and hospital acquired, aka nosocomial.

What are complications of respiratory distress syndrome?

Describe clinical findings in lobar pneumonia.

Most caused by bacterial pathogens, particularly Strep Pneumoniae. Pathogenesis is via inhalation of aerosol from infected person or aspiratin of nasopharyngeal flora while sleeping. Begins as acute bronchitis and spreads locally into the lungs, usually lower lobes or right middle lobes. Causes patchy consolidations and may have microabscesses. Complete or almost complete consolidation of a lobe of the lung. Can be complicated by lung abscesses, empyema or sepsis. See sudden onset of fever with productive cough, chest pain, tachycardia, dullness to percussion, increased tactile fremitus, late inspiratory crackles, bronchial breath sounds, bronchophany and egophany.

Describe clinical findings in atypical pneumonia.

Usually caused by mycoplasma pneumoniae, also chlamydophilia pneumoniae, RSV, influenzavirus, and adenovirus. Contracted by inhalation of droplets. Causes patchy, mononuclear infiltrate but the alveolar spaces are usually free of exudate. Insidious onset with nonproductive cough, low grade fever, chest pain, flu like symptoms including pharyngitis, laryngitis, myalgia and headache. No consolidation.

Describe clinical findings in nosocomial pneumonia.

Happens in patients with severe underlying disease, immunosuppresion, or who are on antibiotic therapy. Respirators are the most common source of infection. Usually gram (-) bacteria, often pseudomonas, E coli, or gram (+) like staph aureus. In immunocompromised, can be opportunistics like CMV, Pneumocystis Jirovecis, Aspergillus-fumigatus.

Describe the pathogenesis of typical pneumonia. Describe the pathogenesis of bronchopneumonia.

Describe pneumonia from Tuberculosis.

From inhalation of Mycobacterium Tuberculosis. Infects phagosomes of alveolar macrophages and produces a protein that prevents fusion of the lysosome with the phagosome. Strict aerobe, acid fast. Cord factor is major virulence factor. Drug resistance by mutations in mycolic acid or catalase peroxidase (activates Isoniazid).

Describe Primary TB Infection.

Subpleural location, usually upper part of lower lobes or lower part of upper lobes. Causes Ghon focus (caseous necrosis) in periphery and Ghon complex in hilar lymph nodes. Produces a calcified granuloma or area of scar tissue

Describe Secondary TB Infection. Describe pneumonia from Mycobacterium Avium Intracellulare What is the most common cause of the common cold? What does Coxsackievirus cause?

Due to reactivation of primary TB. Usually involves apices in upper lobes b/c increased V/Q ratio. Causes cavitary lesions from release of cytokines by T Cells. Causes fever, drenching night sweats, weight loss. May cause miliary TB with invasion into bronchus, lymphatics or extrapulmonary sites like the kidney. Spread to vertebra is called Pott's disease. Atypical mycobacterium causing atypical pneumonia in AIDS patients. Happens when CD4+ T Cell count falls below 50 cells/mm3. Often disseminates and co-occurs with systemic fungal infection. Rhinovirus, transmitted by hand to nose/eye contact. Less common are coronavirus, adenovirus, influenza C and coxsackievirus Acute chest syndrome: fever with pleuritis

What is the most common viral cause of atypical pneumonia and bronchiolitis in children and otitis media in older children? What is the most common viral cause of laryngotracheobronchitis (croup) in infants?

What is the most common viral cause of pneumonia in immunocompromised hosts? What can happen with aspirin ingestion when a child has influenza? What are signs and symptoms of Rubeola infection? What are signs and symptoms of SARS What is Hantavirus pulmonary syndrome? What is the second most common (bacterial) cause of atypical pneumonia?

Respiratory Syncitial Virus. Occurs in late fall and winter. Can give Palivizumab to high risk kids (passive immunity) Parainfluenza. Causes inspiratory stridor from sunmucosal edema obstructing the upper airway. Anterior CXR shows steeple sign in anterior neck.

Cytomegalovirus. Enlarged alveolar macrophages/pneumocytes with basophilic inclusions surrounded by a halo. Reye's Syndrome. Causes fatty liver, severe encephalopathy, palmar rash, comiting, lethargy and stupor. Measles. Fever, cough, conjunctivitis and excessive nasal mucous. Koplik spots in the mouth precede rash. Warthin-Finkeldey multinucleated giant cells are characteristic Infects lower respiratory tract and then spreads systemically thus severe respiratory infection and systemic symptoms. Transmission is via inhalation of urine/feces from deer mice in SW US. Causes ARDS, hemorrhage and renal failure. Chlamydophilia pneumoniae. Has a seroepidemiologic association with coronary artery disease. Treat with doxycycline.

What is a common bacterial cause of newborn pneumonia?

Chlamydia trachomatis from passage through infected birth canal. Afrebile with staccato cough, conjunctivitis and wheezing. Treat with erythromycin.

