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

What are some causes of Impaired O2 delivery to the alveoli for gas exchange, e.g. from
ventilation defects? airway collapse due to respiratory distress syndrome or atelectasis.
What are some causes of Decreased or absent blood flow to the alveoli, e.g. pulmonary
perfusion defects? embolus

What are some causes of O2 cannot diffuse across alveolar-capillary interface, e.g.
diffusion defects? pulmonary fibrosis or pulmonary edema. Causes decreased DLCO

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

Define Functional Residual

Capacity, FRC (Refer to
Pulmonary attachment 1). Total amount of air in the lungs at the end of normal expiration
Define Total Lung Capacity,
TLC Total amount of air in a fully expanded lung
Volume of air left over in the lung after maximal expiration: FRC-
Define Residual Volume, RV ERV
Define Tidal Volume, TV Volume of air that enters/exits the lungs during normal respiration
Define Forced Vital Capacity,
FVC Total amount of air expelled after maximal inspiration
Define Forced Expiratory Amount of air expelled from the lungs in 1 second after maximal
Volume, 1 second, FEV1 inspiration
What is the normal
FEV1/FVC? 70-80%
Define Expiratory Reserve
Volume, ERV Amount of air forcibly expelled at the end of normal expiration

TLC decreased, RV decreased, FEV1 decreased, FVC decreased,

Describe spirometry in FEV1/FVC normal to increased, PaO2 decreased, A-a gradient
restrictive lung disease increased (if disease of lungs, not just restriction of chest wall

Describe spirometry in TLC increased, RV increased, FEV1 decreased, FVC decreased,

obstructive lung disease FEV1/FVC decreased, PaO2 decreased, A-a gradient increased

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,
Define Dyspnea and list interstitial inflammation or fluid accumulation, e.g. left sided heart
some causes. failure.
Where are cough receptors
located? They're at the bifurcation of airways, larynx and distal esophagus
What is the most common
cause of cough with a
normal CXR? Postnasal discharge
What causes nocturnal GERD from acid refluxing into the bronchial tree at night. Bronchial
cough? asthma due to airway constriction
What causes productive Chronic bronchitis, usually associated with smoking cigarettes.
cough? 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
What drugs cause cough? bronchoconstrictors
Define hemoptysis and the Coughing up blood-tinged sputum. Caused by parenchymal
mechanisms. necrosis and/or bronchial/pulmonary vessel damage.
Chronic bronchitis (most common), pneumonia, bronchogenic
What are some causes of carcinoma, tuberculosis, bronchiectasis, aspergilloma (fungus in a
hemoptysis? cavitary lesion)

Rapid, shallow breathing, more than 20 breaths/minute. Causes

Define tachypnea and list the are restrictive lung disease, pleuritic chest pain, pulmonary
causes. embolus with infarction (tachypnea is the key finding)

shift of trachea from large changes in pleural fluid volume. Causes

are pressure in contralateral lung, large tension pneumothorax,
Define tracheal shift and list large pleural effusion; decreased volume in ipsalateral lung, large
the mechanism. spontaneous pneumothorax, resorption atelectasis.
What is vocal tactile Palpable thrill (vibration) transmitted through the chest when the
fremitus? patient says "99," or "E"
What causes decreased Emphysema or asthma with increased AP diameter from increased
tactile fremitus? total lung capacity.
What causes increased Sound travels better through fluid/solid so any type of lung
tactile fremitus? consolidation, pneumonia, etc.
What causes absent tactile Atelectasis/collapse of airways, fluid/effusion, air in pleural space
fremitus? (pneumothorax)
Dull percussion comes from pleural effusions, lung consolidations,
What causes dull and atelectasis. Hyperresonant percussion comes from pneumothorax,
hyperresonant percussion? asthma or emphysema
What is the origin and
mechanism of normal breath Normal breath sounds come from the trachea and are caused by
sounds? air velocity and turbulence inducing vibrations in airway walls
Where does laminar air flow Terminal bronchioles where the increased surface area converts
start? turbulent to laminar flow

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
What are tubular breath longer than inspiration. Means that there is consolidation or patent
sounds? 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
What are vesicular breath to increased AP diameter. Absent in pneumothorax, atelectasis or
sounds? effusion

What are bronchovesicular Normal breath sounds over the main bronchi with an equal
breath sounds? inspiratory and expiratory ratio.

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,
What are crackles and how transudate, pus). These do not clear with coughing and vary from
are they caused? fine to course
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
What is wheezing and how is asthma); pulmonary infarction (release of TXA from platelets in the
it caused? embolus causes bronchoconstriction
Low pitched snoring sounds during inspiration or expiration. Due
What are Rhonchi and how to secretions in large airways (bronchus or trachea). Usually clear
are they caused? with coughing, common in chronic bronchitis
High pitched inspiratory sound. Indicates upper airway
What is inspiratory stridor obstruction. Caused by epiglottitis (H. Influenzae), croup
and how is it caused? (parainfluenza)

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).
What is a pleural friction rub Disappears with alrge effusion bc separates layers and stays with
and how is it caused? holding breath.
What does grunting in a Newborns should not grunt after 24 hours. It's a sign of respiratory
newborn mean? distress syndrome.

Caused by alveolar consolidations. Spoken numbers, syllables are

What is bronchophony and heard more distinctly through stethoscope. Egophany is when the
egophony? patient says E and you hear an A through the stethoscope.
Plot of inspiratory and expiratory flow rate(L/sec) versus lung
What is a flow volume loop? volume(L)
Where is maximal inspiration
on the diagram? (see
Pulmonary attachment 2 for
following) 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
Define Peak Expiratory Flow resistance and large caliber. Slope decreases to point A as
(PEF) resistance increases and airways get smaller.
What is the volume between
points B and C? Vital Capacity
Describe the flow-volume TLC is increased and RV is increased. AKA left shifted curve.
loop in obstructive lung Decreased PEF. Can have concavity at C from mucus plugs or
disease. collapsed airways.
Describe the flow-volume
loop in restrictive lung
disease. 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
What is Choanal Atresia? 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
What is a Nasal Polyp? associated with CF
Define Obstructive Sleep
Apnea Excessive snoring with intervals of breath cessation (apnea)
Most commonly a result of obesity causing the pharyngeal muscles
What causes obstructive to collapse under the weight of the tissue. Can also result from
sleep apnea? tonsilar hypertrophy or nasal septum deviation.
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
What is the pathogenesis daytime somnolence. Can cause pulmonary arterial hypertension
and clinical findings in sleep leading to Right Ventricular Hypertrophy and polycythemia
apnea? secondary to hypoxemia.

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,
Define Sinusitis and describe strep pneumoniae, anaerobes (chronic sinusitis), systemic fungi
its causes. (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
What is a Nasopharyngeal carcinoma or undifferentiated cancers which can metastasize to
Carcinoma? cervical lymph nodes.

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
Define Laryngeal Carcinoma. hoarseness from cervical lymphadenopathy is common.
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.
What is Atelectasis? Treat with incentive spirometry, CPAP or PEEP.

Airway obstruction in bronchiols, segmental bronchi or bronchi, by

thick secretions which prevents air from reaching the alveoli. Can
What is resorption be caused by mucus or mucopruluent plug after surgery, aspiration
atelectasis? of foreign material or centrally located bronchogenic carcinoma.
What is compression Air or fluid in the pleural cavity under increased pressure collapses
atelectasis? small airways beneath the pleura.

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
What is atelectasis due to tension so airways don't collapse. Without surfactant, airways can
loss of surfactant? 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,
What is Respiratory Distress tachypnea, intercostal retractions and hypoxemia with respiratory
Syndrome? acidosis.
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
What are complications of enterocolitis from intestinal ischemia (allows entry of gut bacteria
respiratory distress into intestinal walls) and hypoglycemia leading to seizures and
syndrome? 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
What is Pulmonary Edema resulting from infection. Can be from aspiration, drugs, high
and what are the causes? altitude or 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),
What is Acute Respiratory Heroin, smoke inhalation, acute pancreatitis, cardiopulmonary
Distress Syndrome, ARDS? bypass, DIC, amniotic fluid or fat embolism.

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
What is the pathogenesis of producing hyaline membranes. Neutrophils damage Type I and II
ARDS? pneumocytes, reducing surfactant and causing atelectasis.

Dyspnea/tachypnea, late inspiratory crackles, severe hypoxemia

What are clinical not responsive to 100% O2, increased pulmonary wedge pressure,
signs/symptoms of ARDS? increased A-a gradient, bilateral infiltrates and consolidations.
What are the subtypes of Community acquired which can be typical or atypical and hospital
Pneumonia? acquired, aka nosocomial.
Most caused by bacterial pathogens, particularly Strep
Describe the pathogenesis of Pneumoniae. Pathogenesis is via inhalation of aerosol from
typical pneumonia. infected person or aspiratin of nasopharyngeal flora while sleeping.
Begins as acute bronchitis and spreads locally into the lungs,
Describe the pathogenesis of usually lower lobes or right middle lobes. Causes patchy
bronchopneumonia. 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
Describe clinical findings in inspiratory crackles, bronchial breath sounds, bronchophany and
lobar pneumonia. egophany.

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
Describe clinical findings in symptoms including pharyngitis, laryngitis, myalgia and headache.
atypical pneumonia. No consolidation.

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.
Describe clinical findings in In immunocompromised, can be opportunistics like CMV,
nosocomial pneumonia. Pneumocystis Jirovecis, Aspergillus-fumigatus.
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
Describe pneumonia from resistance by mutations in mycolic acid or catalase peroxidase
Tuberculosis. (activates Isoniazid).

Subpleural location, usually upper part of lower lobes or lower part

of upper lobes. Causes Ghon focus (caseous necrosis) in periphery
Describe Primary TB and Ghon complex in hilar lymph nodes. Produces a calcified
Infection. granuloma or area of scar tissue

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,
Describe Secondary TB lymphatics or extrapulmonary sites like the kidney. Spread to
Infection. vertebra is called Pott's disease.
Atypical mycobacterium causing atypical pneumonia in AIDS
Describe pneumonia from patients. Happens when CD4+ T Cell count falls below 50
Mycobacterium Avium cells/mm3. Often disseminates and co-occurs with systemic fungal
Intracellulare infection.
Rhinovirus, transmitted by hand to nose/eye contact. Less
What is the most common common are coronavirus, adenovirus, influenza C and
cause of the common cold? coxsackievirus
What does Coxsackievirus
cause? Acute chest syndrome: fever with pleuritis
What is the most common
viral cause of atypical
pneumonia and bronchiolitis
in children and otitis media Respiratory Syncitial Virus. Occurs in late fall and winter. Can give
in older children? Palivizumab to high risk kids (passive immunity)
What is the most common
viral cause of Parainfluenza. Causes inspiratory stridor from sunmucosal edema
laryngotracheobronchitis obstructing the upper airway. Anterior CXR shows steeple sign in
(croup) in infants? anterior neck.

What is the most common

viral cause of pneumonia in Cytomegalovirus. Enlarged alveolar macrophages/pneumocytes
immunocompromised hosts? with basophilic inclusions surrounded by a halo.
What can happen with
aspirin ingestion when a Reye's Syndrome. Causes fatty liver, severe encephalopathy,
child has influenza? palmar rash, comiting, lethargy and stupor.
What are signs and Measles. Fever, cough, conjunctivitis and excessive nasal mucous.
symptoms of Rubeola Koplik spots in the mouth precede rash. Warthin-Finkeldey
infection? multinucleated giant cells are characteristic

What are signs and Infects lower respiratory tract and then spreads systemically thus
symptoms of SARS severe respiratory infection and systemic symptoms.
What is Hantavirus Transmission is via inhalation of urine/feces from deer mice in SW
pulmonary syndrome? US. Causes ARDS, hemorrhage and renal failure.
What is the second most
common (bacterial) cause of Chlamydophilia pneumoniae. Has a seroepidemiologic association
atypical pneumonia? with coronary artery disease. Treat with doxycycline.
What is a common bacterial Chlamydia trachomatis from passage through infected birth canal.
cause of newborn Afrebile with staccato cough, conjunctivitis and wheezing. Treat
pneumonia? with erythromycin.

What is the most common Mycoplasma Pneumoniae. Insidious onset with low grade fever. Can
baterial cause of atypical cause bullous myringitis(inflamed Tympanic membrane), cold
pneumonia? autoimmune hemolytic anemia from anti-IgM antibodies.
Describe the signs and
symptoms of Coxiella Atypical pneumonia, myocarditis, granulomatous hepatitis.
Burnetti infection Associated with dairy farmers and vetrinarians.

What is the most common

cause of community acquired Strep pneumoniae. Rapid onset, productive cough and signs of
lobar pneumonia? 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
What are signs/symptoms of sputum, abscess formation and tension pneumatocysts
pneumonia from Staph (intrapleural blebs) which can rupture and produce tension
Aureus? pneumothorax.
Causes toxin-induced pseudomembranous inflammation producing
Describe signs and a shaggy gray membrane in the oropharynx and trachea. Can
symptoms of infection with cause toxic myocarditis from impaired B oxidation of fatty acids in
Corynebacterium Diptheriae. the heart.
Cutaneous anthrax initially looks like a scab but swells to form a
What are signs and black scab (eschar) with an area of central necrosis. Pulmonary
symptoms of infection with anthrax causes necrotizing pneumonia, meningitis, splenomegaly
Bacillus Anthracis? and systemic dissemination.

What are signs and Normal flora in tonsils and adenoids. Can produce draining sinuses
symptoms of Actinomyces in the jaw, chest cavity and abdomen. Pus contains yellow specks
infection? (sulfur granules) which contain the bacteria.
What are signs and
symptoms of Nocardia Granulomatous microabscesses in the lungs. Often disseminates
infection? 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
What are signs and lymphocytosis and coughing. Can cause hemorrhage into skin,
symptoms of infection with conjunctiva, bronchus, brain or rectal prolapse from coughing.
Bordatella Pertussis? Also otitis media and meningoencephalitis.
Common cause of sinusitis, otitis media, conjunctivitis, epiglottitis
What are signs and with inspiratory stridor. Swelling of epiglottis produces a
symptoms of infection with thumbprint sign on lateral xray of the neck. Can cause COPD
H. Influenzae? exacerbation.
What are signs and
symptoms of Moraxella Causes typical pneumonia, especially in the elderly. Causes acute
Catarrhalis infection? COPD exacerbation, chronic bronchitis, sinusitis and otitis media.

What are signs and Green sputum (pyocyanin), nosocomial pneumonia and pneumonia
symptoms of infection with in CF patients. Often associated with infarction from vessel
Pseudomonas Aeruginosa? invasion.
Most common gram negative that causes lobar pneumonia and
What are signs and typical pneumonia in nursing home patients and alcoholics.
symptoms of Klebsiella Associated with blood tinged, thick, mucoid sputum, lobar
Pneumoniae infection? consolidations and abscesses.
Pneumonia associated with high fever, dry cough, flu like
symptoms. May produce tubulointerstitial disease with destruction
What are signs and of the JG apparatus leading to hyporeninemic hypoaldosteronism
symptoms of infection with (type IV renal tubular acidosis-hyponatremia, hyperkalemia,
Legionella Pneumophila? metabolic acidosis). Urine antigen is an excellent screen.

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
What are signs and surface (buboes). Pneumonic and septicemic are just what they
symptoms of infection with sound like. Treat with gentamicin and doxycycline (pneumonic) or
Yersinia Pestis? gentamicin and streptomycin (bubonic)

What are signs and

symptoms of infection with Granulomatous inflammation with caseation. Acquired from pigeon
Cryptococcus Neoformans? feces.

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
What are signs and terminal bronchioles resulting in bronchiectasis and interstitial lung
symptoms of infection with disease. Vessel invasion with hemorrhagic infarctions and
Aspergillus Fumigatus? necrotizing bronchopneumonia.
Happens to diabetic and immunosuppressed patients. Vessel
What are signs and invasion producing hemorrhagic infarcts in the lungs. Invades the
symptoms of infection with frontal lobes when there is diabetic ketoacidosis (rhinocerebral
Mucor species? mucormycosis).
Contracted by inhaling arthrospores in dust in arid areas (increased
What are signs and after earthquakes). Causes flu-like symptoms and erythema
symptoms of infection with nodosum and granulomatous inflammation of the lungs with
Coccidoides Immitis? 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,
What are signs and consolidations, milary spread and cavitation. Causes marked
symptoms of infection with dystrophic calcification of granulomas and multiple calcifications in
Histoplasma Capsulatum? the spleen.
Male dominant disease, common in Great lakes, central and
What are signs and southern US. Causes skin disease that simulates squamous cell
symptoms of infection with carcinoma and lung disease with granulomatous inflammation and
Blastomyces Dermatitidis? caseous necrosis.

Cysts and trophozoites attach to Type I pneumocytes. Most

common AIDS-defining infection, CD4+ count <200. Fever,
What are signs and dyspnea and severe hypoxemia, diffuse intra-alveolar foamy
symptoms of infection with exudates with cup chaped cysts (under silver or Giemsa stain).
Pneumocystis Jiroveci? Diffuse alveolar and interstitial infiltrates.
Aspiration of oropharyngeal material. Risk factors are alcoholism,
loss of consciousness and recent dental work. Can also be a
What are the common complication of pneumonia, a result of septic embolism or from an
causes of lung abscesses? obstructive lung neoplasia.
What are the most common
pathogens in lung Aerobic and anaerobic streptococci, staph species, prevotella,
abscesses? fusobacterium
Right side because the bronchi going to the right lobes are more
Where are most lung direct (straight) so it's easier to aspirate crap into there. Usually in
abscesses due to aspiration the upper portion of the right lower lobe, but it depends on the
located? position of the person when they aspirated.
What are clinical findings in Spiking fever with productive cough and foul smelling sputum.
a lung abscess? CXR shows cavitation with an air/fluid level.

Venous clot, most commonly from the femoral vein. Risk factors
are Virchow's triad-stasis of blood flow, hypercoagulable states and
trauma to the vessel. Clot breaks off and goes to the lung-size of
What is the pathophysiology the embolus determines what it will block. Large embolus blocks
of a pulmonary major vessels (saddle embolus) while small emboli occlude
thromboembolism? medium and small vessels.
Increase in pulmonary artery pressure, decreased flow to
pulmonary parenchyma which can cause hemorrhagic infarct, see a
What are consequences of red-blue, raised, wedge shaped area that extends to the pleural
pulmonary surface. Fibrinous exudate on the pleural surface and hemorrhagic
thromboembolism? pleural effusion.

Sudden increase in PA pressure which can cause right ventricular

What are clinical signs of failure, sudden onset of dyspnea and tachypnea, fever, pleuritic
pulmonary chest pain, plueral friction rub, pleural effusion, expiratory
thromboembolism? wheezing from release of TXA2 from platelets.
What are lab findings of
pulmonary Respiratory alkalosis (PCO2<33mmHg), PaO2<80 mmHg,
thromboembolism? increased A-a gradient, increased D-Dimer

What is Hampton's Hump? Wedge shaped area of consolidation/infarction from PE

Define Pulmonary Mean pulmonary artery pressure >25 mmHg at rest or >30mmHg
Hypertension with exercise.
What causes primary Mutation associated with TGF-B resulting in vascular
pulmonary hypertension? hyperreactivity with proliferation of smooth muscle

Endothelial cell dysfunction, e.g. loss of vasodilation (NO), increase

in vasoconstriction (endothelin). Hypoxemia and respiratory
acidosis stimulate vasoconstriction of pulmonary arteries resulting
in smooth muscle hyperplasia and hypertrophy. Any sort of lung
disease that results in chronic hypoxemia or chronic respiratory
acidosis can do this, e.g. high altitude, chronic bronchitis, sleep
apnea, loss of pulmonary vasculature from emphysema or
What causes secondary recurrent PE, left to right shunting/volume overload, mitral stenosis
pulmonary hypertension? resulting in volume overload.
Exertional dyspnea (common), chest pain, tapering of arteries on
What are clinical findings of CXR, accentuated P2, left parasternal heave or other signs of right
pulmonary hypertension? ventricular hypertrophy.

How do you treat pulmonary Diuretics, O2, vasodilators-Ca channel blockers, prostanoids,
hypertension? endothelin receptor antagonists, lung transplant
Pulmonary hemorrhage with hemoptysis often preceding renal
What is Goodpasture's failure. Autoantibodies to Type IV collagen in basement membrane
Syndrome? of lung and glomerulus.

Chest wall disorders with normal lungs, e.g. kyphoscoliosis, pleural

disease like mesothelioma or obesity. Acute or chronic interstitial
What are common causes of lung diseases, e.g. ARDS, pneumoconiosis or other fibrosing
restrictive lung disease? disorders, granulomatous diseases like amyloidosis or sarcoidosis.
Elveolitis-leukocytes release cytokines which stimulate fibrosis.
Causes functional loss of type I/II pneumocytes and capillaries
(decreased DLCO), and decreased expansion of lung parenchyma
What is the pathogenesis of during inspiration. Increased elasticity to recoil on expiration is
interstitial fibrosis? increased.
What are clinical findings in dry cough and exertional dyspnea, late inspiratory crackles in lower
restrictive lung disease? lung fields, potential cor pulmonale, equal decreases on PFT's.

Inhalation of mineral dust into the lungs leading to interstitial

What is a pneumoconiosis? fibrosis. Can be silica, asbestos, beryllium or others.

"I think I've got the black lung pop…" Coal dust, aka aanthracotic
pigment comes from coal mines, large cities, second hand smoke,
etc. Deposits in alveolar macrophages creating "dust cells."
Fibrotic opacities smaller than 1 cm in upper lobes and coal
deposits adjacent to respiratory bronchioles producing centriacinar
emphysema- simple CWP. Complicated CWP involves large fibrotic
opacities, crippling lung disease (black lung), may have cor
Describe Coal Worker's pulmonale or large cavitating rheumatoid nodules (Caplan
Pneumoconiosis. Syndrome). No increase in TB or primary lung cancers.
Common occupational disease from quartz/silicon dioxide,
foundries, sandblasting and working in mines. Quartz is fibrogenic
and deposits in the upper lungs, activates and is cytolytic to
alveolar macrophages. Macrophages release cytokines resulting in
What is silicosis? fibrosis.
Ground glass appearance on CXR or nodular opacities in more
advanced disease (concentric layers of collagen w/wo central
cavitation). Dystrophic calcification of lymph nodes. Can cause cor
Describe clinical findings in pulmonale or Caplan syndrome and increased risk of lung cancer
silicosis. and TB.
Serpentine asbestos-interstitial fibrosis and lung cancer; amphilobe
asbestos-interstitial fibrosis, lung cancer and mesothelioma.
Deposits in respiratory bronchioles, alveolar ducts and alveoli.
How do asbestos related Comes from insulating pipes, naval shipyards, roofing material,
diseases occur? ceiling tiles, old floor tiles and demolition of old buildings.

Fibers are coated in iron and protein (ferruginous bodies) which are
then pahgocytosed, coated with ferritin and look golden and
beaded in sputum or distal small airways. Causes calcified pleural
plaques which don't predispose to mesothelioma, diffuse interstitial
fibrosis, primary bronchogenic carcinoma (esp if smoker),
What is the pathogenesis of malignant mesothelioma of the pleura arising from serosal cells of
asbestos related disease? the pleura. Can cause cor pulmonale or Caplan syndrome.

Beryllium exposure from nuclear and aerospace industry causes

diffuse interstitial fibrosis with noncaseating granulomas.
What is Berylliosis? Increased risk for cor pulmonale and primary lung cancer.

Multisystem granulomatous disease of unknown origin. Common

in Black women and nonsmokers and causes 25% of chronic
interstitial lung disease. Granulomas in mediastinal/hilar lymph
nodes and interstitium. Granulomas contain multinucleated giant
cells, laminated calcium concretions (Schaumann bodies) and
stellate inclusions (asteroid bodies). Dyspnea is the most common
What is Sarcoidosis? symptom.
Nodular lesions containing granulomas, violaceous rash on the
nose and cheeks (lupus pernio), erythema nodosum-painful
nodules on lower extremities, inflammation of subcutaneous fat.
Eye lesions produce uveitis, blurry vision, glaucoma and corneal
opacities. Can ahve granulomatous hepatitis, enlarged salivary
and lacrimal glands, diabetes insipidus, and granulomas in the
bone marrow and spleen. See increased ACE, hypercalcemia
(increased 1-alpha hydroxylase in granulomas), polyclonal
What are other clinical signs gammopathy, and cutaneous anergy of skin antigens like Candida
in Sarcoidosis? (due to consumption of CD4+ T cells in granulomas)
Idiopathic means the doctor is an idiot!!! Repeated cycles of
alveolitis, release of cytokines producing interstitial fibrosis,
alveolar fibrosis leading to proximal dilation of small airways giving
the lung a honeycomb appearance. See fever, dyspnea on
What is idiopathic pulmonary exertion, chronic, nonproductive cough, and late inspiratory
fibrosis? crackles.
Systemic Lupus causes interstitial disease in 50% of patients and
pleuritis with effusion (serositis). Rheumatoid Arthritis can cause
What collagen vascular rheumatoid nodules (if with a pneumoconiosis, Caplan's
diseases cause lung disease? syndrome).

What is hypersensitivity Extrinsic allergic alveolitis associated with exposure to known

pneumonitis? inhaled antigen. Does not involve IgE or have eosinophilia.
Exposure to thermophilic actinomyces (Saccharopolyspora
rectivirgula) in moldy hay causes precipitating IgG antibodies
which combine with inhaled antigens to form immune complexes.
Type III hypersensitivity. Immune complexes deposit in lung and
cause inflammation which chronically causes granulomatous
What is Farmer's Lung? inflammation (type IV hypersensitivity).

Inhalation of gases (oxides of nitrogen) from plant material causes

What is Silo Filler's Disease? an immediate hypersensitivity reaction associated with dyspnea.

Contact with cotton, linen and hemp in textile factories causes

exposure to gram negative endotoxin growing on the cotton.
Causes dyspnea on exposure to cotton, linen or hemp. Disease
What is Byssinosis? occurs on returning to work-Monday Morning Blues (cyanosis)

What drugs are associated Amiodarone, Bleomycin and Busulfan, Cyclophosphamide,

with interstitial fibrosis? Methotrexate and methysergide, nitrosurea and nitrofurantoin.
What is obstructive lung Obstruction to airflow out of the lungs. Usually loss of elastic recoil
disease? or obstruction of airways.
Permanent enlargement of all or part of the respiratory unit-
What is Emphysema? respiratory bronchioles, alveolar ducts and alveoli.
Smoking is the most common cause. Also can be from Alpha-1
What causes Emphysema? Antitrypsin deficiency

Increased compliance and decreased elasticity (C=V/P). There can

be an imbalance between elastase and anti-elastases (A1AT), or an
imbalance between oxidants and antioxidants. Elastase and
oxidants all derive from macrophages so chronic inflammation
What is the pathogenesis of results in tissue destruction. Smoking produces a functional A1AT
Emphysema? deficiency.
Fibers attach to the outside of the walls of small airways and
provide radial traction to keep the lumen open. Destruction causes
What is the normal function loss of radial traction and small airway collapse, especially on
of elastic fibers in the lung? expiration.
During expiration, the distal terminal bronchioles collapse
preventing egress of air. Trapped air distends parts of the
Where is the site of respiratory unit that have no elastic tissue. Trapped air increases
obstruction in emphysema? TLC and RV
Centriacinar/Centrilobular. Mostly apical segments of upper lobes,
What type of Emphysema is distal terminal bronchioles and respiratory bronchioles lose elastic
most common in smokers? tissue.

Panacinar emphysema. Autosomal dominant disorder. MM

phenotype is normal, Homozygous ZZ phenotype causes disease.
Primarily affects the lower lobes. Tissue destruction happens in
distal terminal bronchioles and all parts of the respiratory units.
What type of Emphysema is See absent alpha-1 globulin peak in serum protein electrophoresis.
most common in Alpha-1 Dyspnea is sever and occurs early, causes pink puffers. Frequently
Antitrypsin deficiency? coexists with chronic bronchitis.

Paraseptal emphysema-localized to the subpleura and targets

alveolar ducts and alveoli. Increased incidence of spontaneous
What are 2 non-obstructive pneumothorax from rupture of subpleural blebs. Irregular
types of Emphysema? Emphysema-localized disease associated with scar tissue.
Productive cough for at least 3 months. Most commonly from
What is Chronic Bronchitis? smoking and Cystic Fibrosis.

Hypersecretion of mucous in bronchi, obstruction to airflow in the

What is the pathogenesis of terminal bronchioles, proximal to the obstruction seen in
chronic bronchitis? emphysema. Causes irreversible fibrosis of terminal bronchioles.
Hypersecretion of submucosal mucus-secreting glands in the
trachea and bronchi are responsible for sputum overproduction.
Acute inflammation with neutrophils are superimposed on chronic
inflammation. Causes loss of ciliated epithelium resulting in
What changes are seen in squamous metaplasia. Mucus plugs can block the exodus of CO2.
the bronchi with chronic GOblet cell metaplasia is seen with hypertrophy of mucus secreting
bronchitis? glands, fibrosis and narrowing of the airway.

Productive cough, dyspnea late in the disease, cyanosis of skin and

membranes, decreased SaO2 from hypoxemia. These patients are
called Blue Bloaters. Tend to be stocky or obese, have expiratory
What are clinical findings of wheezing and siliant rhonchi and often cor pulmonale. Also have
chronic bronchitis? chronic respiratory acidosis with increased bicarb to compensate.
Episodic and reversible obstructive airway disease. Primarily
What is Asthma? targets bronchi and terminal bronchioles.

Type I hypersensitivity reaction with exposure to extrinsic

allergens, typically in children with atopic family history. Initial
sensitization to inhaled allergens stimulates induction of Th2 cells
which release IL-4 and IL-5. IL-4 facilitates isotype switching to
IgE and IL-5 stimulates production and maturation of eosinophils.
Inflammatory mediators like histamine facilitate
bronchoconstriction, mucus production and influx of leukocytes.
Later Eotaxin is released which recruits eosinophils. Eosinophils
release major basic protein which damages epithelial cells and
What is Extrinsic Asthma? produces airway constriction.
What are other chemical
mediators involved in Leukotriene C, D, E4 cause prolonged bronchoconstriction.
Extrinsic Asthma? Acetylcholine causes airway muscle contraction.
Thickening of the basement membrane, edema and mixed
inflammatory infiltrate, hypertrophy of submucosal glands and
hypertrophy/hyperplasia of smooth muscle cells. Also see spiral
shaped mucus plugs which contain old epithelial cells-Curschmann
Spirals. This is a pathologic effect of major basic protein.
What are some histologic Crystalline granules in eosinophils coalesce to form Charcot-Leyden
changes in Extrinsic Asthma? crystals.

Episodic wheezing, nocturnal cough, increased AP diameter from

What are clinical findings in air trapping. Initially have respiratory alkalosis but may turn into
Extrinsic Asthma? respiratory acidosis if bronchospasm is not relieved.
Nonimmune asthma caused by virus-induced respiratory infection,
What is Intrinsic Asthma? or air pollutants.

Permanent dilation of bronchi and bronchioles due to destruction of

What is Bronchiectasis? cartilage and elastic tissue by chronic necrotizing infections.

Cystic Fibrosis, Infection (TB, adenovirus, staph, HiB), bronchial

obstruction (bronchogenic carcinoma), Primary ciliary dyskinesia
What are some causes of (absent dynein arm in cilia aka Kartagener's Syndrome), Allergic
Bronchiectasis? Bronchopulmonary Aspergillosis.
Cough productive of massive amounts of sputum, hemoptysis,
What are some clinical digital clubbing, cor pulmonale, crowded bronchial markings that
findings in Bronchiectasis? extend to lung periphery.
Autosomal Recessive disease. Three nucleotide deletion on
chromosome 7(should be phenylalanine) resulting in defective CF
transmembrane conductance regulator (CFTR) for chloride ions.
Defective protein is degraded in the Golgiso there is decreased
reabsorption of Na+ and Cl- from sweat glands, but decreased
secretion of Na and Cl into luminal secretions. This results in
What is Cystic Fibrosis? dehydrated body secretions which are thick and easily infected.

Nasal polyps, heat exhaustion, respiratory infections/failure, cor

pulmonale, pneumothorax, malabsorption, type I diabetes from
pancreatic destruction, infertility in males (atresia of vas deferens),
What are clinical findings in meconium ileus, rectail prolapse from straining, gallstones from
CF? thick bile and secondary biliary cirrhosis.

Smoking, Radon gas (uranium mining), asbestos, metal exposure-

What are risk factors for lung chromium, cadmium, beryllium, arsenic- secondhand smoke,
cancer? ionizing radiation, air pollution, prior TB

Most common tumor, weakest smoking association, tends to be

What are some features of peripherally located bc filters in cigarettes remove large
adenocarcinoma? carcinogens leaving the small ones that can move peripherally.

What are some features of 2nd most common tumor, greatest smoking association. Tends to
squamous cell carcinoma? be centrally located (mainstem bronchus)
What are common sites for Hilar lymph nodes (most common), adrenal glands, liver, brain,
metastasis? bone
Which cancers are most
commonly responsible for
lung metastasis? Primary breast cancer, colon cancer and renal cell carcinoma.
Where in the lung do tumors Parenchyma, pleura and pleural space (pleural effusions),
commonly metastasize? lymphatics (causes severe dyspnea)

What are common findings Cough, weight loss, chest pain, hemoptysis, dyspnea, superior
in primary lung cancer? vena cava syndrome

Superior sulcus tumor. Usually a primary squamous cancer located

at the extreme apex of the lung. Causes desctruction of superior
What is a Pancoast tumor? cervical sympathetic ganglion producing Horner's syndrome.
What are some
paraneoplastic changes Digital clubbing from reactive periosteal changes in underlying
associated with lung bone. Muscle weakness (Eaton Lambert Syndrome). Ectopic
cancers? hormone secretion (ACTH)

Usually metastatic primary lung cancer in older patients, usually a

primary disease in younger patients. Neurogenic tumors (posterior
mediastinum)- neuroblastoma (malignant in children),
ganglioneuroma (benign in adults). Thymomas, pericardial cysts,
What are the common malignant lymphomas (anterior mediastinum, usually nodular
causes of mediastinal sclerosing Hodgkin's in a woman), teratomas-usually benign, in
masses? anterior mediastinum.

Thymoma is usually benign (70%) neoplastic epithelial tissue.

Most patients have systemic symptoms of Myesthenia Gravis. Most
commonly have follicular B cell hyperplasia in the thymus (that's
where antiacetylcholine antibodies are synthesized). Also can have
What are some symptoms of hypogammaglobulinemia, RBC aplasia and increased incidence of
Thymoma? other autoimmune diseases.
Increased hydrostatic pressure in visceral pleura (CHF), decreased
oncotic pressure (nephrotic syndrome), obstruction of lymphatic
drainage from pleura (lung cancer), increased vessel permeability
What is the etiology of of pleural capillaries (pulmonary infarction, pneumonia),
pleural effusions? metastasis to the pleura (metastatic breast cancer).
Ultrafiltrate of plasma from disturbances in Starling pressures
Describe a transudate (CHF, nephrotic syndrome)

Describe an exudate Protein-rich and cell-rich fluid from increased vessel permeability.
Indicates interruption of the thoracic duct. Turbid, milky
appearance. Can be from malignancy, trauma (iatrogenic) or too
Describe Chylous fluid many chylomicrons
Turbid, milky appearance from increased inflammation with
Describe Pseudochylous fluid necrotic debris. Most often from rheumatoid lung disease.

Ratio of pleural fluid protein and LDH to serum protein and LDH.
How do you distinguish PF protein/serum protein <0.5 is transudate, >0.5 is exudate. PF
between exudate and LDH/serum LDH <0.6 is transudate, >0.6 is exudate. PF LDH
transudate? <200 U/L is transudate, >200 U/L is exudate

Commonly seen in tall, thin young men, 20-40 yrs old, increased
risk with smoking. Can be caused by rupture of apical subpleural
blebs (secondary to high negative intrapleural pressure), COPD,
Marfan syndrome, scuba diving, insertion of a subclavian catheter.
How does a spontaneous Loss of negative intrapleural pressure causes collapse of lung.
pneumothorax happen? Sudden onset of dyspnea with pleuritic chest pain.
Penetrating trauma to the lungs, rupture of tension pneumocytes.
Flap like tear in pleura allows air into pleural cavity but prevents its
release resulting in increasing positive intrapleural pressure. This
results in compression atelectasis. Sudden onset of severe
dyspnea and plueritic chest pain, can cause trachea and
What is the pathogenesis of mediastinal structures to deviate to contralateral side. Can cause
a Tension Pneumothorax? compromised venous return to the heart.
Left Gonadal vein to the left renal vein to the IVC. Right ovary/testis drains to right gonadal vein straight to
What vein drains the ovaries/testes? the IVC.
What is the lymphatic drainage of the
Ovaries/Testes? Ovary/Testis drains to the para-aortic lymph nodes.
Where does lymph from the Distal 1/3 of the vagina/vulva/scrotum drains to the superficial lymph nodes. Proximal 2/3 of vagina/uterus
vagina/vulva/scrotum drain to? drains to the obturator, external iliac and hypogastric lymph nodes
What does the suspensory ligament of
the ovaries connect? Connects ovaries to the lateral pelvic wall and contains the ovarian vessels.
What does the Cardinal ligament
connect? Connects the cervix to the side wall of the pelvis and contains the uterine vessels.
What does the Round ligament of the
uterus connect? Contains the Uterine fundus to the labia majora but carries no structures.
What is the round ligament of the
uterus derive from? Derivative of the Gubernaculum. Travels through the round inguinal canal.
What does the Broad Ligament Connects the uterus, fallopian tubes, and ovaries to the pelvic side wall. Contains the ovaries, fallopian
connects? tubes, and round ligaments of the uterus.
What does the Ligament of the ovary
connect? Connects the ovary to the uterus and does not contain any structures.
What does the Genital Tubercle
become? Becomes the Glans Penis or Clitoris
What does the Urogenital Fold
become? Becomes the shaft of the penis or the labia minora
What does the labioscrotal swelling
become? Scrotum and Labia majora
What is the pathway of sperm during (SEVEN UP) Seminiferous tubules to epididymis to vas deferens to ejaculatory ducts (nothing) to urethra to
ejaculation? the penis

Erection-Parasympathetic nervous system (pelvic nerve). Nitric oxide increases cGMP which causes smooth
What is the autonomic innervation muscle relaxation which causes vasodilation and is proerectile. Also Norepinephrine causes an increase in
causing an erection? Calcium which causes smooth muscle contraction which causes vasoconstriction and is antierectile.

What is the autonomic innervation

causing Sperm Emission? Sympathetic nervous system via the hypogastric nerve
What is the autonomic innervation
causing Ejaculation? Visceral and somatic via the pudendal nerve
What are the different parts of the
sperm? Acrosome, head, nucleus, neck, middle piece, tail
Where do the different parts of the Acrosome-Golgi apparatus, Flagellum/Tail-Centrioles, Middle Piece-contains the mitochondria, Head and
sperm come from? nucleus come from the nucleus.
What is the function of
spermatogonia? Maintain the germ pool and produce primary spermatocytes
Secrete inhibin which inhibits FSH. Secrete Androgen Binding Protein to maintain the level of testosterone.
Form tight junctions between adjacent Sertoli Cells to form the blood-testis barrier, isolating gametes from
immune attack. Support and nourish spermatozoa. Regulate spermatogenesis. Produce Anti-Mullerian
What is the function of Sertoli Cells? hormone.