What is the most common baterial cause of atypical pneumonia? Describe the signs and symptoms of Coxiella Burnetti infection

Mycoplasma Pneumoniae. Insidious onset with low grade fever. Can cause bullous myringitis(inflamed Tympanic membrane), cold autoimmune hemolytic anemia from anti-IgM antibodies.

What is the most common cause of community acquired lobar pneumonia?

Atypical pneumonia, myocarditis, granulomatous hepatitis. Associated with dairy farmers and vetrinarians.

What are signs and symptoms of infection with Bacillus Anthracis?

Strep pneumoniae. Rapid onset, productive cough and signs of lobar consolidation. Can test with urine screen. Commonly superimposed on measles or influenza pneumonia or in CF or IV drug users. Hemorrhagic pulmonary edema, yellow sputum, abscess formation and tension pneumatocysts (intrapleural blebs) which can rupture and produce tension pneumothorax. Causes toxin-induced pseudomembranous inflammation producing a shaggy gray membrane in the oropharynx and trachea. Can cause toxic myocarditis from impaired B oxidation of fatty acids in the heart. Cutaneous anthrax initially looks like a scab but swells to form a black scab (eschar) with an area of central necrosis. Pulmonary anthrax causes necrotizing pneumonia, meningitis, splenomegaly and systemic dissemination.

What are signs and symptoms of Actinomyces infection?

Normal flora in tonsils and adenoids. Can produce draining sinuses in the jaw, chest cavity and abdomen. Pus contains yellow specks (sulfur granules) which contain the bacteria.

What are signs/symptoms of pneumonia from Staph Aureus? Describe signs and symptoms of infection with Corynebacterium Diptheriae.

What are signs and symptoms of Nocardia infection?

What are signs and symptoms of infection with Bordatella Pertussis? What are signs and symptoms of infection with H. Influenzae? What are signs and symptoms of Moraxella Catarrhalis infection? What are signs and symptoms of infection with Pseudomonas Aeruginosa? What are signs and symptoms of Klebsiella Pneumoniae infection?

Granulomatous microabscesses in the lungs. Often disseminates to CNS and kidneys. Produces whooping cough-inspiratory whoop between coughing fits. Catarrhal phase is 1-2 weeks and involves mild coughing, rhinorrhea and conjunctivitis. Paroxysmal phase lasts 2-5 weeks and involves coughing in succession followed by inspiratory whoop and absolute lymphocytosis (20,000-50,000). Convalescent pahse lasts 1-2 weeks or more and involves a slow decline in lymphocytosis and coughing. Can cause hemorrhage into skin, conjunctiva, bronchus, brain or rectal prolapse from coughing. Also otitis media and meningoencephalitis. Common cause of sinusitis, otitis media, conjunctivitis, epiglottitis with inspiratory stridor. Swelling of epiglottis produces a thumbprint sign on lateral xray of the neck. Can cause COPD exacerbation. Causes typical pneumonia, especially in the elderly. Causes acute COPD exacerbation, chronic bronchitis, sinusitis and otitis media. Green sputum (pyocyanin), nosocomial pneumonia and pneumonia in CF patients. Often associated with infarction from vessel invasion. Most common gram negative that causes lobar pneumonia and typical pneumonia in nursing home patients and alcoholics. Associated with blood tinged, thick, mucoid sputum, lobar consolidations and abscesses.

What are signs and symptoms of infection with Legionella Pneumophila?

Pneumonia associated with high fever, dry cough, flu like symptoms. May produce tubulointerstitial disease with destruction of the JG apparatus leading to hyporeninemic hypoaldosteronism (type IV renal tubular acidosis-hyponatremia, hyperkalemia, metabolic acidosis). Urine antigen is an excellent screen.

What are signs and symptoms of infection with Yersinia Pestis?

The plague!!! Macrophages cannot kill bacteria due to protection by V and W antigens so you get really sick. Bubonic causes infected lymph node which enlarge and mat together and drain to the surface (buboes). Pneumonic and septicemic are just what they sound like. Treat with gentamicin and doxycycline (pneumonic) or gentamicin and streptomycin (bubonic)

What are signs and symptoms of infection with Cryptococcus Neoformans?

Granulomatous inflammation with caseation. Acquired from pigeon feces.

What are signs and symptoms of infection with Aspergillus Fumigatus? What are signs and symptoms of infection with Mucor species?

Aspergilloma-fungus ball that develops in a prior cavitary lesion and cause massive hemoptysis. Allergic bronchopulmonary aspergillosis-type I and III hypersensitivity. IgE increase, eosinophilia, intense inflammation of airways and mucous plugs in terminal bronchioles resulting in bronchiectasis and interstitial lung disease. Vessel invasion with hemorrhagic infarctions and necrotizing bronchopneumonia. Happens to diabetic and immunosuppressed patients. Vessel invasion producing hemorrhagic infarcts in the lungs. Invades the frontal lobes when there is diabetic ketoacidosis (rhinocerebral mucormycosis).

What are signs and symptoms of infection with Coccidoides Immitis?

What are signs and symptoms of infection with Histoplasma Capsulatum? What are signs and symptoms of infection with Blastomyces Dermatitidis?

What are signs and symptoms of infection with Pneumocystis Jiroveci?

What are the common causes of lung abscesses? What are the most common pathogens in lung abscesses?

Contracted by inhaling arthrospores in dust in arid areas (increased after earthquakes). Causes flu-like symptoms and erythema nodosum and granulomatous inflammation of the lungs with caseous necrosis. Most common systemic fungal infection, endemic in Ohio and Mississippi river valleys. Causes granulomatous inflammation with caseous necrosis, simulating TB. Produces coin lesions, consolidations, milary spread and cavitation. Causes marked dystrophic calcification of granulomas and multiple calcifications in the spleen. Male dominant disease, common in Great lakes, central and southern US. Causes skin disease that simulates squamous cell carcinoma and lung disease with granulomatous inflammation and caseous necrosis. Cysts and trophozoites attach to Type I pneumocytes. Most common AIDS-defining infection, CD4+ count Ovarian>Cervical. Worst Prognosis- Ovarian>Cervical>Endometrial Premature atresia of ovarian follicles in women of reproductive age. Presents with signs of menopause after puberty but before age 40. See decreased estrogen but increased LH and FSH b/c no feedback. Polycystic ovarian syndrome, obesity, Asherman's Syndrome (adhesions), HPO axis abnormalities, premature ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, Cushing Syndrome and adrenal insufficiency Increased LH production leading to anovulation, hyperandrogenism due to deranged steroid synthesis by theca cells. Enlarged bilateral cystic ovaries manifest clinically with amenorrhea, infertility, obesity and hirsutism. Associated with insulin resistance, increased risk of endometrial cancer. Treatment is weight loss, OCP, gonadotropin analogs, clomiphene or surgery. Increased LH and FSH and increased Testosterone. Distention of a ruptured Grafian Follicle. May be associated with hyperestrinism and endometrial hyperplasia. Hemorrhage into persistent corpus luteum. Commonly regresses spontaneously. Commonly bilateral or multiple cysts. Due to gonadotropin stimulation. Associated with choriocarcinoma and moles.

What is a Chocolate Cyst? What age group most commonly gets Ovarian Cell Tumors? What is a Dysgerminoma?

What is a Choriocarcinoma? What is a yolk sac (endodermal sinus) tumor?

Blood-containing cyst from ovarian endometriosis. Varies with the menstrual cycle. Most common in adolescents Malignant, equivalent to a male seminoma, but rarer (1% vs 30%). Sheets of uniform cells with hCG and LDH. Rare but malignant. Can develop during pregnancy in mother or the baby. Large, hyperchromatic syncitiotrophoblastic cells. Increased frequency of theca-lutein cysts. Along with moles, comprise spectrum of gestational trophoblastic neoplasia. hCG is the tumor marker. Aggressive malignancy in the ovaries (testes in boys) and sacrococcygeal area of young children. These are yellow, friable, solid masses. 50% have Schiller Duval bodies that resemble glomeruli. Alpha fetoprotein is the tumor marker.

What is a serous cystadenoma?

90% of ovarian germ cell tumors. Contain cells from 2-3 germ layers. Mature teratomas/Dermoid cysts are the most frequent benign ovarian tumors/teratomas. Immature teratomas are aggressively malignant. Struma Ovarii contain functional thyroid tissue. Can present as hyperthyroidism. Makes up about 20% of ovarian tumors. Frequently bilateral, lined with Fallopian tube-like epithelium. Benign.

What is a serous cystadenocarcinoma?

Makes up about 50% of ovarian tumors, malignant and frequently bilateral.

What is a Mucinous Cystadenoma? What is a Mucinous Cystadenocarcinoma? What is a Brenner tumor? What is a Fibroma? What is Meigs' Syndrome?

Multilobular cyst lined by mucus-secreting epithelium. Benign. Intestine-like tissue. Malignant! Pseudomyxoma peritonei- intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor. Benign tumor that looks like the bladder. Bundles of spindle shaped fibroblasts. Associated with Fibromas. Triad of ovarian fibroma, ascites and hydrothorax. Causes pulling sensation in the groin.

What is a Granulosa Cell Tumor?

Secretes estrogen-causes precocious puberty. Can cause endometrial hyperplasia or carcinoma in adults. See Call-Exner bodies-small follicles filled with eosinophilic secretions. Abnormal uterine bleeding.

What is a teratoma?

What is a Krukenberg tumor? What causes squamous cell carcinoma of the vagina? What predisposes to Clear Cell Adenocarcinoma? Who is affected by Sarcoma Botryoides (variant of Rhabdomyosarcoma) How do Bartholin's gland cyst present?

GI Malignancy that metastasizes to the ovaries, causing a mucin-secreting signet cell adenocarcinoma. Secondary to squamous cell carcinoma of the cervix. Affects women who had exposure to DES in utero.