What is the function of Leydig Cells? Secrete testosterone

Seminal Vesicle Products(fructose, ascorbic acid, prostaglandins, phosphorylcholine, flavins), Prostate
What is the composition of Semen? Products (Zinc, citrate acid, phospholipids, acid phosphatase, fibrinolysin), Sperm

Describe the general process of Spermatogenesis begins at puberty with spermatogonia. Full development takes 2 months. Occurs in
spermatogenesis seminiferous tubules. Produces spermatids that undergo spermiogenesis to form mature spermatozoa
Maturation of sperm as they lose their cytoplasmic contents, gain an acrosomal cap and become mature
What is spermiogenesis? spermatozoa

Spermatogonium (diploid 2N) copies genome to make Primary spermatid (Diploid 4N). Primary spermatocyte
Describe the process of divides into 2 secondary spermatocytes (Haploid 2N). The Secondary spermatids divide again to produce 4
spermatogenesis. spermatids (Haploid, 1N). These undergo spermiogenesis to form mature spermatozoa

Hypothalamus releases GnRH which causes FSH and LH release from the anterior pituitary. LH stimulates
testosterone release from Leydig cells which release testosterone into the seminiferous tubules and the
blood. FSH stimulates Sertoli cells to produce Androgen Binding Protein and Inhibin. Testosterone from the
Leydig cells stimulates spermatogenesis and stimulates the Sertoli Cells to nurse the Spermatozoa. Inhibin
Describe the hormonal regulation of from the Sertoli cells feeds back and downregulates FSH release. Testosterone from Leydig cells feeds back
Spermatogenesis. and downregulates LH production and GnRH release.

What are the common Androgens? Testosterone (Testes), Dihydrotestosterone (Converted peripherally) and Androstendione (Adrenal)
Differentiation of the Epididymis, Vas deferens and seminal vesicles. Growth spurt of the penis, the seminal
What are the functions of Testosterone vesicles, sperm, muscle, and red blood cell growth. Deepening of voice, closing of epiphyseal plates (via
in development? estrogen converted from testosterone) and Libido.

What is the function of In early differentiation it causes development of the penis, scrotum and prostate. In later/pubertal
Dihydrotestosterone in development? development it causes prostate growth and sebaceous gland activity.
How is testosterone converted to
DHT? 5 Alpha reductase converts Testosterone to DHT.
What are the sources of Estrogen in a Ovary makes 17 Beta estradiol, Placenta makes estriol and blood/peripheral tissues can aromatize androgens
woman? to estrogen.
What is the function of Estrogen in
development? Development of genitalia (external) and breast, and female fat distribution.
Growth of the follicle, endometrial proliferation, increased myometrial excitability. Upregulates LH, FSH and
estrogen receptors and thus upregulates itself. Feedback inhibition of LH and FSH and then the LH surge.
What are the typical functions of Stimulates prolactin secretion but blocks its action at the breast. Increases transport of proteins, Steroid
estrogen beyond development? hormone binding globulin synthesis, increases HDL and decreases LDL.
How much do estrogens increase in
pregnancy? 50 fold increase in estradiol and estrone. 1000 fold increase in estriol indicates fetal well being.

Pulsatile GnRH from the Hypothalamus causes release of FSH and LH from the anterior pituitary. FSH
stimulates the granulosa cells of the ovaries to increase Aromatase which can then convert androstendione to
Describe the hormonal regulation of estrogen. LH acts on the Theca cells to upregulate Desmolase which convert cholesterol to androstendione.
estrogen. The androstendione goes to the granulosa cells to be converted to estrogen.

What is the source of Progesterone? Corpus Luteum, placenta, adrenal cortex and testes (in men obviously)
What does elevation of progesterone
indicate? Ovulation!!!
Stimulation of endometrial glandular secretions and spiral artery development. Maintains pregnancy.
Decreases myometrial excitability. Increases production of thick cervical mucous, which inhibits sperm entry
into the uterus. Increases body temperature (hence why you take your temp), inhibits gonadotropins (LH
and FSH), relaxes uterine smooth muscle (prevents contraction) and decreases estrogen receptor
What is the function of Progesterone? expressivity.
Granulosa cells respond to FSH and stimulate growth of 10-20 follicles. LH responsive Theca cells stimulate
growth of the corpus luteum and produce androgens which are converted to estrogen by granulosa cells (to
stimulate the developing follicle). Estrogen encourages growth of the endometrium and provides positive
feedback to the anterior pituitary to stimulate release of more FSH/LH leading to the midcycle gonadotropin
What happens during the surge. About 1 week before ovulation, one follicle becomes dominant meaning that it becomes more
proliferative/follicular phase of a responsive to FSH. The follicle secretes lots of inhibin which downregulates FSH and causes atresia of the
woman's cycle? other follicles.
When is follicular growth fastest? 2nd week of the proliferative phase.
What stimulates endometrial
proliferation? Estrogen

What maintains the endometrium? Progesterone

What defines Oligomenorrhea? Cycle greater than 35 days
What defines Polymenorrhea? Cycle less than 21 days
What defines Metorrhagia? Frequent but irregular menstruation
What defines Menometrorrhagia? Heavy, irregular menstruation
During the follicular phase, both estrogen and progesterone are low. FSH is fairly low as is LH initially. LH
spikes about halfway through the follicular phase which increases estrogen above its threshold. Estrogen
feeds back onto LH which causes it to spike along with an estrogen spike. FSH is also increased and has a
small spike along with the LH spike. This causes ovulation and begins the secretory/luteal phase. LH and
Describe the hormonal changes during FSH then drop. Estrogen increases again but Progesterone increases a lot throughout the whole phase thus
a woman's cycle (see Reproductive maintaining the lining of the endometrium. Everything drops when entering the menstrual phase which
Attachment 1). allows the endometrial llining to shed.

A primordial follicle consists of an oocyte surrounded by a single layer of squamuos granulosa cells. The
granulosa cells enlarge and become cuboidal turning the follicle into a primary follicle. The primary follicle
then enlarges and the granulosa cells form more than one layer. The Zona Pellucida then forms around the
oocyte. The structure becomes a secondary follicle when fluid filled vesicles develop among the granulosa
cells and a well developed capsule, Theca layer, becomes apparent around the granulosa cells. The Theca
Describe the maturation of the Follicle has both internal and external layers. It becomes a mature follicle when the vesicles form a single antrum.
(see Reproductive Attachment 2). At full maturity, the oocyte is located in the cumulus mass.
During ovulation, the oocyte is released with some granulosa cells called the corona radiata. The remaining
granulosa cells divide rapidly and enlarge to form the corpus luteum which makes progesterone for the
What happens to the follicle during remainder of the cycle or the beginning of pregnancy. The corpus luteum then degenerates to form the
ovulation? corpus albicans and eventually becomes fibrotic.
What hormonal changes are seen Increased estrogen, increased GnRH and increased GnRH receptors on anterior pituitary, estrogen surge
during ovulation? precedes LH surge. Increased temperature from increased progesterone.
What is Mittelschmerz? Blood from ruptured follicles which can cause peritoneal irritation that mimics appendicitis.
Primary oocytes begin Meiosis I during fetal life but don't complete Meiosis I until just before ovulation. Thus
When does oogenesis begin and when Meiosis I is arrested in Prophase for years until ovulation. Meiosis II arrests in metaphase until fertilization.
is it completed? If there is no fertilization, the secondary oocyte degenerates.
Begins with a diploid Oogonium (2N) which replicates (interphase) to become a diploid primary oocyte (4N).
The Primary oocyte then arrests in Prophase I until ovulation. During ovulation it divides to become a
secondary haploid oocyte (2N) and a polar body which degenerates. It arrests in Metaphase II here until
fertilization. The secondary Oocyte divides again to become a Haploid Ovum (1N) and another polar body
What is the process of oogenesis? that degenerates.
Where does Fertilization most Most commonly happens in the upper end of the Fallopian tube (the ampulla). Typically within a day after
commonly happen? ovulation.
When does implantation into the wall 6 days after fertilization. The trophoblast secretes Beta-HCG which is detectable in the blood 1 week after
of the uterus typically occur? conception and in urine (home test) 2 weeks after conception.

How is lactation induces after labor? The decrease in maternal steroids induces lactation.
How is milk production maintained Suckling increases nerve stimulation which increases oxytocin and prolactin production thus maintaining milk
after birth? production.
What is the role of Prolactin in the
female? PRL induces and maintains lactation and decreases reproductive function.
What is the role of Oxytocin in the
female? Helps with milk letdown and may be involved with uterine contractions.
Where is hCG made? Syncytiotrophoblast of the placenta.

Maintains corpus luteum (thus progesterone) for the first trimester by acting LH. The Placenta synthesizes its
What is the function of hCG? own estriol and progesterone during the 2nd and 3rd trimester and the corpus luteum degenerates.
How is pregnancy detected? hCG is used to detect pregnancy because it appears early in the urine.
What changes in hCG are there in hCG is elevated in Hydatidiform moles, Choriocarcinoma, Gestational trophoblastic tumors (and other tumors
pathologic states? I think)
Decreased Estrogen production due to age linked decline in follicles. Significantly increased FSH, increased
What hormonal changes are seen in LH, increased GnRH. Average age of onset is 51, earlier in smokers. Usually preceded by a few years of
menopause? irregular periods.
What is the main source of Estrogen Estrone from peripheral conversion of androgens. Increased androgens can cause hirsutism (that's why your
after menopause? grandma has a mustache)
What are some symptoms of
menopause? HHAVOC-Hirsutism, Hot flashes, Atrophy of the Vagina, Osteoporosis, Coronary artery disease

47 (XXY). Causes testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair
What is Klinefelter's Syndrome? distribution. May cause developmental delay. Usually a Barr body is present (inactive X chromosome)
How does Klinefelter's Syndrome Dysgenesis of seminiferous tubules causes decreased inhibin which leads to increased FSH. Abnormal Leydig
cause infertility? cell function causes decreased testosterone and increased LH and estrogen.
45 (XO). Causes short stature, ovarian dysgenesis (streak ovaries), shield chest, bicuspid aortic valve,
webbing of the neck from cystic hygroma, preductal coarctation of the aorta, no Barr body and primary
What is Turner's Syndrome? amenorrhea.

Describe a double Y male 47 (XYY). Phenotypically normal, very tall, severe acne, antisocial behavior in 1-2%, normal fertility.
What hormonal changes would you
see with a defective androgen
receptor? Increased testosterone and increased LH (female phenotype I think)

What hormonal changes would you

see with a Testosterone-secreting
tumor, or exogenous steroids Increased testosterone but decreased LH from negative feedback

What hormonal changes would you

see with primary hypogonadism? Decreased testosterone and increased LH from gonadal failure and lack of feedback.
What hormonal changes would you
see with Hypogonadotropic
hypogonadism? Decreased testosterone and decreased LH from pituitary failure not stimulating the gonads.
What is pseudohermaphroditism? Disagreement between the phenotypic (external genitalia) and gonadal (testes vs ovaries) sex.
46 (XX). Ovaries are present but the external genitalia are virilized or ambiguous. It's due to excessive or
What is a female inappropriate androgen exposure during early gestation. Usually congenital adrenal hyperpasia or exogenous
pseudohermaphrodite? androgen administration.
46 (XY). Testes are present but external genitalia are female or ambiguous. The most common reason is
What is a male pseudohermaphrodite? androgen insensitivity syndrome aka testicular feminization.
What is a true hermaphrodite? (46, XX or 47, XXY). Both ovaries and testicular tissue present. Ambiguous genitalia. Very rare.
Defect in androgen receptors resulting in normal-appearing female. Female external genitalia with a
rudimentary vagina. Uterus, uterine tubes are generally absent. No sexual hair. Testes are often found in
What is Androgen Insensitivity the labia majora and must be surgically removed to prevent malignancy. Increased testosterone (although
Syndrome? no response), increased estrogen and LH

Inability to convert testosterone to DHT. Ambiguous genitalia until puberty when the massive testosterone
increase causes masculinization and increased growth of the external genitalia. Testosterone/estrogen levels
What is 5 alpha reductase deficiency? are normal; LH is normal or increased. Internal genitalia are normal.
Cystic Swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast) that presents with
abnormal vaginal bleeding. Most common cause of Choriocarcinoma. See increased Beta-hCG, a
honeycombed uterus, looks like a cluster of grapes (if a cluster of grapes is totally disgusting looking). See
What is a Hyaditiform Mole? an abnormally enlarged uterus.
2 sperm with a completely empty egg. Classically have a snowstorm appearance with no fetus during first
sonogram. Moles can lead to uterine rupture. Treat with dilitation and curettage and methotrexate. Monitor
What is a complete Hyaditiform Mole? Beta-hCG.

What characteristics are seen in a Karyotype is 46,XX or 46, XY. Massively increased hCG, increased uterine size, 2% convert to
complete mole? adenocarcinoma, no fetal parts, 2 sperm +empty egg, 15-20% form malignant trophoblastic disease.
What characteristics are seen in a Karyotype is 69,XXY, slightly increased hCG, no change in uterine size, rare for it to convert to
partial mole? choriocarcinoma, 2 sperm+1 egg, risk of malignancy is less than 5%
What are some common causes of during the 1st weeks- low progesterone levels (no response to Beta-hCG, 1st trimester-chromosomal
recurrent miscarriages? abnormalities, 2nd trimester-bicornate uterus
What is pre-eclampsia? Combination of hypertension, proteinuria and edema.
What is eclampsia? Pre-eclampsia + Seizures
What are some risk factors for pre-
eclampsia? Pre-existing hypertension, diabetes, chronic renal disease and autoimmune disorders.
What is the pathogenesis of Pre- Caused by placental ischemia due to impaired vasodilation or spiral arteries, resulting in increased vascular
eclampsia? tone. May be an issue with implantation.
What is HELLP Syndrome? Hemolysis, Elevated LFT's, Low Platelets from Pre-eclampsia
What are some clinical features of Headache, blurred vision, abdominal pain, edema of the face and extremities, altered mentation,
Pre-eclampsia? hyperreflexia. Lab findings include thrombocytopenia and hyperuricemia.

How do you treat Pre-Eclampsia or Delivery of the fetus as soon as it's viable. Otherwise bed rest, salt restriction, and monitoring/treatment of
Eclampsia? hypertension. Treatment is IV magnesium sulfate and diazepam to prevent seizures of eclampsia.
Premature detachment of the the placenta from the implantation site. Fetal death and DIC may occur.
What is Abruptio Placentae? Increase in risk with smoking, hypertension and cocaine use.
Defective decidual layer allows the placenta to attach to the myometrium. No separation of the placenta after
birth. May cause massive bleeding after delivery. Associated with prior C-Section. Acreta does not penetrate
What is Placenta Acreta? the entirety of the myometrium.
What is Placenta Increta? Just like Placenta Acreta but extends further into the myometrium.

The worst form of Placenta Acreta which involves the placenta extending all the way through the myometrium
What is Placenta Percreta? to the serosa. The placenta may then attach to other organs like the bladder or rectum.
Attachment of the placenta to the lower uterine segment. May then occlude the internal os (so baby can't
What is Placenta Previa? get out). Associated with multiparity and prior C-Section.

Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and
What is an Ectopic Pregnancy? sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
What is the problem with retained
placental tissue? May cause postpartum hemorrhage.

What are some risk factors associated History of infertility, Salpingitis/PID, ruptured appendix (at any point), prior tubal surgery or any lower
with ectopic pregnancy? abdominal surgery, endometriosis.
Greater than 1.5-2 Liters of amniotic fluid. Associated with esophageal and duodenal atresia, causing
What is Polyhydramnios? inability to swallow amniotic fluid. Also associated with anencephaly.

Less than 0.5 Liters of amniotic fluid. Associated with placental insufficiency, bilateral renal agenesis or
What is Oligohydramnios? posterior urethral valves (in men) and thus an inability to excrete urine. Can cause Potter's syndrome.
Atypical appearance of the fetus in the womb as a result of oligohydramnios. Causes clubbed feet,
What is Potter's Syndrome? pulmonary hypoplasia and cranial anomalies.

Describe Dysplasia and Carcinoma in Disordered epithelial growth. Begins at the basal layer of the squamo-columnar junction and extends
Situ of the cervix. outward. Classified as CIN I, CIN II or CIN III (Carcinoma in Situ), depending on the extent of the dysplasia.
What virus is associated with Cervical
dysplasia? HPV 16 and 18
What risk factors are associated with
cervical dysplasia? Multiple sexual partners, smoking, early sexual intercourse, HIV infection
Pretty much the cervical cancer gone really nasty. Often squamous cell carcinoma. Papsmear can catch
Describe invasice carcinoma of the cervical dysplasia (koilocytes) before it becomes invasive carcinoma. Lateral invasion can block ureters
cervix causinf renal failure.
Cervical cell infected with HPV that is undergoing dysplasia. See large nuclei and large ring of cytoplasm.
What is a Koilocyte? See Attachment 3 for some pics.

Non-neoplastic endometrial glands/stroma in an abnormal location outside the uterus. Characterized by

cyclic bleeding from the ectopic endometrial tissue resulting in blood filled "chocolate cysts." Does anyone
What is Endometriosis? else want to puke right now? Often in the ovary or on the peritoneum.
How does Endometriosis manifest
clinically? Severe menstrual-related pain.
What are possible complications of
Endometriosis? Often causes infertility, possibly due to retrograde mentrual flow or ascending infection.
What is Adenomyosis? Endometrium within the myometrium
Abnormal endometrial gland proliferaton usually caused by excess estrogen stimulation. Associated with
What is Endometrial Hyperplasia? increased risk for endometrial carcinoma.
How does Endometrial Hyperplasia
manifest clinically and what are some Postmenopausal vaginal bleeding. Risk factors are anovulatory cycles, hormone replacement therapy,
risk factors? polycystic ovarian syndrome and granulosa cell tumors.
Most common gynecologic malignancy, usually between 55 and 65 years of age. Usually a progression of
endometrial hyperplasia so presents with vaginal bleeding after menopause. Risk factors are prolonged
estrogen exposure without progesterone, obesity, diabetes, hypertension, nulliparity and late menopause.
What is Endometrial Carcinoma? The more it's invaded the myometrium, the worse the prognosis.

Most common cause of all tumors in females. Essentially a Fibroid. Often causes multiple tumors with well
demarcated borders. This is a benign smooth muscle tumor and malignant transformation is very rare.
Mostly occurs between 20-40 years old and is often asymptomatic. may cause abnormal uterine bleeding or
result in miscarriage. If bleeding is severe it may cause Iron deficiency anemia. See a whorled pattern of
Describe a Leiomyoma? smooth muscle bundles (doesn't become Leiomyosarcoma). See attachment 4 for a picture.

Bulky, irregularly shaped tumor with areas of necrosis and hemorrhage. Nasty tumor. Typically arises de
novo, not from a Leiomyoma. Highly aggressive tumor with a tendency to recur. May protrude out of the
What is a Leiomyosarcoma? cervix and bleed (yuck!). More common in middle aged women and African American women.
What is the epidemiology of
gynecologic tumors? Incidence- Endometrial>Ovarian>Cervical. Worst Prognosis- Ovarian>Cervical>Endometrial

Premature atresia of ovarian follicles in women of reproductive age. Presents with signs of menopause after
What is premature Ovarian failure? 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
what are the most common causes of ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, Cushing Syndrome and adrenal
anovulation? 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,
What is Polycystic Ovarian Syndrome? OCP, gonadotropin analogs, clomiphene or surgery.
What hormonal changes do you see in
PCOS? Increased LH and FSH and increased Testosterone.

What is a Follicular Cyst? Distention of a ruptured Grafian Follicle. May be associated with hyperestrinism and endometrial hyperplasia.
What is a Corpus Luteum cyst? Hemorrhage into persistent corpus luteum. Commonly regresses spontaneously.
Commonly bilateral or multiple cysts. Due to gonadotropin stimulation. Associated with choriocarcinoma and
What is a Theca Lutein Cyst? moles.
What is a Chocolate Cyst? Blood-containing cyst from ovarian endometriosis. Varies with the menstrual cycle.
What age group most commonly gets
Ovarian Cell Tumors? Most common in adolescents
Malignant, equivalent to a male seminoma, but rarer (1% vs 30%). Sheets of uniform cells with hCG and
What is a Dysgerminoma? 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
What is a Choriocarcinoma? 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
What is a yolk sac (endodermal sinus) yellow, friable, solid masses. 50% have Schiller Duval bodies that resemble glomeruli. Alpha fetoprotein is
tumor? the tumor marker.

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.
What is a teratoma? 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.
What is a serous cystadenoma? Benign.

What is a serous cystadenocarcinoma? Makes up about 50% of ovarian tumors, malignant and frequently bilateral.