Affects girls < 4 years of age. Spindle shaped tumor cells that are desmin positive. Rare. Present with pain in the labia majora. Can result from previous infection.

What is a Fibroadenoma of the breast? What is an Intraductal Papilloma? What is a Phyllodes Tumor? How do malignant breast tumors arise and when/where are they most common? What are some risk factors for malignant breast tumors? What is a Ductal Carcinom in Situ (DCIS)? What is invasive ductal carcinoma? What is What is breast? What is breast? What is breast?

an invasive Lobular tumor? a medullary tumor of the

Small, mobile, firm mass with sharp edges. Most common tumor in those 30 years of age. Breast abscess. During breast feeding. Increases risk of bacterial infection through cracks in the nipple. Staph Aureus is the most common pathogen. A benign, painless lump. Forms as a result of injury to breast tissue. Up to 50% of patients may not report trauma. Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter's syndrome or drugs (estrogen, marijuana, heroin, psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol, Ketoconazole).

What is the order of structures in the breast starting at the nipple?

Nipple, Lactiferous sinus, major duct, terminal duct, lobules. All surrounded by stroma

What tumors occur at each of these structures? How does prostatitis present?

Nipple-Paget's disease, breast abscesses. Lactiferous sinus-Intraductal papilloma, breast abscess, mastitis. Major duct-Fibrocystic change, ductal cancer. Terminal ducts-Tubular carcinoma. Lobules-lobular carcinoma, sclerosing adenitis. Stroma-Fibroadenoma, phyllodes tumor. Dysuria, frequency, urgency, low back pain.

What are causes of acute prostatitis? What are causes of chronic prostatitis?

What is Benign Prostatic Hyperplasia (BPH)? How do you treat BPH?

What is Prostatic adenocarcinoma?

What is cryptorchidism? How common are testicular germ cell tumors?

What is a Seminoma?

What is an embryonal carcinoma? What is a yolk sac (endodermal sinus) tumor in a man? What is a Choriocarcinoma in a man? What is a teratoma in a man? How common are testicular non-germ cell tumors?

Usually bacterial, especially E. Coli May be bacterial or abacterial. Hyperplasia (not hypertrophy) of the prostate gland. May be due to an age related increase in estradiol with possible sensitization of the prostate to the growth-promoting effects of DHT. Characterized by a nodular enlargement of the periurethral (lateral and middle) lobes, which compress the urethra into a vertical slit. Often present with increased frequency of urination, nocturia, difficulaty starting and stopping the stream of urine and dysuria. May lead to distention and hypertrophy of the bladder, hydronephrosis and UTI's. Not considered premalignant. Do see increased free PSA but not rapidly increasing like in cancer. Use alpha antagonists like Terazosin, tamulosin, which cause relaxation of smooth muscle. Common in men >50. Arises most frequently from the posterior lobe of the prostate(peripheral zone) and is most commonly diagnosed by digital rectal exam and prostate biopsy. Prostatic acid phosphatase and PSA are the most useful tmor markers. See increased total PSA with decreased fraction of free PSA. Osteoblastic metastases in bone may develop in later stages and appears as lower back pain and an increase in serum alkaline phosphatase and PSA. Undescended testis. Lack of spermatogenesis due to increased body temperature. Also associated with increased risk of germ cell tumors. Prematurity increases the risk of cryptorchidism. 95% of all testicular tumors. May present as a mixed germ cell tumor. Malignant, painless, homogenous testicular enlargement. Most common testicular tumor, mostly affecting males age 15-35. See large cells in lobules with watery cytoplasm and a fried egg appearance. These are radiosensitive, only metastasize late and have a great prognosis. Malignant, painful tumor with a worse prognosis than a seminoma. Often glandular or papillary morphology. Can differentiate and become other tumors and is associated with increased AFP and hCG. Yellow, mucinous tumor analagous to an ovarian yolk sac tumor. See Schiller Duval bodies which resemble primitive glomeruli. Malignant, hCG secreting tumor. Has distinct syncytiotrophoblastic and cytotrophoblastic elements. Causes hematogenous metastases. Similar to females except that mature teratomas in men are usually malignant. 5% of all testicular tumors, most of which are benign.

What is a Leydig Cell Tumor? What is a Sertoli Cell Tumor? What is testicular lymphoma? What What What What

is is is is

a a a a

tunica vaginalis lesion? Variocele? Hydrocele? spermatocele?

Androgen producing tumor which causes gynecomastia in men, precocious puberty in boys. Contains Reinke crystals and is golden brown in color. Androblastoma from the sex cord stroma. Most common testicular cancer in older men. It's pretty much lymphoma in the testicles.

What is Bowen's Disease? Qhat is Erythroplasia of Queyrat? What is Bowenoid papulosis? What is Squamous Cell Carcinoma of the penis? What is Peyronie's Disease? What changes are seen in Decidualization?

A lesion in the serous covering of the testis. Presents as testicular masses that can be transilluminated. Dilated vein in pampinoform plexus which can result in infertility. Looks like a bag of worms. Increased fluid secondary to incomplete fusion of the processus vaginalis Dilated epididymal duct Gray, solitary, crusty plaque, usually on the shaft of the penis or on the scrotum. Peak incidence is in the 5th decade of life. Progresses to invasive squamous cell carcinoma in 2. Increased serum testosterone and androstendione. Increased serum estrogen. Weight reduction in obese women. Low dose OCP's or medroxyprogesterone to suppress steroidogenesis and LH. Can use Spironolactone if OCP's are unacceptable to block androgen receptors on the hair follicle. LHreleasing hormone analogs inhibit ovarian androgen production. Loss of blood >80 mL per period. It's likely if sheets are stained despite heavy protection. Excessive passage of clots indicates that plasmin does not have enough time to dissolve clot. Painful menses, occuring in approximately 50% of women. Primary type occurs in ovulatory cycles due to increased prostaglandin PGF-2alpha. See increased uterine contractions from increased prostaglandins. The secondary type is from endometriosis, adenomyosis, leiomyomas, or cervical stenosis. NSAID's, OCP, nifedipine, magnesium sulfate Essentially deal with the underlying disease. Abnormal uterine bleeding that is unrelated to an anatomic cause. Note that this is a diagnosis of exclusion. Menorrhagia, Hypomenorrhea, Metrorrhagia, Menometrorrhagia, Oligomenorrhea, Polymenorrhea

What is Primary Amenorrhea? What is Secondary Amenorrhea?

Anovulatory cycle in 90% of cases but less than 10% due to anovulation during reproductive years. Excessive estrogen stimulation relative to progesterone resulting in an absent secretory phase. It produces excessive endometrial hyperplasia and excessive bleeding. Inadequate luteal phase resulting in inadequate maturation of the corpus luteum. This causes inadequate synthesis of progesterone and delay in the development of the secretory phase. May see decreased 17-OH progesterone . If the follicle size is normal, supplement progesterone. If the follicle size is inadequate, give clomiphene sulfate. Absence of menses by age 16. Most cases are due to constitutional delay with a family history of delayed menses. Absence of menses for 3 months, most commonly due t pregnancy.

What are some causes of amenorrhea?

Hypothalamic or pituitary dysfunction resulting in decreased LH and FSH which results in decreased estrogen and progesterone. Ovarian disorders cause problems in synthesis of estrogen or progesterone.

What are causes of abnormal vaginal bleeding in a pre-pubertal girl? What are some causes of abnormal vaginal bleeding between menarche and 20 years?

Vulvovaginitis, poor hygeine, infection, gonrrhea, sexual abuse, foreign bodies, embryonal rhabdomyosarcoma

What causes ovulatory dysfunctional uterine bleeding? How do you treat ovulatory dysfunctional uterine bleeding?

Anovulatory dysfunctional uterine bleeding, Von Willebrand's disease

What are some causes of abnormal vaginal bleeding between ages 20-40? What are some causes of abnormal vaginal bleeding after age 40? What part of the placenta covers the fetal surface? What covers the chorion? What covers the maternal surface of the placenta?

Pregnancy and related complications, ovulatory dysfunctional uterine bleeding, PID, hypothyroidism, submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis

Anovulatory dysfunctional uterine bleeding, endometrial hyperplasia, cancer. Entirely covered by the chorionic plate. The chorionic villi vessels converge with the umbillical cord. Chorion is covered with amnion Contains cotyledons covered by decidua basalis.

Where do the chorionic villi project? What does the intervillous space contain? What lines the chorionic villi? What forms the outside layer of the trophoblast? What does the Syncytiotrophoblast do? What forms the inside layer of the trophoblast? How many vessels are contained in the umbillical cord? What risks are related to a single umbillical artery? What causes most placental infections?

Into the intervillous space Maternal blood that delivers oxygen and nutrients and spiral arteries from the uterus that empty into the space Trophoblastic tissue

How should you treat a placental infection even if culture is negative? What is Funisitis? What is Placentitis? What is chorioamnionitis? What complications might arise from chorioamnionitis? What is Placenta Previa?

Treat prophylactically with IV Ampicillin+Erythromycin followed by PO amoxicillin and erythromycin. If culture positive you can give IV penicillin or ampicillin Infection of the umbillical cord Infection of the placenta Infection of the fetal membranes

How does Placenta Previa present? How do you diagnose Placenta Previa?

Syncytiotrophoblast. Synthesizes hCG, and HPL which directly correlates with placental mass and has anti-insulin activity. Cytotrophoblastic tissue One umbillical vein and two umbillical arteries. The vein carries the oxygenated blood in this case Increased incidence of congenital anomalies, defects including cardiovascular defects, trisomy 18 and esophageal atresia. Ascending infections, often from premature rupture of membranes

Neonatal sepsis and meningitis. Treat with Cefoxitin or Ticaricillin-Clavulanate Implantation over cervical os. Previous C Section is major risk factor Painless vaginal bleeding, usually second or third trimester. The uterus is soft and non-tender and fetal distress is usually not present. Do not do a pelvic exam. Transabdominal ultrasound localizes the placenta and transvaginal ultrasound confirms placenta previa.