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

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

What is a Krukenberg tumor? GI Malignancy that metastasizes to the ovaries, causing a mucin-secreting signet cell adenocarcinoma.
What causes squamous cell carcinoma
of the vagina? Secondary to squamous cell carcinoma of the cervix.
What predisposes to Clear Cell
Adenocarcinoma? Affects women who had exposure to DES in utero.
Who is affected by Sarcoma
Botryoides (variant of
Rhabdomyosarcoma) Affects girls < 4 years of age. Spindle shaped tumor cells that are desmin positive.
How do Bartholin's gland cyst
present? Rare. Present with pain in the labia majora. Can result from previous infection.
Small, mobile, firm mass with sharp edges. Most common tumor in those <25 years. See increasing siza
What is a Fibroadenoma of the breast? and tenderness with increasing estrogen such as during menstruation. Not a precursor to breast cancer.
Small tumor that grows in lactiferous ducts. Typically beneath areola. See serous or bloody nipple
What is an Intraductal Papilloma? discharge. Slight (1.5-2X) increased risk for breast carcinoma.
Large bulky mass of connective tissue and cysts with "Leaf like projections." Most common in the 6th
What is a Phyllodes Tumor? decade. Some may become malignant.

How do malignant breast tumors arise Common postmenopause. Arise from mammary duct epithelium or lobular glands. Overexpression of
and when/where are they most estrogen/progesterone receptors on erb-B2 (HER-2 and EGF Receptor) is common. Affects therapy and
common? prognosis. Axillary lymph node involvement is the single most important prognostic factor.
Risk factors are increased estrogen exposure. Increased total number of menstrual cycles, older age at 1st
What are some risk factors for live birth, obesity (adipose tissue serves as a major source of estrogen in post-menopausal women by
malignant breast tumors? converting androstenedione to estrone).
What is a Ductal Carcinom in Situ Malignant tumor of the breast that fills the ductal lumen. Arises from ductal hyperplasia. Early malignancy
(DCIS)? without basement membrane penetration.
Worst and most invasive ductal carcinoma but also most common. Forms firm, fibrous, rock hard masses
What is invasive ductal carcinoma? with sharp margins and small, glandular duct like cells.

What is an invasive Lobular tumor? Malignant breast tumor, often multiple and often bilateral. See an orderly row of cells.
What is a medullary tumor of the
breast? Malignant tumor with a good prognosis. See fleshy, cellular, lymphatic infiltrate.
What is a comedocarcinoma of the
breast? Subtype of DCIS. See ductal caseous necrosis.
What is an inflammatory tumor of the Nasty, malignant tumor with a 50% 5 year survival. See dermal lymphatic invasion by breast carcinoma.
breast? See Peau d'orange-breast skin looks like orange peel.
Eczematous patches on nipples. Paget cells are large cells in the epidermis with clear halo around them.
What is Paget's disease? May also be seen on the vulva. Suggests an underlying carcinoma.
Most common cause of breast lumps after age 25. Presents with premenstrual breast pain and multiple
lesions, often bilaterally. See a fluctuation in size of the mass. Usually does not indicate increased risk of
What is Fibrocystic disease? carcinomas.
Fibrosis-hyperplasia of breast stroma. Cystic-fluid filled, blue dome. Ductal dilation. Sclerosing adenosis-
increases acini and intralobular fibrosis. Associated with calcifications. Epithelial hyperplasia-increase in
What are the histologic subtypes of number of epithelial cell layers in terminal duct lobule. Increases risk of carcinoma with atypical cells.
Fibrocystic disease? Occurs in women >30 years of age.
Breast abscess. During breast feeding. Increases risk of bacterial infection through cracks in the nipple.
What is acute mastitis? 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
What is Fat Necrosis? trauma.
Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter's syndrome or drugs
(estrogen, marijuana, heroin, psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol,
What is Gynecomastia? 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

Nipple-Paget's disease, breast abscesses. Lactiferous sinus-Intraductal papilloma, breast abscess, mastitis.
What tumors occur at each of these Major duct-Fibrocystic change, ductal cancer. Terminal ducts-Tubular carcinoma. Lobules-lobular carcinoma,
structures? sclerosing adenitis. Stroma-Fibroadenoma, phyllodes tumor.
How does prostatitis present? Dysuria, frequency, urgency, low back pain.

What are causes of acute prostatitis? Usually bacterial, especially E. Coli

What are causes of chronic
prostatitis? 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
What is Benign Prostatic Hyperplasia urine and dysuria. May lead to distention and hypertrophy of the bladder, hydronephrosis and UTI's. Not
(BPH)? considered premalignant. Do see increased free PSA but not rapidly increasing like in cancer.
How do you treat BPH? 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
What is Prostatic adenocarcinoma? alkaline phosphatase and PSA.

Undescended testis. Lack of spermatogenesis due to increased body temperature. Also associated with
What is cryptorchidism? increased risk of germ cell tumors. Prematurity increases the risk of cryptorchidism.
How common are testicular germ cell
tumors? 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
What is a Seminoma? radiosensitive, only metastasize late and have a great prognosis.

Malignant, painful tumor with a worse prognosis than a seminoma. Often glandular or papillary morphology.
What is an embryonal carcinoma? Can differentiate and become other tumors and is associated with increased AFP and hCG.
What is a yolk sac (endodermal sinus) Yellow, mucinous tumor analagous to an ovarian yolk sac tumor. See Schiller Duval bodies which resemble
tumor in a man? primitive glomeruli.
Malignant, hCG secreting tumor. Has distinct syncytiotrophoblastic and cytotrophoblastic elements. Causes
What is a Choriocarcinoma in a man? hematogenous metastases.
What is a teratoma in a man? Similar to females except that mature teratomas in men are usually malignant.
How common are testicular non-germ
cell tumors? 5% of all testicular tumors, most of which are benign.
Androgen producing tumor which causes gynecomastia in men, precocious puberty in boys. Contains Reinke
What is a Leydig Cell Tumor? crystals and is golden brown in color.
What is a Sertoli Cell Tumor? Androblastoma from the sex cord stroma.
What is testicular lymphoma? Most common testicular cancer in older men. It's pretty much lymphoma in the testicles.

What is a tunica vaginalis lesion? A lesion in the serous covering of the testis. Presents as testicular masses that can be transilluminated.
What is a Variocele? Dilated vein in pampinoform plexus which can result in infertility. Looks like a bag of worms.
What is a Hydrocele? Increased fluid secondary to incomplete fusion of the processus vaginalis
What is a spermatocele? Dilated epididymal duct
Gray, solitary, crusty plaque, usually on the shaft of the penis or on the scrotum. Peak incidence is in the 5th
What is Bowen's Disease? decade of life. Progresses to invasive squamous cell carcinoma in <10% of cases.
Qhat is Erythroplasia of Queyrat? Red, velvety plaques, usually involving the glans penis. Otherwise similar to Bowen's disease.
What is Bowenoid papulosis? Multiple papular lesions. Affects younger men but isn't usually invasive
What is Squamous Cell Carcinoma of Essentially like any other SCC, just on the penis. Commonly associated with HPV and lack of circumcision.
the penis? More common in Asia, Africa and South America.
What is Peyronie's Disease? Bent penis due to acquired fibrous tissue formation.
What changes are seen in Glycogen and lipid accumulation, extra-cellular matrix changes, prolactin and IGF binding proteins increased,
Decidualization? COX-2 increase which increases PGE2, and influx od dedidual NK cells.

When does Blastocyst hatching occur? When the blastocyst enters the endometrial cavity, about 5 days after fertilization.
What is the Zona Pellucida? Non-cellular, porous layer of glycoproteins around the oocyte.

What proteins characterize Early pregnancy factor, Platelet activating factor, human Chorionic Gonadotropin, Matrix Metalloproteinases
preimplantation of the embryo? and Inhibitors of Matrix Metalloproteinases, Heparin binding-EGF like growth factor receptors
What are the three stages of
implantation? Apposition, Adhesion and Invasion
What is the Decidua Basalis? Decidua that forms underneath the embryo
What is the Decidua Capsularis? Capsule of decidua over the embryo
What is the Decidua Paritalis? Other decidua lining the uterine cavity
What happens to RBC and Plasma
volume and mass in pregnancy? Both are increased but plasma is increased more than RBC. This results in a dilutional effect in hematocrit.
Creatinine clearance is increased. GFR increases fairly significantly. Increased clearance of creatinine and
What happens to GFR and Creatinine urea results in serum creatinine and urea that are really low. Thus normal creatinine and urea are
Clearance during pregnancy? problematic.
Estrogen and progesterone both stimulate the respiratory center. Greater tidal volume and increased
Why does respiratory alkalosis happen respiration rate also cause increased minute ventilation, thus more CO2 is blown off. Thus respiratory
during pregnancy? alkalosis from decreased PaCO2
Why do women get dyspnea during
pregnancy? May be due to decreased CO2 stimulating the respiratory center and causing subjective shortness of breath.
hCG simulates TSH since they share the same alpha subunit. Thus it stimulates T4 secretion during the first
Why are Thyroxin and Cortisol 10 weeks. Estrogen promotes growth of the pituitary and the thyroid and synthesis of thyroid binding
increased in pregnancy? globulin. Thus T4 and cortisol are increased but free T4 and cortisol are the same.
What defines menopause? No menses for one year after age 40.
Waxing and waning of estrogen levels from decreased ovarian function. Depletion of granulosa and thecal
What are the physiologic causes of cells. Lack of response to gonadotropins. Increased LH stimulates androgen production in stromal cells
menopause? (thus hirsutism)
What are non-physiologic causes of Surgical removal or radiation of ovaries. Turner syndrome. Family history of early menopause and left
menopause? handedness (seriously???)
What is the average age of
menopause and how is age at Average age is 51. The age at which it's determined is genetically determined, but smokers reach
menopause determined? menopause early and peri-menopause is mid-to late 40's.

Secondary amenorrhea, hot flushes, night sweats, atrophic vaginitis with pruritis, burning, bleeding and
What are some clinical findings in dyspareunia. Also see mood swings, anxiety, depression, insomnia, decreased libido, urinary incontinence,
menopause? headaches, tiredness, lethargy, and osteoporosis with increased risk of Colle's and vertebral fractures.
What are some labroratory findings in
menopause? Increase in LH and FSH from a drop in estrogen (LH) and progesterone (FSH)
What are some treatment options for
symptomatic menopause? Estrogen replacement, progestins added if the uterus is still present to prevent endometrial adenocarcinoma.
What are risks of long term hormone Thromboembolism, Coronary heart disease, stroke, slightly increased risk for breast cancer, increased risk for
replacement? dementia in women over 65.
What is Hirsutism? Excess hair in normal hair-bearing areas.
What is virilization? Hirsutism plus male secondary sex characteristics
What are male secondary sex
characteristics? Increased muscle mass, acne, enlarged clitoris
Both caused by increased androgens of either ovarian or adrenal origin. In the ovaries, the androgen is
What causes virilization or hirsutism? testosterone, in the adrenals it's DHEA-S
Polycystic ovary syndrome, idiopathic causes, adrenogenital syndrome, insuline resistance, drugs like
androgenic progestins, phenytoin, cyclosporin, minoxidil. Can also be from ovarian tumors like a leydig or
What are some causes of virilization sertoli-leydig cell tumor, adrenal tumors producing Cushing syndrome, decreased steroid hormone binding
and hirsutism? globulin from obesity and hypothyroidism.

Syndrome that occurs around menarche. See increased synthesis of LH and decreased synthesis of FSH.
Increased LH increases androgen synthesis resulting most often in hirsutism. Androgens are then aromatized
to estrogen in adipose cells increasing the risk of endometrial carcinoma. The increased estrogen feeds back
positively on LH and negatively on FSH. Suppression of FSH causes follicle degeneration resulting in fluid
What is Polycystic Ovarian Syndrome? accumulating and producing subcortical cysts that then enlarge the ovaries.
What are clinical findings in polycystic
ovarian syndrome? Menstrual irregularities, mostly oligomenorrhea and often hirsutism, infertility or obesity.
What are some lab findings in PCOS? LH:FSH ratio >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. LH-
What is the treatment in PCOS? releasing hormone analogs inhibit ovarian androgen production.
Loss of blood >80 mL per period. It's likely if sheets are stained despite heavy protection. Excessive
What is Menorrhagia? 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
What is Dysmenorrhea? secondary type is from endometriosis, adenomyosis, leiomyomas, or cervical stenosis.
What is the treatment for Primary
Dysmenorrhea? NSAID's, OCP, nifedipine, magnesium sulfate
What is the treatment for secondart
Dysmenorrhea? Essentially deal with the underlying disease.
What is dysfunctional uterine
bleeding? Abnormal uterine bleeding that is unrelated to an anatomic cause. Note that this is a diagnosis of exclusion.
What are some types of dysfunctional
uterine bleeding? Menorrhagia, Hypomenorrhea, Metrorrhagia, Menometrorrhagia, Oligomenorrhea, Polymenorrhea
What is most common cause of
irregular bleeding? Anovulatory cycle in 90% of cases but less than 10% due to anovulation during reproductive years.
What causes anovulatory Excessive estrogen stimulation relative to progesterone resulting in an absent secretory phase. It produces
dysfunctional uterine bleeding? excessive endometrial hyperplasia and excessive bleeding.
Inadequate luteal phase resulting in inadequate maturation of the corpus luteum. This causes inadequate
What causes ovulatory dysfunctional synthesis of progesterone and delay in the development of the secretory phase. May see decreased 17-OH
uterine bleeding? progesterone .
How do you treat ovulatory If the follicle size is normal, supplement progesterone. If the follicle size is inadequate, give clomiphene
dysfunctional uterine bleeding? sulfate.
Absence of menses by age 16. Most cases are due to constitutional delay with a family history of delayed
What is Primary Amenorrhea? menses.
What is Secondary Amenorrhea? Absence of menses for 3 months, most commonly due t pregnancy.

What are some causes of Hypothalamic or pituitary dysfunction resulting in decreased LH and FSH which results in decreased estrogen
amenorrhea? and progesterone. Ovarian disorders cause problems in synthesis of estrogen or progesterone.

What are causes of abnormal vaginal Vulvovaginitis, poor hygeine, infection, gonrrhea, sexual abuse, foreign bodies, embryonal
bleeding in a pre-pubertal girl? rhabdomyosarcoma
What are some causes of abnormal
vaginal bleeding between menarche
and 20 years? Anovulatory dysfunctional uterine bleeding, Von Willebrand's disease
What are some causes of abnormal Pregnancy and related complications, ovulatory dysfunctional uterine bleeding, PID, hypothyroidism,
vaginal bleeding between ages 20-40? submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis

What are some causes of abnormal

vaginal bleeding after age 40? Anovulatory dysfunctional uterine bleeding, endometrial hyperplasia, cancer.
What part of the placenta covers the
fetal surface? Entirely covered by the chorionic plate. The chorionic villi vessels converge with the umbillical cord.
What covers the chorion? Chorion is covered with amnion
What covers the maternal surface of
the placenta? Contains cotyledons covered by decidua basalis.

Where do the chorionic villi project? Into the intervillous space

What does the intervillous space Maternal blood that delivers oxygen and nutrients and spiral arteries from the uterus that empty into the
contain? space
What lines the chorionic villi? Trophoblastic tissue
What forms the outside layer of the
trophoblast? Syncytiotrophoblast.
What does the Syncytiotrophoblast
do? Synthesizes hCG, and HPL which directly correlates with placental mass and has anti-insulin activity.
What forms the inside layer of the
trophoblast? Cytotrophoblastic tissue
How many vessels are contained in
the umbillical cord? One umbillical vein and two umbillical arteries. The vein carries the oxygenated blood in this case
What risks are related to a single Increased incidence of congenital anomalies, defects including cardiovascular defects, trisomy 18 and
umbillical artery? esophageal atresia.
What causes most placental
infections? Ascending infections, often from premature rupture of membranes

How should you treat a placental Treat prophylactically with IV Ampicillin+Erythromycin followed by PO amoxicillin and erythromycin. If
infection even if culture is negative? culture positive you can give IV penicillin or ampicillin
What is Funisitis? Infection of the umbillical cord
What is Placentitis? Infection of the placenta
What is chorioamnionitis? Infection of the fetal membranes
What complications might arise from
chorioamnionitis? Neonatal sepsis and meningitis. Treat with Cefoxitin or Ticaricillin-Clavulanate
What is Placenta Previa? 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
How does Placenta Previa present? distress is usually not present.
Do not do a pelvic exam. Transabdominal ultrasound localizes the placenta and transvaginal ultrasound
How do you diagnose Placenta Previa? confirms placenta previa.
Premature separation of the placenta due to formation of a retroplacental clot. This separates the placenta
What is Abruptio Placentae? from the implantation site. This is most common cause of late pregnancy bleeding
Hypertension, smoking, cocaine, advanced maternal age, trauma, chorioamnionitis, premature membrane
What are risks for abruptio placentae? rupture, previous abruptio placentae.
What are the clinical signs of abruptio Painful uterine bleeding, forceful uterine contractions or signs of preterm labor, usually see evidence of fetal
placentae? distress
Direct implantation into muscle without intervening decidua. Causes great risk for hemorrhage during
What is Placenta Acreta? 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
What is Velamentous insertion? Section to avoid vessel tear.
What risks do accessory lobes of the
placenta pose? Increased risk of hemorrhage if they are detached.

What can cause an enlarged placenta? Diabetes mellitus, Rh hemolytic disease of the newborn, congenital syphilis
What type of placentas do
Monozygotic twins have? Monochorionic and monoamniotic although they can have dichorionic placentas

What risks are associated with

monochorionic, diamnionic placentas? Twin Twin Transfusion syndrome.
What is Preeclampsia? Toxemia of pregnancy

What are risk factors for First pregnancy, more common in women <20 years and >35 years, history of previous preeclampsia,
Preeclampsia? positive family history, multiple gestations, african american, thrombocytosis, obesity
Abnormal placentation causing mechanical or functional obstruction of the spiral arteries. The abnormal
What is the pathogenesis of Pre- trophoblastic tissue invades the spiral arteries. Imbalance favors vasoconstriction over vasodilation
eclampsia? (decreased PGE2 and NO, increased TXA2, Ang II and increased sensitivity to Ang II)
What are pathologic findings in Pre-
Eclampsia? Premature aging of the placenta, multiple placental infarctions, spiral arteries show atherosclerosis
Hypertension, proteinuria from leaky capillaries (increased inflammation), dependent pitting edema from loss
What are clinical findings in Pre- of albumin, weight gain, seizures in eclampsia, swollen endothelial cells in glomerular capillaries producing
Eclampsia? oliguria.
What are some other symptoms in Right upper quadrant pain and hepatomegaly, periportal necrosis with increased transaminases, HELLP
Pre-Eclampsia? syndrome
What is a Hyaditiform Mole? 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
What is a complete Hyaditiform Mole? or duplicated 23X sperm in the ovum
Complete mole. Presents with painless vaginal bleeding in fourth, fifth month of pregnancy. Causes severe
Which type of Mole has an increased vomiting, pre-eclampsia, uterus that is too large for gestational age, increased hCG for gestational age, and
risk of Choriocarcinoma? snowstorm appearance on ultrasound.
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
What is a partial Hyaditiform Mole? choriocarcinoma.
malignant tumor composed of syncytiotrophoblast and cytotrophoblast without chorionic villi. Risks are
What is a Choriocarcinoma? complete mole, spontaneous abortion and normal pregnancy
Where does Choriocarcinoma
metastasize? Lungs and vagina-hemorrhagic lesions
What is the composition of amniotic Predominantly fetal urine, initially plasma ultra-filtrate from mom. High salt content causes ferning when
fluid? dried on a slide-good sign of premature rupture of amniotic sac.
What is the quantity of amniotic flud
maintained? Swallowed and recycled by the fetus.
Excessive amniotic fluid. Causes are tracheoesophageal fistula, duodenal atresia, maternal diabetes-
What is Polyhydramnios? maternal hyperglycemia causes fetal hyperglycemia resulting in fetal polyuria.
Decreased amount of amniotic fluid. Caused by juvenile polycystic kidney disease, fetal genitourinary
What is Oligohydramnios? obstruction, uteroplacental insufficiency and premature rupture of membranes.
What can Alpha Fetoprotein indicate in Increased maternal AFP indicates open neural tube defects (often related to Folate deficiency). Decreased
pregnancy? maternal AFP can indicate Down syndrome.
What does the Lecithin to Lecithin is synthesized by type II Pneumocytes which decreases alveolar tension to prevent atelectasis. L:S
Sphingomyelin ratio indicate? ratio >2 indicates adequate surfactant.