What is Abruptio Placentae? What are risks for abruptio placentae? What are the clinical signs of abruptio placentae? What is Placenta Acreta?

What is Velamentous insertion? What risks do accessory lobes of the placenta pose? What can cause an enlarged placenta? What type of placentas do Monozygotic twins have? What risks are associated with monochorionic, diamnionic placentas? What is Preeclampsia? What are risk factors for Preeclampsia? What is the pathogenesis of Preeclampsia? What are pathologic findings in PreEclampsia? What are clinical findings in PreEclampsia? What are some other symptoms in Pre-Eclampsia? What is a Hyaditiform Mole?

What is a complete Hyaditiform Mole? Which type of Mole has an increased risk of Choriocarcinoma?

Premature separation of the placenta due to formation of a retroplacental clot. This separates the placenta from the implantation site. This is most common cause of late pregnancy bleeding Hypertension, smoking, cocaine, advanced maternal age, trauma, chorioamnionitis, premature membrane rupture, previous abruptio placentae. Painful uterine bleeding, forceful uterine contractions or signs of preterm labor, usually see evidence of fetal distress Direct implantation into muscle without intervening decidua. Causes great risk for hemorrhage during delivery, commonly requiring surgery to control bleeding. Often requires hysterectomy. Umbilical cord inserts away from the placental edge-the vessels pass to the placenta through the membranes between the amnion and chorion. Causes increased risk for hemorrhage if the vessels are torn. Deliver by C Section to avoid vessel tear. Increased risk of hemorrhage if they are detached. Diabetes mellitus, Rh hemolytic disease of the newborn, congenital syphilis Monochorionic and monoamniotic although they can have dichorionic placentas

Twin Twin Transfusion syndrome. Toxemia of pregnancy First pregnancy, more common in women 35 years, history of previous preeclampsia, positive family history, multiple gestations, african american, thrombocytosis, obesity Abnormal placentation causing mechanical or functional obstruction of the spiral arteries. The abnormal trophoblastic tissue invades the spiral arteries. Imbalance favors vasoconstriction over vasodilation (decreased PGE2 and NO, increased TXA2, Ang II and increased sensitivity to Ang II) Premature aging of the placenta, multiple placental infarctions, spiral arteries show atherosclerosis Hypertension, proteinuria from leaky capillaries (increased inflammation), dependent pitting edema from loss of albumin, weight gain, seizures in eclampsia, swollen endothelial cells in glomerular capillaries producing oliguria. Right upper quadrant pain and hepatomegaly, periportal necrosis with increased transaminases, HELLP syndrome Benign tumor of the chorionic villus from an empty egg and 2 sperm or an egg and 2 sperm. The entire placenta is neoplastic. Dilated swollen villi without fetal blood vessels. No embryo is present. Ovum 46, XX, lacking maternal chromosomes. The chromosomesare derived from the father, either 2 sperm or duplicated 23X sperm in the ovum Complete mole. Presents with painless vaginal bleeding in fourth, fifth month of pregnancy. Causes severe vomiting, pre-eclampsia, uterus that is too large for gestational age, increased hCG for gestational age, and snowstorm appearance on ultrasound.

What is a partial Hyaditiform Mole? What is a Choriocarcinoma? Where does Choriocarcinoma metastasize? What is the composition of amniotic fluid? What is the quantity of amniotic flud maintained?

Not all villi are neoplastic or dilated? Embryo is present but this is triploid. Egg with 23X is fertilized by 23X and 23Y sperm. (Not that if the embryo is doubled, it's not considered a mole). This has a low risk of choriocarcinoma. malignant tumor composed of syncytiotrophoblast and cytotrophoblast without chorionic villi. Risks are complete mole, spontaneous abortion and normal pregnancy Lungs and vagina-hemorrhagic lesions Predominantly fetal urine, initially plasma ultra-filtrate from mom. High salt content causes ferning when dried on a slide-good sign of premature rupture of amniotic sac.

What is Oligohydramnios? What can Alpha Fetoprotein indicate in pregnancy? What does the Lecithin to Sphingomyelin ratio indicate?

Swallowed and recycled by the fetus. Excessive amniotic fluid. Causes are tracheoesophageal fistula, duodenal atresia, maternal diabetesmaternal hyperglycemia causes fetal hyperglycemia resulting in fetal polyuria. Decreased amount of amniotic fluid. Caused by juvenile polycystic kidney disease, fetal genitourinary obstruction, uteroplacental insufficiency and premature rupture of membranes. Increased maternal AFP indicates open neural tube defects (often related to Folate deficiency). Decreased maternal AFP can indicate Down syndrome. Lecithin is synthesized by type II Pneumocytes which decreases alveolar tension to prevent atelectasis. L:S ratio >2 indicates adequate surfactant.

What can increase surfactant production in the fetus?

Cortisol and thryroxine increase surfactant synthesis. Maternal administration of glucocorticoids can increase surfactant if the baby must be delivered before term. Insulin inhibits surfactant synthesis.

Where is estriol made in pregnancy?

Derived from fetal adrenal gland (DHEA-S) which is aromatized by the placenta.

What is Polyhydramnios?

What part of estriol synthesis does the fetal adrenal cortex control? What does the fetal liver do in estriol synthesis? What does the maternal placenta do in estriol synthesis? What does the maternal liver do to estriol? What does decreased estriol indicate? What is the triad of markers in Down syndrome? What is the most high density location of breast tissue? What effects do sex hormones have on the breast during the menstrual cycle?

Fetal adrenal cortex converts pregnenolone from the placenta to DHEA-S. Hydroxylates DHEA-S to 16-OH-DHEA-S Initially converts LDL to pregnenolone for fetal processing. Placental sulfatase then cleaves off the sulfate from 16-OH-DHEA-S and converts it to free unbound estriol via aromatase. Conjugates it to estriol sulfate and estriol glucosiduronate which is then excreted in the maternal urine and bile. Sign of fetal-maternal-placental dysfunction Decreased urine estriol, decreased AFP, increased serum Beta-hCG Upper outer quadrant-thus cancer is most commonly located in this location. Also underneath the nipple.

Estrogen stimulates ductal and alveolar growth. Progesterone stimulates alveolar differentiation.

What hormones affect lactation? Where do outer quadrant breast cancers drain? Where do inner quadrant breast cancers drain? What are normal causes of Galactorrhea? What are pathologic causes of Galactorrhea? What causes Bloody nipple discharge? What causes prululent nipple discharge? What causes Green-Brown nipple discharge? What is the most common cause of Breast Pain? What is Mondor's disease?

Prolactin-stimulates and maintains lactogenesis. Oxytocin-released by the suckling reflex which causes expulsion of milk into the ducts. Axillary lymph nodes Internal mammary lymph nodes. Mechanical stimulation of the nipple from prolonged suckling or sexual intercourse. Prolactinoma, primary hypothyroidism (decreased T4 causes increased TRH which stimulates PRL), drugs like OCP's, phenothiazines, methyldopa, H2-Receptor blockers and angiolytics. Intraductal papilloma, ductal cancer Acute mastitis due to Staph A., usually related to breast feeding Mammary duct ectasia (plasma cell mastitis)

What is sclerosing adenosis?

Fibrocystic change Superficial thromboplebitis of veins overlying the breast, presenting as a palpable, painful cord. Most common painful breast mass in women HCO3 - Metabolic alkalosis + metabolic acidosis. AG15 because proportionately more Urea is reabsorbed from the low flow rate.

What is Renal Azotemia and what are some causes?

Increased BUN and Cr from parenchymal damage to the kidneys. Some causes are Acute Tubular Necrosis and Chronic Renal Failure. BUN:Cr 15. Obstruction to flow decreases GFR resulting in back diffusion of urea (not Cr) into blood and a disproportionate increase in BUN. 97-137 mL/minute. Less than 100 mL/minute is abnormal.

What are some causes of decreased CR Clearance?

Normal pregnancy (Increased plasma volume means increased GFR), early diabetic glomerulopathy (constricted efferent arteriole from hyaline sclerosis causing increased GFR) Elderly people (decreasing GFR with age), Acute and Chronic Renal disease (ARF from tubular sclerosis, CRF from diabetic glomerulopathy)

What does dark yellow color indicate in Urinalysis?

Concentrated urine, Bilirubinemia, Increased UBG, Vitamins

What does Red or Pink color indicate in Urinalysis?

Hematuria, hemoglobinuria, myoglobinurua, drugs (phenazopyridine), porphyria

What are some causes of increased Cr Clearance?

What does smoky-colored urine indicate?

Acid pH converts Hb to hematin. Common in nephritic glomerulonephritis

What does black urine after exposure to light indicate?

Alkaptonuria. Deficiency of homogentisate oxidase resulting in buildup of homogentisic acid

What does clarity of the urine indicate?

Cloudy urine with alkaline pH is normal, probably from phosphates. Cloudy urine with acid pH is normal probably from uric acid. Otherwise, bacteria, WBC's, Hb, myoglobin

What does the specific gravity of the urine indicate?

What does the pH of the urine indicate? What does glucose indicate in the urine? What does microalbuminuria indicate? What do ketones in the urine indicate? What does bilirubin in the urine indicate?

What does Urobilinogen indicate? What does blood in the urine indicate? What do nitrites in the urine indicate?

Urine concentration and dilution. SG>1.023 indicates urine concentration and excludes intrinsic renal disease. Hypotonic 3.5 g/24 hr, pitting edema and ascited due to hypoalbuminemia. Increased risk for spontaneous peritonitis from strep pneumoniae. Sometiems there is hypertension from salt retention. Hypercoagulability due to loss of Antithrombin III causing potential for renal vein thrombosis. Hypercholesterolemia from increased synthesis (after albumin loss). Hypogammaglobulinemia from protein loss. Fatty casts with maltese crosses and oval fat bodies. Nephrotic syndrome with Nodular Glomerulosclerosis (Kimmelstiel-Wilson disease). Risk factors are poor glycemic control, hypertension and high correlation with coexisting diabetic retinopathy.