What can increase surfactant Cortisol and thryroxine increase surfactant synthesis. Maternal administration of glucocorticoids can increase
production in the fetus? 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 part of estriol synthesis does the

fetal adrenal cortex control? Fetal adrenal cortex converts pregnenolone from the placenta to DHEA-S.
What does the fetal liver do in estriol
synthesis? Hydroxylates DHEA-S to 16-OH-DHEA-S
What does the maternal placenta do Initially converts LDL to pregnenolone for fetal processing. Placental sulfatase then cleaves off the sulfate
in estriol synthesis? from 16-OH-DHEA-S and converts it to free unbound estriol via aromatase.
What does the maternal liver do to Conjugates it to estriol sulfate and estriol glucosiduronate which is then excreted in the maternal urine and
estriol? bile.

What does decreased estriol indicate? Sign of fetal-maternal-placental dysfunction

What is the triad of markers in Down
syndrome? Decreased urine estriol, decreased AFP, increased serum Beta-hCG
What is the most high density location
of breast tissue? Upper outer quadrant-thus cancer is most commonly located in this location. Also underneath the nipple.
What effects do sex hormones have
on the breast during the menstrual
cycle? Estrogen stimulates ductal and alveolar growth. Progesterone stimulates alveolar differentiation.
Prolactin-stimulates and maintains lactogenesis. Oxytocin-released by the suckling reflex which causes
What hormones affect lactation? expulsion of milk into the ducts.
Where do outer quadrant breast
cancers drain? Axillary lymph nodes
Where do inner quadrant breast
cancers drain? Internal mammary lymph nodes.
What are normal causes of
Galactorrhea? Mechanical stimulation of the nipple from prolonged suckling or sexual intercourse.
What are pathologic causes of Prolactinoma, primary hypothyroidism (decreased T4 causes increased TRH which stimulates PRL), drugs like
Galactorrhea? OCP's, phenothiazines, methyldopa, H2-Receptor blockers and angiolytics.

What causes Bloody nipple discharge? Intraductal papilloma, ductal cancer

What causes prululent nipple
discharge? Acute mastitis due to Staph A., usually related to breast feeding
What causes Green-Brown nipple
discharge? Mammary duct ectasia (plasma cell mastitis)
What is the most common cause of
Breast Pain? Fibrocystic change
What is Mondor's disease? Superficial thromboplebitis of veins overlying the breast, presenting as a palpable, painful cord.
Most common painful breast mass in women <50 years old. Causes distortion of normal cyclic breast
changes. Some cysts have hemorrhage into the cyst fluid-called blue-domed cysts. Vary in size with the
What is Fibrocystic change? menstrual cycle but have no malignant potential
Proliferation of small ductules/acini in the lobule-pattern is often confused with infiltrating ductal cancer.
What is sclerosing adenosis? Often contains microcalcifications.

Ducts are estrogen sensitive. See papillary proliferation called papillomatosis, apocrine metaplasia (change
What is Ductal Hyperplasia? to sweat producing glands), and atypical ductal hyperplasia (increased risk for carcinoma)

What is Mammary duct Main ducts fill up with debris causing dilation, rupture and inflammation. Results in greenish-brown nipple
ectasia/plasma cell mastitis? discharge. May result in skin and nipple retraction stiulating cancer but no increased risk for breast cancer.
Trauma to breast tissue. Microscopic findings are lipid-laden macrophages with foreign body giant cells,
fibrosis and dystrophic calcification. See a painless indurated mass which is painful in the acute stage and
What is traumatic fat necrosis? may produce skin retraction stimulating cancer.
Most common breast tumor in women <35 years. Discrete movable, painless or painful mass. It's a benign
tumor derived from the stroma which proliferates and compresses the ducts. The duct epithelium is not
neoplastic. Estrogen sensitive so increases in size during pregnancy. May spontaneously involute during
What is a Fibroadenoma of the breast? menopause.
Bulky tumor derived from stromal cells. Most commonly benign but can be malignant in some cases-see
hypercellular stroma with signs of mitoses in malignancy. Lobulated tumor with cystic spaces containing leaf-
What is a Phyllodes tumor? like extensions.
Most common cause of bloody nipple discharge in women <50. Develops in the lactiferous ducts or sinuses.
What is an Intraductal Papilloma? No increased risk for cancer.
What are risk factors for breast Prolonged estrogen stimulation, genetic susceptibility, especially if first generation relatives. Prolonged
cancer? estrogen stimulation from either early menarche or late menopause or nulliparity.
What are some genetic markers for
breast cancer? BRCA 1 and BRCA 2, Li-Fraumeni, RAS oncogene, ERBB2, RB suppressor gene
What decreases risk for breast
cancer? Breast feeding, moderate or vigorous physical training, healthy body weight.
What are clinical findings in breast Painless mass in the breast, usually the upper outer quadrant. Skin or nipple retraction, painless axillary
cancer? lymphadenopathy, hepatomegaly and bone pain if there are metastases.

What is the primary screening test for Mammography-detects 80-90% of non-palpable breast masses. Does not distinguish benign from malignant
breast cancer? lesions. Can identify microcalcifications and spiculated masses with or without microcalcification.
Where do microcalcifications most Ductal carcinoma in situ, and sclerosing adenosis. Five or more microcalcifications that are punctate,
commonly occur? microlinear or branching all suggest malignancy
How is estrogen and progesterone
receptor expression related to
prognosis? ER/PR expression generally confers a good prognosis whereas ERB2/NEU has a poor prognosis if amplified.
What is a Ductal Carcinom in Situ Nonpalpable mass. Forms a cribiform pattern (seive like) or comodo like pattern (necrotic center).
(DCIS)? Commonly contains microcalcifications which allow it to be detected on mammogram.
Nonpalpable mass. Virtually always an incidental finding on breast biopsy for something else. Not
What is a Lobular Carcinoma in Situ identifiable on mammography. Lobules are distended with bland neoplastic cells. Usually ER/PR positive.
(LCIS)? Increased incidence of cancer in the opposite breast, that isn't LCIS.
Malignant, invasive breast tumor. Has a stellate morphology. Indurated, gray-white tumor. 1/3 have ERB2
amplification conferring poor prognosis. These look gritty on cut section and have reactive desmoplasia
What is Infiltrating Ductal Carcinoma? causing induration.
Extension of DCIS into the lactiferrous ducts and skin of the nipple producing a rash with or without nipple
What is Paget's disease? retraction. Palpable mass often present, see Paget's cells as well.
What is Medullary Carcinoma of the Invasive tumor associated with BRCA1 mutations. Bluky, soft tumor with large cells and a lymphoid infiltrate.
breast? Most are ER/PR negative.
Invasive tumor that presents with erythematous breast with dimpling of the skin like an orange peel from
What is inflammatory carcinoma of fixed opening of the sweat glands. Plugs of tumor block the lumen of dermal lymphatics causing localized
the breast? lymphedema. Has a very poor prognosis.

What is Invasive Lobular Carcinoma? Invasive mass of neoplastic cells arranged in a linear fashion or in concentric circles.

What is Tubular Carcinoma? Invasive mass that develops in terminal ductules. Increased incidence of cancer in the opposite breast.
What is a Colloid (Mucinous)
Carcinoma? Invasive mass that usually occurs in older women. Neoplastic cells surrounded by extracellular mucin.
Benign glandular proliferation in the male breast due to estrogen from increased enstrogens, decreased
androgens or a defect in androgen receptors. Most often unilateral. Normal in newborns, puberty or the
What is Gynecomastia? elderly.
Cirrhosis causes an inability to metabolize estrogen or to metabolize 17-ketosteroids which are then
aromatized to estrone. Genetic diseases like Klinefelter's and testicular feminization cuase gynecomastia.
Drugs that displace estrogen from SHBG, such as spironolactone or ketoconazole or drugs with estrogen
What causes pathologic activity like DES or digoxin, or androgen blocking drugs like spironolactone or flutamide or that decrease
gynecomastia? androgen production like leuprolide. These all increase estrogen.
What is the most common cause of
Bartholin gland abscesses? Infection with Neisseria Gonorrhea

What is Lichen Sclerosis? Thinning of the epidermis with parchment appearing skin. Most commonly in post-menopausal women.
White plaque like skin lesion (leukoplakia) due to squamous cell hyperplasia. Small risk for developing
What is Lichen Simplex Chronicus? Squamous Cell Carcinoma.
What is a Papillary Hidradenoma? Benign tumor of the apocrine sweat gland. Causes painful nodule on the labia majora.
What is Vulvar Intraepithelial Dysplasia of the vulva, ranging from mild to carcinoma in situ. Strong association with HPV 16 and high risk
Neoplasia? of developing squamous cell carcinoma

What are risk factors for squamous

cell carcinoma of the vulva? HPV 16, smoking, immunodeficiency.
Red, crusted vulvar lesion. Intraepithelial adenocarcinoma derived from primitive epithelial progenitor cells.
What is extramammary Paget's Malignant Paget cells contain mucin which is Periodic Acid Schiff positive. Spreads along the epithelium but
disease? rarely invades the dermis.
What is Malignant melanoma of the
vulva? Melanoma cells, histologically similar to Paget cells except these are PAS negative.

What type of lesion results from

infection with Calymmatobacterium Gram negative coccobacilli that causes granuloma inguinale. It's phagocytosed by macrophages forming
Granulomatis? Donovan bodies and results in creeping, raised sores that heal by scarring. Treat with bactrim or doxy.

What types of lesions result from Yeast and pseudohyphae which should be part of the normal vaginal flora. Causes vaginitis, pruritic vaginitis
infection with Candida Albicans? with a white discharge and fiery red mucosa. Risk factors are diabetes, antibiotics, pregnancy and OCP's
STD-commonly coinfecting with Neisseria Gonorrhea. See red inclusions (reticulate bodies) in squamous
cells which then divide and form elementary bodies which can reinfect other cells. Causes sterile pyuria,
epididdmitis, proctitis (in males obviously) and urethritis, cervicitis, PID, perihepatitis (Fitz-Hugh Curtis),
What type of lesion results form proctitis and bartholin gland abscesses (in females obviously). Can also cause conjunctivitis and pneumonia
infection with Chlamydia Trachomatis? in a newborn.
What types of lesions result from Lymphogranuloma venerum, papules with no ulceration, inguinal lymphadenitis with granulomatous
infection with Chlamydia Trachomatis microabscesses and draining sinuses. Lymphedema of the scrotum or vulva and possibly rectal strictures in
subspecies? women

What types of lesions are seen with Gram negative rod that causes bacterial vaginosis. Most common vaginitis which presents with malodorous
infection by Gardnerella Vaginalis? discharge. Organisms adhere to the squamous epithelium forming clue cells.
What types of lesions result from Gram negative rod that causes Chancroid. Male dominant disease, often correlated with HIV. Causes painful
infection with Hemophilus Ducreyi? genital warts and perianal ulcers with suppurative inguinal nodes which main have draining sinuses.

What types of lesions result from STD with the virus remaining latent in the sensory ganglia. Causes recurrent vesicles that ulcerate on the
infection with HSV-2? vulva, penis, cervix and perianal area. See multinucleated squamous cells on Tzanck prep

Types 6 and 11 associated with Condyloma Acuminata (warts)-fernlike or flat lesions in the genital area.
What types of lesions result from Types 16 and 18 associated with dysplasia and squamous cell carcinoma. See koilocytes in squamous
infection with HPV? epithelium. Cells have wrinkled, pyknotic nuclei surrounded by a clear halo.
How do you treat HPV? Vaccine! Topical podophyllin, alpha-IFN injections and imiquimod cream
Gram negative diplococcus that infects glandular transitional epithelium in sites similar to Chalmydia. Causes
What types of lesions result from prululent lesions and urethritis. Can cause ectopic pregnancy, male sterility, disseminated gonococcemia,
infection with Neisseria Gonorrhoeae? septic arthritis, and Fitz Hugh Curtis.
What are signs of disseminated
Gonococcemia? Septic arthritis in the knee, tenosynovitis of the hands and feet, pustules on the hands and feet

Gram negative spirochete that causes syphillis. Primary syphillis presents with a solitary, painless, indurated
chancre on the penis, labia or mouth. Secondary presents with a maculopapular rash on the trunk, palms
What types of lesions result from and soles along with generalized lymphadenopathy, condylomata lata (flat lesions) and alopecia. Tertiary
infection with Treponema Pallidum? syphillis presents with neurosyphillis, aortitis and gummas.
What are the non-specific screening
tests for Syphillis? RPR or VDRL. Titers should decrease after treatment.
What are the confirmatory tests for
Syphillis? FTA-ABS which is positive with or without treatment
What is the Jarisch-Herxheimer Intensification of rash in primary or secondary syphillis after proteins are released from the dead organisms
reaction? following penicillin treatment

what types of lesion results from Flagellated protozoan with jerky motility which produces vaginitis, cervicitis and urethritis. Causes a
infection with Trichamonas Vaginalis? strawberry colored cervix and fiery red vaginal mucosa with greenish, frothy discahrge.
What is Rokitansky-Kuster Hauser
Syndrome? Absence of the upper vagina and uterus resulting in primary amenorrhea

What is a Gartner's Duct cyst? Remnant of the Wolffian/mesonephric duct which presents as a cyst on the lateral wall of the vagina.
What is a Rhabdomyoma? Benign tumor of skeletal muscle in the vagina (can also be on the tongue or heart)
What is an Embryonal
Rhabdomyosarcoma? Necrotic, grape like mass protruding from the vagina, most often in girls <5 years

What is clear cell adenocarcinoma of Adenocarcinoma of the vaginal wall (pretty self explanatory). Occurs in women with DES exposure since DES
the vagina? inhibits mullerian differentiation-tubes, uterus, cervix and upper third of the vagina
Precursor lesion for squamous cell carcinoma. Produces red, superficial ulcerations in the upper portion of
What is Vaginal Adenosis? the vagina
What are some other DES related Abnormally shaped uterus that thwarts implantation (T shape). Cervical incompetence which can cause
abnormalities? recurrent miscarriage.
What is vaginal squamous cell It's what it sounds like. That said, primary SCC is associated with HPV 16. Most of these are actually
carcinoma? extensions of cervical SCC into the vagina.
What does the cervix actually consist
of? Endocervix and exocervix. The exocervix begins at the cervical os
What lines the exocervix? squamous epithelium
What lines endocervical glands? Mucus secreting columnar cells
How does the endocervical epithelium Endocervical epithelium migrates down to the exocervix where exposure to the acid pH of the vagina causes
transform into the exocervical squamous metaplasia. This area is called the transformation zone and is the most likely location for
epithelium? squamous dysplasia and cancer.
What is the pathogenesis of a Metaplastic squamous cells block endocervical gland orifices resulting in obstruction to outflow of mucus.
Nabothian cyst? This is a normal finding however.
Acute inflammation is often present in the transformation zone, however pathologic acute inflammation may
What is acute cervicitis? be due to infection-Chlamydia, Neisseria, Trichomonas, Candida, HSV, HPV.
What are clinical findings in acute Vaginal discharge, pelvic pain, dyspareunia, pain on palpation (chandelier sign), easy bleeding and
cervicitis? erythematous or exudative cervical os.
What causes chronic cervicitis? Essentially persistence of acute cervicitis
What is follicular cervicitis? Pronounced lymphoid infiltrate with germinal centers caused by Chlamydia Trachomatis.
What is the purpose of a Cervical Pap
test? Screening test for squamous dysplasia and cancer. Evaluate the hormone status of the patient.
What do superficial squamous cells
indicate on Pap? Adequate estrogen
What do intermediate squamous cells
on Pap indicate? Adequate progesterone
What do parabasal cells on Pap
indicate? Lack of estrogen and progesterone.
What types of cells are seen on Pap
from a non-pregnant and pregnant Non-pregnant: 70% superficial, 30% intermediate squamous cells. Pregnant: 100% intermediate squamous
woman? cells from progesterone effect.
Non-neoplastic polyp that protrudes from the cervical os. Arises from the endocervix, most commonly in
What is a Cervical Polyp? perimenopausal or multigravida women.

Describe Cervical Intraepithelial Most cases associated with HPV which produces koilocytes in squamous cells. Associated with early age of
Neoplasia, CIN sexual intercourse, multipe high-risk partners, high risk HPV types, smoking, OCP's and immunodeficiency.
What is CIN I? Mild dysplasia involving the lower third of the epithelium
What is CIN II? Moderate dysplasia involving the lower 2/3 of the epithelium
What is CIN III? Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium
What is the epidemiology of cervical Least common GYN cancer with higher incidence in developing countries. Most are squamous cell carcinomas
cancer? with the same risk factors as CIN
What are clinical findings in cervical
cancer? Abnormal vaginal bleeding, often post coital, malodorous discharge
Cancer often extends down into the vagna and out into the lateral wall of the cervix and vagina. May
What are some characteristics of infiltrate the bladder wall and obstruct the uterus causing postrenal azotemia and possibly death. May
cervical cancer? metastasize distantly, e.g. to the lungs.

What is the sequence to menarche? Breast budding (Thelarche), growth spurt, pubic hair, axillary hair, menarche (mean age is 12.8 years).
When does ovulation occur? Between days 14 and 16
What mediates the secretory phase of
the cycle? Progesterone

Fertilization usually occurs in the ampullary portion of the Fallopian tube. The fertilized egg spends 3 days
there, 2 days in the uterine cavity and then implants in the endometrial mucosa on day 21. There is an
What changes occur after fertilization? exaggerated secretory phase in pregnancy called the Arias-Stella phenomenon.
What initiates menses? Drop-off in serum estrogen and progesterone signalling endometrial cells to undergo apoptosis.
Prepares the follicle of the month, increases aromatase synthesis in the granulosa cells, increased synthesis
What are the functions of FSH? of LH receptors.

Increases synthesis of 17-ketosteroids in the theca interna (DHEA and androstenedione). Convert DHEA to
androstenedione and androstenedione to testosterone. Increase aromatization of testosterone. (Obviously
What are the functions of LH? LH isn't doing these things directly but it uprgulates necessary enzymes)
What hormonal changes are seen in Human chorionic gonadotropin-synthesized in the syncytiotrophoblast lining the chorionic villus. hCG acts as
pregnancy? an LH analog and maintains the corpus luteum to produce progesterone.
Mixture of estrogens and progestins which then prevent the midcycle LH surge and ovulation. Progestin
What is in Oral Contraceptive Pills and arrests the proliferative phase and cause gland atrophy and also inhibit LH directly. OCP's also render the
how do they work? cervical mucus hostile to sperm and alter Fallopian tube motility.
Where does Estradiol come from? Aromatized testosterone in granulosa cells. Primary estrogen in non-pregnant women.
Where does Estrone come from? Weak estrogen produced during menopause from adipose cell aromatization of androstendione
End product of estradiol metabolism. Primary estrogen of pregnancy derived from fetal adrenal, placenta and
Where does Estriol come from? maternal liver.
Where does androstendione come
from in a woman? Equal derivation from ovaries and adrenal cortex
Where does DHEA come from in a
woman? Almost exclusively from the adrenal cortex
Where does testosterone come from derived from conversion of androstenedione to testosterone in the ovaries and adrenal glands. Can be
in a woman? converted to DHT peripherally.
What is Sex Hormone Binding Binding protein for both estrogen and testosterone, mostly synthesized in the liver. Androgens, obesity and
Globulin? hypothyroidism all decrease SHBG
What does SHBG have a greater
affinity for? SHBG preferentially binds testosterone over estrogen thus lack of SHBG can cause hirsutism in women.

Acute inflammation of the endometrium, most commonly as a result of bacterial infection following delivery
What is acute endometritis? or miscarriage. Group B strep, staph a, bacteroides, C. trachomatis, N. Gonorrhoeae, E Coli.
What are clinical findings in acute
endometritis? Fever, uterine tenderness, prululent or foul vaginal discharge and abdominal pain.

What causes chronic endometritis? Retained placenta, gonorrhea, IUD (with infection)
What is the key histologic finding in
chronic endometritis? Like all chronic inflammatory conditions, you see plasma cells
Invagination of the stratum basalis into the myometrium. See glands and stroma thickening in the
What is Adenomyosis? myometrium and general enlargement of the uterus.
What are clinical findings in
adenomyosis? Menorrhagia, dysmenorrhea or pelvic pain
Functioning endometrial glands and stroma located outside the uterus causing cyclic bleeding of gland and
stromal implants. Essentially reverse menses through the Fallopian tube allows inplantation of viable
endometrial cells. Can also be from vascular spread. Most common sites are ovaries, rectal pouch, Fallopian
What is Endometriosis? tubes and intestines.

What are clinical findings in Dysmenorrhea, abnormal bleeding, painful stooling during menses, intestinal obstruction and bleeding during
Endometriosis? menses, increased risk for ectopic pregnancy and enlargement of the ovaries with blood filled cysts
Benign polyp on the endometrium that enlarges with estrogen stimulation. Does not progress to endometrial
What is an endometrial polyp? carcinoma but it can protrude through the cervix into the vagina.
What are clinical findings of an
endometrial polyp? Common cause of menorrhagia, spotting in between periods or after menopause

What is a Hyatid Cyst of Morgagni? Cystic mullerian remnant most often in the fibriated end of the tube. May undergo torsion causing pain.
Inflammation in the pelvis, often due to N. Gonorrhoeae or C. Trachomatis. See Fallopian tubes that are filled
with pus or see hydrosalpinx (clear fluid in Fallopian tube). Causes fever, lower abdominal pain, cervical
motion tenderness, abnormal uterine bleeding, vaginal discharge, mucopurulent discharge in the cervical os,
What is pelvic inflammatory disease? and right upper quadrant pain (FHC Syndrome)

What are some risk factors for PID? Multiple sex partners, vaginal douching, prior PID, unprotected sex

What is Salpingitis Isthmica Nodosa Invagination of the mucosa of the tube into muscle (tubal diverticulosis). Produces nodules in the tube that
(SIN)? narrow the lumen. Most likely a result of infection and can result in infertility and ectopic pregnancy.

Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and
What is ectopic pregnancy? sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
What are risk factors for ectopic Scarring from previous PID, Endometriosis, Altered tubal motility (SIN), progestin only pill, previous tubal
pregnancy? ligation, prior abdominal surgery.

Where in the tubes do ectopic

pregnancies most commonly implant? Most occur in the broad ampullary region below the fimbriae.
What are some clinical findings in Sudden onset of lower abdominal pain and tenderness, usually about 6 weeks after LMP, adnexal tenderness,
ectopic pregnancy? peritoneal signs, abnormal uterine bleeding, hypovolemic shock as a result of intraperitoneal hemorrhage.
How do you diagnose ectopic Beta hCG is a good screening test but a positive hCG doesn't mean that there is an ectopic pregnancy.
pregnancy? Vaginal ultrasound showing an amniotic sac is confirmatory.
What is Oophoritis? Inflammation of the ovary, possible as a result of mumps or PID.
Bilateral ovarian enlargement from hypercellular ovarian stroma. Stroma have vacuolated (leutenized)
stromal hilar cells which synthesize excess androgens. May cause hirsutism or virilization. Associated with
What is stromal hyperthecosis? obesity, acanthosis nigracans, insulin resistance, and hypertension.

Nulliparity-increased number of ovulatory cycles increases risk, also causes increased risk for surface-derived
ovarian tumors. Genetic factors are BRCA1 and BRCA2 suppressor gene mutations, Lynch syndrome, Turner
What are risk factors for Ovarian syndrome (dysgerminoma), Peutz-Jeghers syndrome (sex cord tumors with annular tubules), history of
cancer? breast cancer, postmenopausal estrogen replacement, obesity
cancers are similar to those seen in the testicle, not many are malignant. Sex cord stromal tumors-derive
from stromal cells, may be hormone producing, most are benign. Metastases-most commonly from breast,
How can ovarian tumors be classified? and stomach (Krukenberg tumors)
Abdominal enlargement from fluid. Malignant ascites may cause induration in the rectal pouch on digital
rectal exam and intestinal obstruction with colicky pain. Palpable ovarian mass in postmenopausal woman,
What are some clinical findings in malignant pleural effusion, torsion and infarction (cystic teratomas), signs of hyperestrinism in estrogen
Ovarian tumors? secreting tumors or virilization in androgen secreting tumors.
What is a common tumor marker of
malignant ovarian tumors? Increased CA-125- only in surface derived tumors
Most common group of primary benign and malignant tumors, many are bilateral. Cysts are lined by ciliated
cells (like Fallopian tubes). A Serous Cystadenoma is benign. A Serous Cystadenocarcinoma is malignant
What is a Serous Ovarian tumor? and has psammoma bodies and dystrophic calcification.

Cysts lined by mucus-secreting cells (like endocervical cells). Cause large multi-nucleated tumors. Seeding
What is a Mucinous tumor of the of tumor produces pseudomyxoma peritonei. A mucinous cystadenoma is benign and may be associated with
ovary? Brenner tumors. A mucinous cystadenocarcinoma is malignant.
What is an endometroid tumor? Malignant tumor associated with endometrial carcinoma. Commonly bilateral
What is a Brenner tumor? Usually a benign tumor that contains Walthard's rests (traditional-like epithelium)
Most common benign germ cell tumor. See ectodermal differentiation (hair, sebaceous glands, teeth) mostly
found in a nipple like structure called Rokitansky Tubercle. A Struma Ovarii subtype has functioning thyroid
What is a cystic teratoma? tissue

What is a Thecoma-Fibroma? Benign tumor associated with Meigs' syndrome (ascited, right sided pleural effusions). Commonly calcify.

What is a Granulosa-Theca cell tumor? Low grade malignant tumor which produces estrogen and contains Call-Exner bodies

What is a Sertoli-Leydig cell tumor? Benign tumor that produces androgens. Pure leydig cell tumors contain cells with crystals of Reinke.
Malignant tumor with a mixture of germ cells (dysgerminoma) and sex-cord stromal cells. Associated with
What is a Gonadoblastoma? abnormal sexual development. May calcify
What is a Krukenberg tumor? Metastasis to the ovary. Contains signet ring cells from hematogenous spread of gastric cancer.
What does the urinary system Intermediate mesoderm of the posterior wall of the abdominal
derive from? cavity.
How many sets of kidneys are Three sets of kidneys-pronephros, mesonephros and
there? metanephros
What is the pronephros? First kidney. Nonfunctional and disappears by week 4

Forms after the pronephros and forms the mesonephric/Wolffian

duct. That eventually connects the mesonephros to the cloaca
What is the mesonephros? and forms adult genital structures.
What is the metanephros? Forms the definitive kidney
Primary ureteric bud. Becomes the glomerulus, Bowman's
What is the excretory system capsule, Loop of Henle, Distal Collecting tubule and collecting
of the kidneys derived from? system
Outgrowth of the Mesonephric duct which joins the
What are the collecting ducts metanephros to form the ureteric bud. Forms the major and
of the kidney derived from? minor calyces, renal pelvis and ureters.

Allantois goes to Urachus and becomes the Median umbilical

What adult structure does the ligament. Don't confuse this with the medial umbilical ligament
Allantois become? which is a remnant of the umbilical artery.

Malformation of the Ureteric Bud which results in bilateral renal

What is Potter's Sequence? agenesis. Results in oligohydramnios/Potter's syndrome

What are the limb deformities Clubfoot, flipper hands, hyperextensible joints, and compressed
in Potter's Syndrome? thorax
Sloping forehead, flattened nose, recessed chin, low floppy
What are the facial deformities ears. Results from compression of the fetus against the wall of
in Potter's Syndrome? the the amniotic sac.
Why does Pulmonary Fetal lungs mature through swallowing of amnion which allows
Hypoplasia result from Potter's the lungs to expand. Thus decreased amnion causes decreased
Syndrome? expansion of the lungs.

What can occur if the allantois

fails to obliterate? Patent Urachus results in Urachal fistula at birth
What does the urogenital sinus
become? Urinary bladder and urethra
During development, the embryologic kidneys must ascend and
pass under the umbilical arteries. If a kidney can't pass, it
Wat causes a pelvic kidney? remains in the pelvis
How do pelvic kidneys Obstructive hydronephrosis and vesicoureteric reflux. May have
present? pain or infection.

Kidneys are pushed close together while ascending under the

umbilical arteries. Causes the lower poles to fuse which causes
it to look like a horseshoe and get trapped underneath the
What is a Horseshoe kidney? inferior mesenteric artery. Associated with Turner's
What is the most common Most are asymptomatic but can present with UTI followed by
presentation of horseshoe obstructive hematuria or abdominal pain. Predisposes to
kidney? nephrolithiasis
What is required for definitive
diagnosis of Horseshoe IV pyelogram shows rotated calyces but doesn't show the
kidney? isthmus. Need a Dimercaptosuccinic Acid Scan (DMSA)

What is the origin and Origin-vertebral column (T12-L5), insertion-lesser trochanter of

insertion, innervation, blood the femur. Innervation-Ventral rami of L1-3. Blood supply-
supply and action of the Psoas mucular branches of the medial femoral and circumflex artery.
major muscle? Actions-flex thigh and trunk and laterally rotate the hip.
What is the origin and Origin-Vertebral column (T12-L1), insertion-pectinate line.
insertion, innervation, blood Innervation-Anterior rami of lumbar nerves L1-2. Actions-with
supply and action of the Psoas the Psoas major, flexes the trunk at the hip and stabilizes the
minor muscle? thigh
What is the origin and Origin-Iliac fossa, insertion-lesser trochanter of the femur.
insertion, innervation, blood Innervation-femoral nerve L3-4. Blood supply-Muscular
supply and action of the branches of the medial femoral circumflex artery. Actions-
Iliacus muscle? powerful hip flexor and lateral rotator

What is the origin and

insertion, innervation, blood Origin-Transverse process of L3-5, insertion-lower border of the
supply and action of the 12th rib. Innervation-Ventral branches of T12 and L1-4.
Quadratus Lumborum muscle? Action-extends and laterally flexes vertebral column.
Pancreas (except tail), Duodenum (second, third and fourth
Which structures are parts), ascending and descending colon, aorta, IVC, rectum,
retroperitoneal? adrenal glands, and since this is the renal section-the kidneys!!!
Where are the kidneys Located at T12-L3 on the left and slightly lower on the right,
located? embedded in Gerota's Fascia.

Where do the ureters pass in Water goes under the bridge. Pass across the bifurcation of the
relation to the uterine artery common iliac and pass under the uterine arteries or vas
or vas deferens? deferens and then join the bladder on the posteroinferior side.
What is the arterial supply to
the kidneys? Renal arteries which branch off the abdominal aorta
What is the venous return
from the kidneys? Renal veins drain into the IVC
What is unique about the Left It also drains blood from the left gonad and is longer than the
Renal Vein? right renal vein since it must cross the IVC
Glomerulus surrounded by Bowman's capsule then proximal
What are the structures of the convoluted tubule the the straight portion of the proximal
Renal filtration system in the tubule, then thick descending, the Loop of Henle, then thick
order in which filtrate would ascending limb, then the distal collecting tubule followed by the
pass through? collecting duct.
What is the direction of
urinary drainage out of the Renal pyramids to the renal papillae to the minor calyces to the
kidneys? major calyces
Transitional epithelium as it exits the bladder, then stratified
What types of epithelium line columnar epithelium followed by stratified squamous
the Urethra? epithelium.

Prostatic, Membranous (surrounded by striated muscle forming

the voluntary external urethral sphincter), Bulbous then
What are the anatomic Pendulous (surrounded by Littre's glands. Does that mean it
divisions of the male urethra? swings like a pendulum? Just wondering
Much shorter so not really divided. Lined by stratified
squamous and pseudostratified columnar epithelium. At the
What are the anatomic mid-portion it's surrounded by the striated muscle of the
divisions of the female voluntary external urethral sphincter. Also surrounded by
urethra? Littre's glands
What comprises a Renal Primary filtering component, comprised of the glomerulus and
Corpuscle? Bowman's capsule
Collection of dilated capillaries with a fenestrated endothelium,
which emerge from the afferent arteriole and drain into the
What is the glomerulus? efferent arteriole
Double-walled epithelial capsule enclosing the glomerulus.
Consists of visceral and parietal layers with urinary space in
between. Visceral layer filters the blood while the parietal layer
covers the outside and is continuous with the proximal
What is Bowman's capsule? convoluted tubules.
What is special about the
visceral layer of Bowman's Specialized filtration lining that is made of Podocytes resting on
capsule? a basement membrane, primary processes and foot processes.
Yes! It's a fused basement membrane full of heparan sulfate
which gives it a negative charge and makes it more
Is the basement membrane of impenetrable to things like albumin that are also negatively
the Glomerulus charged? charged.
Lined by simple cuboidal epithelium with a microvilli brush
Describe the histology of the border. Interdigitations between the cells prevent loss of fluid
Proximal Convoluted Tubule and solutes
Specialized system for absorption and secretion of electrolytes.
Consists of the thick descending, thin descending, thin
Describe the histology of the ascending and thick ascending loops (see more about transport
Loop of Henle later)

Describe the histology of the

Distal Convoluted Tubule Lined by simple cuboidal epithelium without a brush border
Describe the histology of the Lined by simple cuboidal epithelium. Transports urine from the
collecting tubule functional nephron to the hilum
Describe the histology of the
Collecting Ducts Lined by columnar epithelium
Exceptionally long Loops of Henle allow them to set up a
What doe Juxtamedullary hypertonic gradient in the kidney, regulating the production of
nephrons do? concentrated urine
Consists of macula densa cells in the proximal portion of the
distal tubule and juxtaglomerular cells in the afferent and
efferent arterioles. Controls GFR in response to BP in the
afferent arterioles. JG cells secrete Renin leading to increased
angiotensin II and aldosterone in response to decreased renal
What is the Juxtaglomerular blood pressure, decreases sodium delivery to the distal tubule
Apparatus? and increases sympathetic tone (Beta 1).
Group of epithelial cells in the distal tubules that contact the
afferent and efferent arterioles (JGA). Cells are sensitive to
sodium concentration and rates of flow through the Distal
Convoluted Tubule. Regulates GFR through locally active
What is the Macula Densa? hormones.
Specialized myoepithelial cells located on the afferent arterioles
What are Juxtaglomerular which act as baroreceptors. Monitor BP and maintain GFR
cells? through Renin release

What are extraglomerular Contractile cells with receptors for angiotensin II and natriuretic
mesangial cells? factor allowing them to regulate glomerular flow.

Transitional epithelium-can stretch and thin as it's distended.

Smooth muscle in 3 layers arranged in multiple dimensions
What types of cells line the which evevntually become three distinct layers at the bladder's
bladder? neck. Innermost is the involuntary sphincter.
Diagram shows volume of ICF and ECF in the body. Osmolarity
Walk through a Darrow-Yannet should be equal between ICF and ECF. Normovolemia is 42
Diagram (see following liters total with 28L in the ICF. See Attachment 1 and walk
questions as well) through the diagram.
ICF decreased, ECF increased, osm increased. Technically
What are clinical implications volume contraction and hypotonic but water more contracted
of Water deprivation? that solute.

What are the clinical No change in ICF, ECF decreased, no change in osm.
implications of Diarrhea? Essenitally volume and solute contraction but equal contraction.
What are the clinical
implications of Adrenal ICF increased, ECF decreased, Osm decreased. Volume and
Insufficiency? solute contracted because not holding onto water and salt
What are the clinical
implications of Infusion of ICF unchanged, ECF increased, osm unchanged. Giving
isotonic NaCl? increasing amounts of fluid and solute so volume expansion.
What are the clinical
implications of high NaCl ICF decreased, ECF increased, osm increased. Volume
intake? expansion but solute pulls water into ECF
What are the clinical ICF increased, ECF increased, osm decreased. Holding onto
implications of SIADH? water and salt but water in excess of salt.
Cx=UxV/Px Volume of plasma from which the substance is
completely cleared per unit of time. C-clearance of X, U-urine
concentration of X, V-urine flow rate, P-plasma concentration of
What is Renal Clearance? X. (mL/minute)

What does is mean if Cx<GFR? Net tubular reabsorption of X

What does it mean if Cx>GFR? Net tubular secretion of X.

What does it mean if Cx=GFR? Neither secretion or reabsorption of X

How is Inulin used to calculate Inulin can be used because it is freely filtered and neither
GFR? reabsorbed nor secreted. GFR=Uinulin *V/Pinulin = Cinulin
Creatinine Clearance is an approximate measure of GFR.
How are Creatinine Clearance Slightly overestimates GFR because there is moderate secretion
and GFR related? of creatinine by the renal tubules.

Clearance Ratio=Cx/Cinulin. 1 if equal to inulin. <1 means

that clearance is less than inulin so either not filtered or filtered
What is the Clearance ratio and reabsorbed. >1 means that clearance is more than inulin
(with Inulin)? so filtered and excreted/activelly pumped.

Fenestrated capillary endothelium. Glomerular basement

membrane-composed of type IV and V collagen, laminin,
heparan sulfate. Three layers-Lamina rara interna, lamina
What forms the Glomerular densa and lamina rara externa. Epithelial layer consists of
Filtration Barrier? podocytes which help form a barrier.
How can you estimate Estimate using PAH clearance because it's filtered and actively
Effective Renal Plasma Flow secreted in the proximal tubule-thus all PAH is excreted.
How do you estimate Renal RBF=RPF/(1-Hct). Note that ERPF underestimates RPF by
Blood Flow? about 10% so RBF is overestimated.
Dopamine dilates the vessels and suppresses sodium
reabsorption in the proximal tubule by inhibiting the action of
the basolateral Na/K ATPase. Released directly by the proximal
What is Dopamine's effect on tubule in response to an increase in BP resulting in decreased
the nephron? RBF and GFR.

How does Afferent arteiole

constriction affect RPF, GFR
and Filtration Fraction? Decreased RPF, Decreased GFR, No change in filtration fraction

How does Efferent arteiole

constriction affect RPF, GFR
and Filtration Fraction? Decreased RPF, Increased GFR, increased filtration fraction

How does increased Plasma

protein affect RPF, GFR and
Filtration Fraction? No change in RPF, decreased GFR and filtration fraction

How does decreased plasma

protein affect RPF, GFR and
Filtration Fraction? No change in RPF, increased GFR and increased filtration fraction
How does constriction of the
ureter affect RPF, GFR and
Filtration Fraction? No change in RPF, decreased GFR, decreased filtration fraction

Two autoregulatory mechanisms-stretch/myogenic and

tubuloglomerular feedback. Stretch-when BP increases,
arterioles are stretched leading to vasoconstriction in the
afferent arteriole thus maintaining constant RBF.
Tubuloglomerular feedback- increased arterial pressure leads to
increased RBF and increased flow to the distal tubule which is
Describe autoregulation of sensed by the macula densa. This results in constriction of the
blood flow in the kidneys afferent arteriole, attenuating RBF.

Fraction of plasma filtered across the membrane of the

What is Filtration Fraction? glomerular capillaries. FF=GFR/RPF. Normal FF is about 20%
What is Filtered Load? GFR * Plasma concentration.
Ability to dilute urine. Free water (Ch2o)= V-Cosm
What is Free Water Clearance? (Cosm=Uosm*V/Posm)
Where does free water Thick ascending limb and early distal tubule. NaCl is
clearance occur? reabsorbed without reabsorption/permeability to H2O.
ADH causes retention of free water so Ch2o<0. Concentrated
How does ADH affect Ch2o? urine
How can you calculate
Excretion rate? Excretion rate= V*Ux
How can you calculate
Reabsorption? Reabsorption=Filtered-Excreted
How can you calculate
Secretion? Secretion=Excreted-Filtered

Should be completely reabsorbed in the proximal tubule by

Na/Glucose cotransport. At a plasma glucose >160-200 mg/dL
you start to see glucosuria because the transport is being
How is glucose reabsorbed overwhelmed. At 350 mg/dL, all transporters are fully
and how does it go wrong? saturated so clinical glucosuria develops
Shouldn't be cleared. Na dependent transporters in the
proximal tubules reabsorb amino acids with multiple carrier
How are amino acids cleared? systems.
Deficiency of neutral amino acid (tryptophan) transporter.
What is Hartnup's Disease? Causes Pellagra.
Unit composed of the glomerulus, through which fluid is filtered,
and the tubular system where filtered fluid is modified through
the reabsorption and secretion of various solutes to produce
Define the Nephron. urine.
How do tubules of the nephron
maintain low intracellular Na
and the Na gradient across the Na/K ATPase on the basolateral membrane maintains the Na
tube? gradient from the lumen to the cell.
The proximal tubule is the major site of reabsorption, based on
the transmembrane Na gradient. Reabsorbs all filtered glucose
Describe transport across the and amino acids via cotransport with Na. Reabsorbs most
luminal and basolateral side of bicarb, sodium, chloride and water. Isotonic absorption.
the Proximal Tubule (see Generates and secretes ammonia which buffers secreted H. Na
attachment 2). and H are exchanged, Cl is absorbed in exchange for bicarb.
How is bicarb CO2 and H2O cross the membrane and are made into bicarb by
regulated/excreted in the carbonic anhydrase. That is excreted and then made into CO2
Proximal tubule? and H2O again.