What is Diabetic Microangiopathy? What microscopic changes are seen in Diabetic Glomerulopathy?

Nonenzymatic glycosylation of the GBM, also affecting the tubule basement membranes. Results in increased vessel and tubular permeability to proteins. NEG of the afferent and efferent arterioles also results in hyaline arteriolosclerosis (efferent first). There is also osmotic damage to the glomerular capillary endothelium because glucose is converted to sorbitol by aldolase reductase resulting in an osmotic gradient. Selective hyaline arteriolosclerosis of the efferent arterioles results in increased GFR and causes hyperfiltration damage to the mesangium. Increased Type IV collagen deposition in the GBM, tubular basement membrane and mesangium results in a microangiopathic state. Fusion of podocytes, afferent and efferent hyaline arteriolosclerosis, nodular masses of type IV collagen and trapped proteins in the mesangium

What lab values are significant in Diabetic Glomerulopathy?

Microalbuminuria

What is the pathogenesis of Diabetic Glomerulopathy?

Are there any other diseases of the kidney associated with Diabetic Glomerulopathy?

What is Alport's Syndrome?

Renal papillary necrosis and acute or chronic pyelonephritis Amyloid deposits in the kidney secondary to primary or secondary amyloidosis X-Linked recessive (sometimes AR or AD) mutations in A chains of type IV collagen in the GBM. Lipid accumulates in VEC's producing foam cells. Also see sensorineural hearing loss and ocular abnormalities

What is Thin Basement Membrane Disease?

Benign familial hematuria. AD disorder with extremely thin basement membranes in the setting of normal renal functin. See mild proteinuria and persistent microscopic hematuria

What is renal amyloidosis?

What are the common causes of Chronic Glomerulonephritis? What are gross and microscopic findings in chronic glomerulonephritis?

What is ischemic Acute Tubular Necrosis?

What segments of the nephron are damaged in ischemic ATN?

What is Nephrotoxic Acute Tubular Necrosis? What is the epidemiology of Acute Tubular Necrosis?

What is Acute Renal Failure?

Rapidly progressive glomerulonephritis, focal segmental glomerulosclerosis, type I membranoproliferative glomerulonephritis, membranous glomerulopathy, type IV diffuse proliferative glomerulonephritis in SLE, IgA nephropathy.

Shrunken kidenys with glomerular sclerosis and tubular atrophy

Most often caused by prerenal azotemia due to hypovolemia. Ischemia damages endothelial cells decreasing vasodilators and increasing vasoconstrictors, thus worsening the situation and further decreasing GFR. Ischemia also damages tubular cells which then detach into the lumen, cause obstruction and produce pigmented renal tubular cell casts. The casts further obstruct the lumen increasing tubular pressure, decreasing GFR and pushing fluid into the interstitium resulting in oliguria. Straight segment of the Proximal tubule (part of the degree most susceptible to hypoxia), Medullary segment of the thick ascending limb (location of the NK2C transporter), and the Tubular basement membrane (interferes with renal tubular cell regeneration) ATN from nephrotoxic substances. Aminoglycosides are most common, radiocontrast agents and heavy metal poisoning are also causes. Most commonly see oliguria, occasionally polyuria. This primarily damages proximal tubule while the tubular basement membrane is intact. Also see pigmented renal tubular cell casts, hyperkalemia and anion gap metabolic acidosis, increased BUN and Cr with ratio of BUN:Cr 50% of patients with septic shock Acute suppression of renal function developing in 24 hours, accompanied by oliguria or anuria. Most commonly caused by ATN.

What are some causes of Acute Renal Failure? What is RPGN?

Postrenal obstruction, vascular disease (malignant htn), RPGN, drugs, DIC, urate nephropathy. Rapidly progressive glomerular nephritis

What are common causes of acute pyelonephritis?

Treat prerenal azotemia-volume expansion if hypovolemic to increase renal blood flow. Low dose dopamine. Fenoldopam (dopamine Alpha-1-receptor agonist), Dialysis Acute or chronic inflammation of tubules and interstitium. May be caused by acute pyelonephritis, drugs, infections (legionaire's, leptospirosis), SLE, lead poisoning, Urate nephropathy and multiple myeloma. E Coli is most common followed by Enterococcus. Risk factors are indwelling catheter, obstruction, medullary sponge kidney, DM, pregnancy and sickle cell

How does vesicoureteral reflux cause pyelonephritis? What is Oliguria? What are common causes of Oliguria? What does decreased Urine Osm indicate?

Intravesical portion of the ureter is not compressed during micturition so urine refluxes up. Causes ascending infection into the renal pelvis and parenchyma. Urine output