How do Angiotensin II and

Atrial Natriuretic Peptide act Ang II stimulates Na reabsorption which ANP blocks Na
on the Proximal tubule? reabsorption.
How does Parathyroid
hormone affect PTH inhibits Na/Phosphate cotransport resulting in phosphate
excretion/absorption? excretion.

Thin descending loop absorbs about 20% of filtered water but

no solute via medullary hypertonicity. Thin ascending limb is
impermeable to water and has no significant reabsorption.
Thick ascending limb is the diluting segment of the tubular
system. Actively absorbs Na, K and Cl (NK2Cl). This induces
the paracellular absorption of Mg and Ca because K leaks back
Describe transport across the into the lumen creating a positive charge in the lumen. It's
Loop of Henle. impermeable to H2O so it dilutes urine.

Impermeable to water and urea. Early distal tubule actively

Describe transport across the reabsorbs Na and Cl making urine hypotonic. PTH increases
distal convoluted tubule. Ca/Na exchange thus increasing Ca absorption.
Describe transport across the
late distal tubule and Principle cells reabsorb Na and H2O and secrete K via the Na/K
collecting ducts. ATPase. Intercalated cells secrete H and reabsorb K and HCO3.
How does Aldosterone affect Inserts more Na channels on the luminal side increasing Na
the collecting ducts? reabsorption.
How does ADH affect the Acts at V2 receptors and inserts aquaporins H2O channels into
collecting tubules? the luminal side.
U shaped capillaries which are freely permeable to H2O and
solutes except protein. Situated close to the Loop of Henle.
Enables the cortico-medullary osmolar concentration gradient.
Preserves hyperosmolarity of renal medulla to maintain
What is the Vasa Recta? absorption.

What does it mean if Tubular Solute is being reabsorbed more slowly than water or there is
Fluid (TF)/Plasma (P) >1? net secretion of solute.

What does it mean if TF/P=1 Solute and water are reabsorbed at equal rates

What does it mean if TF/P<1 Solute is reabsorbed more quickly than water.
Affects baroreceptors, limits reflex bradycardia which would
normally accompany pressors. Constricts efferent arterioles-
increased FF to maintain GFR in low volume states. Increases
What is the function of proximal tubule Na/H activity and can stimulate thirst in the
Angiotensin II? hypothalamus.
Released from the atria in response to low volume. Relaxes
vascular smooth muscle via cGMP resulting in increased GFR
What is the function of ANP? and decreased renin.

Regulates osmolarity and responds to low blood volume which

takes precedence over osmolarity. Increases H2O channel
What is the function of ADH? insertion in principle cells resulting in H2O reabsorption.
Increases Na channel, increases Na/K pump insertion in
principle cells, enhances K and H excretion creating a favorable
What is the function of Na gradient for Na and H2O reabsorption. Primarily regulates
Aldosterone? blood volume.
Glycoprotein hormone that stimulates RBC production in
response to hypoxia. Released from endothelial cells of
peritubular capillaries. Epo receptors are on proerythroblasts
What is Erythropoietin? which mature in response.
Active Vitamin D. Proximal tubule cells convert 25-OH-Vitamin
What is 1, 25-(OH)2 Vitamin D to the dihydroxy form. This increases intestinal reabsorption
D? of both calcium and phosphate.
PTH directly acts on the kidney to increase renal calcium
How does Parathyroid reabsorption and decrease renal phosphate excretion. Also
Hormone affect the kidney's stimulates proximal tubule cells to make 1, 25
endocrine function? dihydroxycholicalciferol.
Secreted by JG cells in response to increased renal arterial
pressure and increased renal sympathetic discharge (Beta 1
What is Renin? effect). Stimulates Angiotensin
Paracrine secretion of PGE2 vasodilates the afferent arterioles to
increase GFR. NSAIDs can cause acute renal failure by
What do prostaglandins do in inhibiting PGE thus preventing the arterioles to vasodilate to
the kidney? maintain GFR.

ANP is secreted in response to increased atrial pressure.

Causes increased GFR and increased Na filtration. Acts right at
the beginning of proximal convoluted tubule. PTH is secreted in
response to decreased plasma Ca, increased plasma PO4 or
decreased plasma vitamin D. Causes increased Ca reabsorption
in the distal convoluted tubule, decreased PO4 reabsorption at
the proximal convoluted tubule, increased Vitamin D production
and increased Ca and PO4 absorption from gut. Renin is
released from the JGA and acts on the distal convoluted tubule.
Ang II is synthesized in response to decreased BP and causes
the efferent arteriole constriction thus increasing GFR and FF
but with compensatory Na reabsorption. ADH is secreted in
response to increased plasma osmolarity and decreased blood
volume. Binds receptors on principal cells causing increased
Where do each of the above aquaporins. Acts on collecting ducts. Aldosterone is secreted
hormones act on the kidney? in response to decreased blood volume and increased plasma K,
(this rehashes all the functions resulting in increased Na reabsorption and increased Kand H
as well) secretion. Acts on collecting duct.

Insulin deficiency (decreased Na/K ATPase), Beta Adrenergic

antagonists (decreased Na/K ATPase), Acidosis or severe
What causes K shift out of exercise (K/H exchange), Hyperosmolarity, Digitalis (blocks
cells? Na/K ATPase), Cell lysis
Insulin (increased Na/K ATPase), Beta Adrenergic agonists
(increased Na/K ATPase), Alkalosis (K/H exchanger), Hypo-
What causes K shift into cells? osmolarity.

What is normal pH of blood? About 7.4

What is metabolic acidosis? Decreased Bicarb. Compensation by hyperventilation

What is metabolic alkalosis? Increased bicarb. Compensation by hypoventilation.

Respiratory compensation in response to metabolic acidosis.
What is Winter's Formula? PCO2=1.5 (HCO3) +8 (+/-2)
How much should PCO2
increase when bicarb
increases? PCO2 increases 0.7 mmHg for every 1 mEq/L HCO3
Increased PCO2. Compensation with increased bicarb
What is respiratory acidosis? absorption

What is respiratory alkalosis? Decreased PCO2. Compensate with less bicarb reabsorption.

What are some causes of Hypoventilation-Airway obstruction, acute lung disease, chronic
Respiratory Acidosis? lung disease, opiods/narcotics, weak respiratory muscles.
MUDPILES-Methanol, Uremia, Diabetic Ketoacidosis,
What are some causes of Paraldehyde or Phenformin, Iron tablets or INH, Lactic Acidosis,
Anion Gap Metabolic Acidosis? Ethylene glycol, Salicylates

What are some causes of non-

Anion Gap Metabolic Acidosis? Diarrhea, Glue sniffing, Renal Tubular Acidosis, Hyperchloremia
What are some causes of Hyperventilation-(early) high altitude exposure, Aspirin
Respiratory Alkalosis? ingestion (early)
What are some causes of
Metabolic Alkalosis? Diuretic use, vomiting, antacid use, hyperaldosteronism.

What is Type 1 (Distal) Renal Defect in the collecting tubule's ability to excrete H. Associated
Tubular Acidosis? with hypokalemia and risk for Ca containing kidney stones.

What is Type 2 (proximal) Defect in proximal tubule HCO3 reabsorption. Associated with
Renal Tubular Acidosis? hypokalemia and hypophosphatemic rickets.
Hyperaldosteronism or lack of collecting tubule response to
aldosterone causes hyperkalemia- inhibition of ammonia
What is Type 4 (hyperkalemic) excretion in proximal tubule. Leads to decreased urine pH due
Renal Tubular Acidosis? to decreased buffering capacity.

Stimulated Mineralocorticoid receptors on Principal Cells. This

increases their permeability to sodium and potassium by adding
Na channels and increases enzymes of the citric acid cycle thus
increasing ATP to pump Na/K out the basolateral side. Also
How does Aldosterone act on stimulated alpha-intercalated cells to secrete more H, thus
the Late Distal Tubule? regulating plasma HCO3 and acid-base balance.
How do you calculate the
anion gap? Na- (HCO3 + Cl) normal =10-12

Secondary to a loss of bicarb or an excess of acid. Essentially

there's a lot of something in the blood that's neither Na, HCO3
Why does an anion gap occur? or Cl that isn't being accounted for so there's a gap in the math.
Comparison of change in anion gap to change in bicarbonate.
Can tell you what there is in excess if there is a mixed acid base
What is a delta delta? disorder.
How do you calculate a delta Change in anion gap = AG-12. Change in Bicarb = 24-
delta? measured HCO3. Delta delta is ratio of the two
AG>HCO3 - Metabolic alkalosis + metabolic acidosis.
How do you interpret a delta AG<HCO3 -Wide AG + non AG metabolic acidosis. Equal-wide
delta? anion gap metabolic acidosis.

How much should CO2 rise in For every 10 mmol/L rise in HCO3, PCO2 should increase
response to increased bicarb? 6mmHg
Excretes harmful waste (urea, creatinine, uric acid, etc.),
Maintains acid-base homeostasis, Reabsorbs essential
substances, Regulates water and sodium metabolism, Maintains
What are the general functions vascular tone, Produces erythropoeitin, Maintains calcium
of the Kidneys? homeostasis.
Blood in the urine. Causes fro, the upper urinary tract- renal
stone, glomerulonephritis (dysmorphic RBC's), Renal cell
carcinoma. Causes from the lower urinary tract- Infection,
transitional cell carcinoma, benign prostatic hyperplasia. Drug
What is hematuria and what related causes-anticoagulants, cyclophosphamide (hemorrhagic
are some common causes? cystitis and risk for transitional cell carcinoma)
What is Proteinuria? Protein >150 mg/24 hours or >30 mg/dL via dipstick.
What are diagnostic tests for Dipstick-detects albumin only. Sulfosalicylic acid-detects
proteinuria? albumin and globulins.
Protein <2g/24 hour, not associated with renal disease. Causes
What is Functional Proteinuria? are fever, exercise, CHF.
Postural-only occurs when standing. First void in the morning
What is Orthostatic has no protein but subsequent during the day does have
Proteinuria? protein. No association with renal disease.
Variable protein loss with LMW proteins. Essentially the amount
filtered is greater than the tubular reabsorption. Causes are
multiple myeloma with Bence Jones proteinuria, Hemoglobinuria
from intravascular hemolysis, myoglobinuria from crush
injuries, McArdle's glycogenosis and increases in serum creatine
What is Overflow proteinuria? kinase.

BUN is a normal end product of amino acid and pyrimidine

metabolism that is produced by the liver in the urea cycle. It is
filtered in the kidneys and partially reabsorbed in the proximal
What is Serum BUN? tubule (amount reabsorbed is flow dependent).
What does serum BUN depend GFR, protein content of the diet, proximal tubule reabsorption
on? and the functional status of the urea cycle.
Decreased cardiac output (decreased GFR), increased protein
intake/breakdown, increased tissue catabolism (burns, surgery,
What are some causes of etc), acute glomerulonephritis, acute or chronic renal failure,
increased BUN? postrenal disease.
Increased plasma volume (pregnancy, SIADH, etc), decreased
urea synthesis (cirrhosis, Reye syndrome, fulminant liver
What are some causes of failure), decreased protein intake (Kwashiorkor, starvation
decreased BUN? gluconeogenesis in kideys)
Metabolic end product of creatine in muscle. Filtered in the
kidneys and not reabsorbed or secreted. Serum concentration
What is Serum Creatinine? varies with age and muscle mass.
What is Azotemia? Increased serum BUN and creatinine
15. Urea is filtered and partly reabsorbed whereas Creatinine is
What is a normal Serum BUN: filtered entirely. BUN:Cr ratio depends on changes-can be
Creatinine ratio? prerenal, renal or postrenal
Increased BUN and creatinine caused by something before the
kidneys. Most common cause is decreased cardiac
output/hypoperfusion of the kidneys decreasing GFR. BUN:Cr
What is Prerenal Azotemia and >15 because proportionately more Urea is reabsorbed from the
what are some causes? low flow rate.

Increased BUN and Cr from parenchymal damage to the

kidneys. Some causes are Acute Tubular Necrosis and Chronic
What is Renal Azotemia and Renal Failure. BUN:Cr <15. Both are filtered, there is
what are some causes? extrarenal loss of urea and urea may not be reabsorbed as well.

Increased BUN and Cr from urinary obstruction below the

kidneys. Prostate hyperplasia, blockage or ureters by stones or
cancer. Serum BUN:Cr ratio >15. Obstruction to flow
What is Postrenal Azotemia decreases GFR resulting in back diffusion of urea (not Cr) into
and what are some causes? blood and a disproportionate increase in BUN.
What is a normal Cr
Clearance? 97-137 mL/minute. Less than 100 mL/minute is abnormal.

Normal pregnancy (Increased plasma volume means increased

What are some causes of GFR), early diabetic glomerulopathy (constricted efferent
increased Cr Clearance? arteriole from hyaline sclerosis causing increased GFR)
Elderly people (decreasing GFR with age), Acute and Chronic
What are some causes of Renal disease (ARF from tubular sclerosis, CRF from diabetic
decreased CR Clearance? glomerulopathy)

What does dark yellow color

indicate in Urinalysis? Concentrated urine, Bilirubinemia, Increased UBG, Vitamins

What does Red or Pink color Hematuria, hemoglobinuria, myoglobinurua, drugs

indicate in Urinalysis? (phenazopyridine), porphyria
What does smoky-colored Acid pH converts Hb to hematin. Common in nephritic
urine indicate? glomerulonephritis

What does black urine after Alkaptonuria. Deficiency of homogentisate oxidase resulting in
exposure to light indicate? buildup of homogentisic acid

Cloudy urine with alkaline pH is normal, probably from

What does clarity of the urine phosphates. Cloudy urine with acid pH is normal probably from
indicate? uric acid. Otherwise, bacteria, WBC's, Hb, myoglobin

Urine concentration and dilution. SG>1.023 indicates urine

concentration and excludes intrinsic renal disease. Hypotonic
What does the specific gravity <1.015. Fixed SG (1.008-1.010) may indicate a lack of
of the urine indicate? concentration and dilution possibly renal failure.
Determined by diet and acid base status of person. Vegan often
have alkaline pH, meat eaters have acidic pH. An alkaline pH
What does the pH of the urine plus strong ammonia smell indicates a urease producing
indicate? pathogen.
Increased serum glucose means glucosuria and DM. Normal
What does glucose indicate in serum glucose and glucosuria can happen in normal pregnancy,
the urine? benign glucosuria
What does microalbuminuria
indicate? First sign of diabetic nephropathy

What do ketones in the urine Acetone and acetoacetic acid. Ketonuria from DKA, starvation,
indicate? ketogenic diets, pregnancy and isopropyl alcohol poisoning
What does bilirubin in the
urine indicate? Bilirubinuria may indicate hepatitis or obstructive jaundice

Trace amounts are normal. No UBG with increased urine

bilirubin may be obstructive jaundice. Increased UBG with
What does Urobilinogen absent urine bilirubin means extravascular hemolytic anemia.
indicate? Increased UBG with increased urine bilirubin means hepatitis
Hematuria from renal stone, hemoglobinuria from intravascular
What does blood in the urine hemolytic anemia, myoglobinuria from increased serum creatine
indicate? kinase and crush injuries.
What do nitrites in the urine
indicate? Nitrites produced by nitrate reducing uropathogens.
Esterase in neutrophiles (pyuria). Infections from urethritis,
What does Leukocyte Esterase cystitis, pyelonephritis. Sterile pyuria-Chalmydia trachomatis
in the urine indicate? urethritis, TB, drug induced interstitial nephritis

Bacteria-UTI, RBC's-hematuria from renal stones, cancer,

glomerulonephritis. Dysmorphic RBC's-hematuria of glomerular
What do cells in the urine origin. Neutrophils-pyuria from UTI or sterile pyuria. Oval fat
indicate? bodies-renal tubular cells with lipids (nephrotic syndrome)
Casts are formed in tubular lumens in the kidney and are
composed of a protein matrix with entrapped cells, debris or
What do casts indicate in the protein leaking through the glomeruli. Proves renal origin of
urine? the disease.
Acellular, ghost like cast containing protein. Only significant if
What is a hyaline cast? there is accompanying proteinuria
Nepritic type of glomerulonephritis resulting in a cast made of
What is a RBC Cast? RBC's
Cast of WBC's indicating acute pyelonephritis, acute
What is a WBC cast? tubulointerstitial nephritis
Cast of a sloughed off renal tubule. Indicates acute tubular
What is a renal tubular cast? necrosis

What is a fatty cast? Cast of cells with lots of lipid. Indicates nephrotic syndrome

What is a Waxy/Broad cast? Refractile, acellular cast seen in chronic renal failure.
Calcium oxalate crystals-pure vegan diet, ethylene glycol
poisoning, calcium oxalate stone. Uric acid crystals-
hyperuricemia from gout or massive cell destruction after
What types of crystals can be chemotherapy. Triple phosphate crystals-sign of UTI from
seen in the urine and what do urease producing pathogens like Proteus. Cystine crystals-
they indicate? hexagonal crystals seen in Cystinuria
Renal cortex receives 90% of the blood supply. Medulla is
relatively ischemic from reduced blood supply. Renal vessels
are all end arteries with no collateral circulation so occlusion of
any branch produces infarction. Afferent blood flow is
Describe the blood supply to controlled by renal-derived PGE2 and renin. Efferent blood flow
the kidney. is controlled by ATH (vasoconstrictor)
What is minimal change Loss of charge of the glomerular basement membrane which
disease? produces selective proteinuria.
What protein produces the
charge on the glomerular
basement membrane? Heparan Sulfate
Deposition of immunocomplexes such as in membranous
What are some causes of GBM glomerulopathy. Increased synthesis of Type IV Collagen such
thickening? as in DM.
Production of the GBM. Contain podocytes and slit pores
between podocytes which serve as a distal barrier to prevent
What do Visceral Epithelial protein loss in the urine. Podocytes fuse in nephrotic
Cells do in the glomerulus? syndrome, no matter what the cause.

Support the glomerular capillary. Can release inflammatory

What do Mesangial Cells do in mediators and proliferate-IgA glomerulopathy has mesangial
the glomerulus? immune complex deposits.

What do parietal epithelial Lining cells of Bowman's capsule. Proliferation causes crescents
cells do in the glomerulus? that encroach upon and destroy the glomerulus.

Most common cystic disease in children. See abnormal

development of one or both kidneys with abnormal structures
persisting in the kidneys (cartilage, immature collecting
ductules). Present as enlarged, cystic, unilateral or bilateral
What is Renal Dysplasia? flank mass. May lead to chronic renal failure.
AR disease. Bilateral cystic disease with cysts involving all
What is Juvenile Polycystic parts of the nephron in the cortex and medulla. Bilaterally
Kidney Disease? palpable kidneys.

What other types of conditions Cysts present in liver. Associated with congenital hepatic
are seen in Juvenile Polycystic fibrosis which leads to portal hypertension. Also associated
Kidney Disease? with oligohydramnios and Potter's Syndrome.

AD disease with defect on chr 16. Bilateral cystic disease with

What is Adult Polycystic the cysts involving all parts of the cortex and medulla. Develop
Kidney Disease? chronic renal failure a lot of the time.
Cysts may be present in the liver, pancreas and spleen. Also
have intracerebral Berry aneurysms. May cause hemorrhage if
hypertension results in rupture, intracerebral hemorrhage and
lacunar infarcts. Other associations are sigmoid diverticulosis,
What other conditions are hematuria, mitral valve prolapse, and risk for developing renal
associated with Adult PKD? cell carcinoma.
Multiple cysts in the collecting ducts present in the medulla.
See striations in the papillary ducts of the medulla (swiss
What is Medullary Sponge cheese appearance). Recurrent UTI's, hematuria and renal
Disease? stones.
Most commonly caused by renal dialysis. Tubules become
What is Acquired Polycystic obstructed by interstitial fibrosis or oxalate crystals. Small risk
Kidney Disease? for renal cell carcinoma.

Most common adult renal cyst. Derived from tubular

What are simple retention obstruction. May cause hematuria and may resemble renal cell
cysts? carcinoma. Needle aspiration will distinguish it from RCC
What is Focal
Glomerulonephritis? Only a few glomeruli are abnormal
What is Diffuse
Glomerulonephritis? All glomeruli are abnormal
What is Proliferative
Glomerulonephritis? >100 nuclei in affected glomeruli
What is Membranous
Glomerulonephropathy? Thick GBM, no proliferative change

What is Membranoproliferative
Glomerulonephritis? Thick GBM, hypercellular glomeruli
What is Focal Segmental
Glomerulosclerosis? Fibrosis involving only a segment of the involved glomerulus
What is Crescentic Proliferation of the parietal cells around the glomerulus (in
Glomerulonephritis? Bowman's Space, thus forming a crescent)
What is Primary Glomerular Involves only glomeruli and no other target organs. Essentially
Disease? something like minimal change disease.
What is Secondary Glomerular
Disease? Involves glomeruli and other organs, e.g. SLE
Look at Golijan page 400 and
go through all the histology Ya, definitely do that :-)
What does a Linear pattern
indicate on Antibodies line upagainst evenly distributed antigens in the
Immunofluorescence? GBM. Think Goodpasture's Syndrome
What does a Granular or
Lumpy Bumpy appearance
indicate on Think immunocomplex deposits in the glomerulus forming
Immunofluorescence? lumps of Ig. Not attached to the GBM.
Electron dense giving them a dark color. Subendothelial are
trapped between the endothelial cell and GBM. Subepithelial
What do immune complexes has passed through the GBM but is stuck in the podocytes.
look like on Electron Intramembranous is within the GBM and Mesangial is within the
Microscopy? mesangium.

How does Type III Immune Circulate and deposit in glomeruli or develop in situ. Immune
complex disease cause complexes then activate complement, procude C5a which is
glomerular disease? chemotactic to neutrophils which attack the GBM.
How does something like
Goodpasture's Disease cause
glomerular damage? Anti GBM antibodies attack the glomerular basement membrane

How does T Cell production of Cytokines cause the GBM to lose its negative charge. Cytokines
cytokines damage the GBM? also damage podocytes causing them to fuse.
What are clinical
manifestations of glomerular Nephritic syndrome, nephrotic syndrome and chronic
disease? glomerulonephritis

Glomerular injury primarily occurs due to neutrophils which

damage See hypertension from salt retention, periorbital
puffiness from salt retention, oliguria (decreased GFR from
inflamed glomeruli) and Hematuria. The hematuria features
dysmorphic RBC with irregular membranes from inflamed
glomeruli with IC deposition. Often see neutrophils in the
Describe the pathophysiology sediment, especially if immune complex. RBC casts are a key
of Nephritic Syndrome? finding, and occasionally there are WBC casts.
Proteinuria>150mg/day but less than 3.5 g/day. Azotemia with
What are some lab findings in BUN:Cr ratio >15 because tubular function is intact in acute
Nephritic syndrome? glomerulonephritis
Most common nephropathy, mostly nephritic. Increased
mucosal synthesis and decreased clearance of IgA with
increased serum IgA. Produces Focal Proliferative
Glomerulopathy. Also see Mesangial IgA immune complex
What is IgA Nephropathy deposits with granular immunofluorescence. IC's activate the
(Berger's Disease)? alternative complement pathway.
What does Berger's disease
often immitate? Henoch Schonlein Purpura
What happens after a URI in Episodic hematuria and hypertension following URI because of
Berger's disease? increased IgA deposits.
Most common type of post-infectious glomerulonephritis,
usually after group A strep infection of skin (scarlet fever) or
pharunx. Subepithelial immune complex deposits with granular
immunofluorescence. IC's activate the alternative complement
What is Post-Streptococcal pathway. See a diffuse proliferative pattern with neutrophilic
Glomerulonephritis? infiltrate.

Hematuria, 1-3 weeks following group A strep infection by a

nephritogenic strain (never produces rheumatic fever). Causes
How does Post-Streptococcal periorbital edema from sodium retention not hypoalbuminemia,
Glomerulonephritis present? transient, sometimes severe hypertension.

What lab tests are indicative of Increased DNAase B titers. ASO is degraded by oil in the skin
Post-Strep and is thus not increased. Streptozyme test is positive (anti-
Glomerulonephritis? DNAase B, ASO, anti-AH and anti-NAD antibodies).

Most common type of glomerular disease in SLE.

Subendothelial IC deposits with granular immunofluorescence.
DNA-anti-DNA IC's activate the classical complement pathway.
What is Diffuse Proliferative See "wire looping of capillaries" as well as neutrophil infiltration
Glomerulonephritis? with hyaline thrombi in capillary lumens.

What does the serum ANA test

look like in Diffuse Proliferative Serum ANA has a rim pattern, corresponding to the presence of
Glomerulonephritis? anti-ds DNA antibodies
How do you treat Diffuse
Glomerulonephritis? Corticosteroids and Cyclophosphamide
Clinical syndrome that may be either primary or secondary
disease. See a rapid loss of renal function that progresses to
What is Rapidly progressive acute renal failure within weeks. May or may not be associated
Crescentic Glomerulonephritis? with crescent formation.

Which diseases are associated

with Rapidly Progressive Goodpasture's syndrome, microscopic polyarteritis (p-ANCA),
Crescentic Glomerulonephritis? Wegener's granulomatosis (c-ANCA)

What HLA type is common in

Goodpasture's syndrome? 80% are HLA-BR2 positive

How do you treat Plasma exchange to remove antibodies, immunosuppressive

Goodpasture's syndrome? therapy with steroids and cyclophosphamide or renal transplant
Glomerular injury due to cytokines not neutrophils. Cytokines
released from T Cells destroy the negative charge of the
membrane thus allowing protein leak. They also cause the
What is Nephrotic Syndrome? podocytes to fuse together.

Proteinuria >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
What are the key findings in loss). Hypogammaglobulinemia from protein loss. Fatty casts
nephrotic syndrome? with maltese crosses and oval fat bodies.
Nephrotic syndrome with Nodular Glomerulosclerosis
What type f kidney disease (Kimmelstiel-Wilson disease). Risk factors are poor glycemic
does Diabetic Glomerulopathy control, hypertension and high correlation with coexisting
cause? diabetic retinopathy.
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
What is the pathogenesis of increased GFR and causes hyperfiltration damage to the
Diabetic Glomerulopathy? mesangium.
Increased Type IV collagen deposition in the GBM, tubular
What is Diabetic basement membrane and mesangium results in a
Microangiopathy? microangiopathic state.
What microscopic changes are Fusion of podocytes, afferent and efferent hyaline
seen in Diabetic arteriolosclerosis, nodular masses of type IV collagen and
Glomerulopathy? trapped proteins in the mesangium

What lab values are significant

in Diabetic Glomerulopathy? Microalbuminuria

Are there any other diseases

of the kidney associated with
Diabetic Glomerulopathy? Renal papillary necrosis and acute or chronic pyelonephritis
Amyloid deposits in the kidney secondary to primary or
What is renal amyloidosis? 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
What is Alport's Syndrome? ocular abnormalities

Benign familial hematuria. AD disorder with extremely thin

What is Thin Basement basement membranes in the setting of normal renal functin.
Membrane Disease? See mild proteinuria and persistent microscopic hematuria
Rapidly progressive glomerulonephritis, focal segmental
glomerulosclerosis, type I membranoproliferative
What are the common causes glomerulonephritis, membranous glomerulopathy, type IV
of Chronic Glomerulonephritis? diffuse proliferative glomerulonephritis in SLE, IgA nephropathy.
What are gross and
microscopic findings in chronic
glomerulonephritis? 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
What is ischemic Acute obstruct the lumen increasing tubular pressure, decreasing GFR
Tubular Necrosis? 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
What segments of the nephron Tubular basement membrane (interferes with renal tubular cell
are damaged in ischemic ATN? 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
What is Nephrotoxic Acute acidosis, increased BUN and Cr with ratio of BUN:Cr <15. Often
Tubular Necrosis? have issues with hypokalemia in the diuresis phase.
What is the epidemiology of 10% of ICU patients, 40% iatrogenic, 20% of patients with
Acute Tubular Necrosis? sepsis and >50% of patients with septic shock
Acute suppression of renal function developing in 24 hours,
accompanied by oliguria or anuria. Most commonly caused by
What is Acute Renal Failure? ATN.
What are some causes of Postrenal obstruction, vascular disease (malignant htn), RPGN,
Acute Renal Failure? drugs, DIC, urate nephropathy.
What is RPGN? Rapidly progressive glomerular nephritis

Treat prerenal azotemia-volume expansion if hypovolemic to

How do you treat Acute Renal increase renal blood flow. Low dose dopamine. Fenoldopam
Failure? (dopamine Alpha-1-receptor agonist), Dialysis
Acute or chronic inflammation of tubules and interstitium. May
be caused by acute pyelonephritis, drugs, infections
What is Tubulointerstitial (legionaire's, leptospirosis), SLE, lead poisoning, Urate
Nephritis? nephropathy and multiple myeloma.
E Coli is most common followed by Enterococcus. Risk factors
What are common causes of are indwelling catheter, obstruction, medullary sponge kidney,
acute pyelonephritis? DM, pregnancy and sickle cell

Intravesical portion of the ureter is not compressed during

How does vesicoureteral reflux micturition so urine refluxes up. Causes ascending infection
cause pyelonephritis? into the renal pelvis and parenchyma.
What is Oliguria? Urine output <400 mL/day or less than 20 mL/hr.
What are common causes of Prerenal azotemia, acute glomerulonephritis, acute tubular
Oliguria? necrosis/renal azotemia, and postural azotemia.
What does decreased Urine Urine osm <350 mOsm/kg indicates poor concentrating ability
Osm indicate? and thus tubular dysfunction

How do you calculate a FENa? FENa = (Una * PCr)/(PNa * Ucr) *100

What does a FENa less than Sodium filtration closely mimics creatinine filtration. FENa less
1% indicate? than 1% means good tubular function
What does a FENa greater
than 2% indicate? Tubular dysfunction. Good predictor of ATN

UNa<20 mEq/L indicates good tubular function aka you're not

What can UNa tell you about dumping salt like crazy. UNa >40 mEq/L indicates poor tubular
tubular function? function aka you're not reabsorbing salt.

How do you distinguish ATN usually presents with pigmented tubular casts. In
postrenal azotemia from ATN? postrenal azotemia, the sediment is usually normal.
What should you suspect if
there is staph a. cultured in
the urine? Hematogenous spread of the infection to the kidneys.
What are gross and Grayish white areas of abscess formation in the cortex and
microscopic findings in medulla. Microabscesses form in the tubular lumens and
pyelonephritis? interstitium.

What are the clinical and lab Clinical-spiking fever, flank pain, frequency and dysuria. Lab-
findings in pyelonephritis? WBC casts, pyuria, bacteruria, hematuria
What are complications of Chronic Pyelonephritis, Perinephric Abscess, Renal Papillary
Acute Pyelonephritis? necrosis, septicemia with endotoxic shock

What are pathological findings U shaped cortical scars overlying a blunt calyx, visible on IV
in Chroninc Pyelonephritis? pyelogram.
What pathological findings are
seen in obstructive Chronic Uniform dilation of the calyces and diffuse thinning of cortical
Pyelonephritis? tissue.
Chromic inflammation with scarring of the glomeruli. Tubular
What are microscopic findings atrophy-tubules contain eosinophilic material resembling thyroid
of Chronic Pyelonephritis? tissue (thyroidization)

What can reflux nephropathy

cause in children? Hypertension

What drugs are associated Penicillin esp. methicillin. Rifampin, sulfonamides, NSAIDs,
with acute drug induced ATN? diuretics
Combination of Type I and IV hypersensitivity. Abrupt onset of
fever, oliguria and rash that resolves with withdrawal of the
What is the pathogenesis of drug. Causes tubular disease with a BUN:Cr <15, eosinophilia
Drug induced ATN? and eosinophiluria

Chronic drug induced Tubulointerstitial nephritis. Chronic use of

Acetominophen with Aspirin because Acetominophen causes
free radical damage while aspirin inhibits renal synthesis of
What is Analgesic Nephritis? PGE2 leaving AT II unopposed.
Renal papillary necrosis-sloughing of renal papillae producing
gross hematuria, proteinuria and colicky flank pain. Ring defect
What are complications of where papillae used to reside. Hypertension, CRF and Renal
Analgesic Nephritis? pelvic and bladder transitional cell carcinomas.
Deposition of Urate crystals in the tubules and interstitium.
May be caused by massive release of purines (often after
What is Urate Nephropathy? chemo), lead poisoning or gout.
How does lead poisoning Decreased excretion of uric acid from the lead. Also direct toxic
cause Urate Nephropathy? effects cause TIN

What is seen microscopically

in Urate Nephropathy resulting
from lead poisoning? Nuclear acid-fast inclusions in the proximal tubule

Bence Jones light proteins are toxic to the tubular epithelium

and result in tubular casts. Casts obstruct the lumen and incite
a foreign body giant cel reaction of the tubules and interstitium,
leading to renal failure. Nephrocalcinosis from bone
breakdown/hypercalcemia also causes metastatic calcification of
the basement membrane collecting tubules. Finally, BJ proteins
How does Multiple Myeloma may be converted to amyloid and cause primary amyloidosis
cause renal disease? resulting in nephrotic syndrome.
Normocytic anemia with low corrected reticulocyte count. Due
What are hematologic findings to decreased Erythropoietin production. Also see qualitative
in Chronic Renal Failure? platelet defects.

Chronic kidney disease-mineral bone disorder. Osteitis fibrosia

cystica due to hypovitaminosis D. Causes hypocalcemia which
then stimulates the production of PTH-secondary
hyperparathyroidism. Hyperparathyroidism causes bone
resorption causing cystic lesions in the bone. Hemorrhage into
What is Renal Osteodystrophy? cysts caused brown discoloration.
Osteomalacia from decreased mineralization of the osteoid.
Osteoporosis from loss of organic bone mass and minerals
What are some complications (often due to chronic metabolic acidosis because excess H is
of Renal Osteodystrophy? buffered by bone minerals).
What are some cardiovascular
findings in Chronic Renal Hypertension from salt retention, hemorrhagic fibrinous
Failure? pericarditis, CHF and accelerated atherosclerosis.
What are some other clinical
consequences of Chronic Renal Hemorrhagic gastritis and uremic frost (urea crystals deposit on
Failure? the skin). Also hyperkalemia and anion-gap metabolic acidosis.

Hypovitaminosis D from decreased 1-Alpha Hydroxylase and

thus decreased reabsorption of calcium from the small
Why does renal failure cause intestines. Also hyperphosphatemia from decreased renal
hypocalcemia? excretion drives calcium into bone and soft tissue.

Cystatin in a Cysteine protease inhibitor produces by the

Why is there increased Serum nucleus of all cells. It should be filtered by the glomerulus but
Cystatin C? not secreted so it's a good marker of renal function.
What is seen on urinalysis in Fixed specific gravity because no concentrating ability, free
Chronic Kidney Failure? water clearance is 0, waxy/broad casts are present.

Why do you give ACE

inhibitors in kidney disease? Reduce proteinuria and treat hypertension.
Common renal disease in essential hypertension caused by
hyaline arteriolosclerosis of arterioles in the renal cortex.
Results in tubular atrophy, interstitial fibrosis and glomerular
What is benign sclerosis. See small kidneys with a finely granular cortical
nephrosclerosis? surface.
Sudden onset of accelerated hypertension with end organ
damage. Risk factors are pre-existing BNS, Hemolytic Uremic
What is Malignany syndrome, thrombotic thrombocytopenic purpura and systemic
Hypertension? sclerosis
Fibrinoid necrosis and necrotizing arteriolotis and glomerulitis
with pinpoint hemorrhages on the cortical surface. Also
What microscopic changes are hyperplastic arteriolosclerosis (onion skin lesions) with smooth
seen in Malignant muscle hyperplasia and reduplication of the basement
Hypertension? membrane.
Hypertensive encephalopathy-cerebral edema, papilledema,
What are clinical findings in retinopathy with flame hemorhages and potential for an
Malignant Hypertension? intracerebral bleed.
Embolization from thrombi in the left heart, atheroembolic renal
What causes Renal infarction? disease, vasculitis especially polyarteritis nodosa.
What is the gross and
microscopic appearance of a Irregular wedge-shaped pale infarct in the renal cortex. Old
renal infarction? infarct have a V shape from scar tissue.

Complication of obstetric emergencies. Due to DIC in the renal

cortex which results in fibrin clots in arterioles and glomerular
What is Diffuse cortical capillaries and bilateral, diffuse, pale infarcts of the renal
necrosis? cortex. See anuria in a pregnant woman followed by ARF.
What are some causes of
Hydronephrosis? Renal stones, retroperitoneal fibrosis, cervical cancer and BPH

What are some clinical Compression atrophy of the renal medulla and cortex and
findings of hydronephrosis? dilated ureters and renal pelvis

Hypercalcuria in the absence of hypercalcemia (absorptive

hypercalcuria), decreased urine volume, reduced urine citrate
(citrate chelates calcium), primary hyperparathyroidism, diet
high in dairy (contains phosphates or oxalate), and urinary
What causes Urolithiasis? infections due to urease producers (proteus)
Calcium oxalate stone-from vegans or people with Crohn's.
Calcium Phosphate stone-dairy products and distal renal tubular
What is a calcium stone? acidosis.
Struvite stone causing a Staghorn calculus. Associated with
What is a Magnesium urease producing bugs. Urine is alkaline and smells like
Ammonium Phosphate stone? ammonia.
Most pass. Can give hydrochlorothiazide which increases renal
How do you treat a calcium tubule reabsorption of calcium. Cellulose phosphate binds
stone? calcium in the intestine.
Allopurinol, increase urinary pH to make the stone soluble.
How do you treat a Uric Acid Cotreat chemo patients with allopurinol to prevent urate
stone? nephropathy.
How do you treat a struvite Surgical removal because of size. Antibiotic to eliminate urease
stone? producer.
Hamartoma composed of blood vessels, smooth muscle and
adipose cells. Associated with tuberous sclerosis causing
What is an Angiomyolipoma? mental retardation and multisystem hamartomas.

What are risks for Renal Cell Smoking, Von Hippel-Lindau, Adult PKD, obesity, asbestos and
Carcinoma? lead exposure, and gasoline or petroleum product exposure.
AD disease with defect on chr 3. Increased VEGF causes
What is Von Hippel Lindau hemangiobalstomas of the cerebellum and retina and bilateral
disease? renal cell carcinomas.

What are some gross and Upper pole mass with cysts and hemorrhage composed of clear
microscopic findings in Clear cells that contain lipids and glycogen. Tendency for renal vein
Cell renal carcinoma? invasion and invasion into the IVC and right heart.

Hematuria, abdominal mass, flank pain, hypertension, triad of

What are clinical signs of clear hematuria, abdominal mass and flank pain. Constitutional
cell renal carcinoma? symptoms. Left sided variocele from blocking of left renal vein.
What hormonal changes are
seen in renal clear cell EPO is elevated causing secondary polycythemia. PTH-related
carcinoma? protein produces hypercalcemia.
Transitional cell carcinoma. Risk factors are smoking,
Phenacetin abuse, aromatic amines (aniline dyes),
What is Renal Pelvic Cancer? cyclophosphamide.
AD tumor with the defect on chromosome 11. WAGR
Syndrome-wilms tumor, aniridia (absent iris), genital
abnormalities, retardation. Beckwith-Wiedmann syndrome-
wilms tumor with enlarged body organs, hemihypertrophy of
What is a Wilm's Tumor? extremities.
Large necrotic gray tumors derived from mesonephric
Where do Wilm's tumors come mesoderm, containing abortive glomeruli and tubules with
from? primitive blastemal cells and rhabdomyoblasts.
How does a Wilm's tumor Unilateral palpable mass in a child with hypertension (renin
present? secretion). Metastasis to the lungs.