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Pulmonary

How do you calculate the A-a


gradient?
What causes an A-a gradient
and how is it useful in
differentiating causes of
hypoxemia?

Difference in partial pressure of Oxygen, PO2, between the alveolar


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

What are some causes of


ventilation defects?
What are some causes of
perfusion defects?

Impaired O2 delivery to the alveoli for gas exchange, e.g. from


airway collapse due to respiratory distress syndrome or atelectasis.
Decreased or absent blood flow to the alveoli, e.g. pulmonary
embolus

What are some causes of


diffusion defects?

O2 cannot diffuse across alveolar-capillary interface, e.g.


pulmonary fibrosis or pulmonary edema. Causes decreased DLCO

What are some causes of


shunting?

A shunt is technically blood going from right to left because of


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

What are some causes of


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

Total amount of air in the lungs at the end of normal expiration


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

Define Tidal Volume, TV


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

Volume of air that enters/exits the lungs during normal respiration


Total amount of air expelled after maximal inspiration
Amount of air expelled from the lungs in 1 second after maximal
inspiration
70-80%
Amount of air forcibly expelled at the end of normal expiration

Describe spirometry in
restrictive lung disease

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


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

Describe spirometry in
obstructive lung disease

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


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

Define Dyspnea and list


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

Difficulty breathing. Can be due to stimulation of J receptors


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

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

What causes productive


cough?

What are some causes of


hemoptysis?

Chronic bronchitis, usually associated with smoking cigarettes.


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

Define tachypnea and list the


causes.

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


are restrictive lung disease, pleuritic chest pain, pulmonary
embolus with infarction (tachypnea is the key finding)

What drugs cause cough?


Define hemoptysis and the
mechanisms.

Define tracheal shift and list


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

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


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

What is the origin and


mechanism of normal breath
sounds?
Where does laminar air flow
start?

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

What are vesicular breath


sounds?

Sound like air blowing through a tube-this is normal over the


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

What are bronchovesicular


breath sounds?

Normal breath sounds over the main bronchi with an equal


inspiratory and expiratory ratio.

What are crackles and how


are they caused?

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

What are tubular breath


sounds?

What is inspiratory stridor


and how is it caused?

High pitched musical sound usually in expiration. Caused by


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

What is a pleural friction rub


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

Two inflamed surfaces (pleural and parietal) rubbing against each


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

What is wheezing and how is


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

What is bronchophony and


egophony?
What is a flow volume loop?

Caused by alveolar consolidations. Spoken numbers, syllables are


heard more distinctly through stethoscope. Egophany is when the
patient says E and you hear an A through the stethoscope.
Plot of inspiratory and expiratory flow rate(L/sec) versus lung
volume(L)

Where is maximal inspiration


on the diagram? (see
Pulmonary attachment 2 for
following)

Define Peak Expiratory Flow


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

What is Choanal Atresia?

What is a Nasal Polyp?


Define Obstructive Sleep
Apnea

Begins at point A, RV and goes to point B, TLC


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

TLC is decreased, RV is decreased. AKA right shifted curve.


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

What causes obstructive


sleep apnea?

Most commonly a result of obesity causing the pharyngeal muscles


to collapse under the weight of the tissue. Can also result from
tonsilar hypertrophy or nasal septum deviation.

What is the pathogenesis


and clinical findings in sleep
apnea?

Airway obstruction causes CO2 retention resulting in hypoxemia.


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

What is a Nasopharyngeal
Carcinoma?

Inflammation of the sinuses, most often maxillary or ethmoid


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

Define Laryngeal Carcinoma.

Carcinoma most commonly located on the true vocal cords. Mostly


keratinizing squamous cell carcinomas, mostly in med. Related to
cigarette smoking, alcohol (synergistic with cigarettes), HPV 6 and
11 and squamous papillomas and papillomatosis. Persistent
hoarseness from cervical lymphadenopathy is common.

Define Sinusitis and describe


its causes.

What is Atelectasis?

Loss of lung volume due to inadequate expansion of the airspaces


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

What is resorption
atelectasis?
What is compression
atelectasis?

Airway obstruction in bronchiols, segmental bronchi or bronchi, by


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

What is atelectasis due to


loss of surfactant?

What is Respiratory Distress


Syndrome?

Synthesized by Type II pneumocytes starting in the 28th week of


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

What is Pulmonary Edema


and what are the causes?

Superoxide radicals from O2 therapy can cause blindness


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

What is Acute Respiratory


Distress Syndrome, ARDS?

Noncardiogenic pulmonary edema from acute alveolar-capillary


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

What is the pathogenesis of


ARDS?

Acute damage to alveolar capillary walls and epithelial cells results


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

What are clinical


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

Dyspnea/tachypnea, late inspiratory crackles, severe hypoxemia


not responsive to 100% O2, increased pulmonary wedge pressure,
increased A-a gradient, bilateral infiltrates and consolidations.
Community acquired which can be typical or atypical and hospital
acquired, aka nosocomial.

What are complications of


respiratory distress
syndrome?

Describe clinical findings in


lobar pneumonia.

Most caused by bacterial pathogens, particularly Strep


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

Describe clinical findings in


atypical pneumonia.

Usually caused by mycoplasma pneumoniae, also chlamydophilia


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

Describe clinical findings in


nosocomial pneumonia.

Happens in patients with severe underlying disease,


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

Describe the pathogenesis of


typical pneumonia.
Describe the pathogenesis of
bronchopneumonia.

Describe pneumonia from


Tuberculosis.

From inhalation of Mycobacterium Tuberculosis. Infects


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

Describe Primary TB
Infection.

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


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

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

Due to reactivation of primary TB. Usually involves apices in upper


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

What is the most common


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

What is the most common


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

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

Cytomegalovirus. Enlarged alveolar macrophages/pneumocytes


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

What is a common bacterial


cause of newborn
pneumonia?

Chlamydia trachomatis from passage through infected birth canal.


Afrebile with staccato cough, conjunctivitis and wheezing. Treat
with erythromycin.

What is the most common


baterial cause of atypical
pneumonia?
Describe the signs and
symptoms of Coxiella
Burnetti infection

Mycoplasma Pneumoniae. Insidious onset with low grade fever. Can


cause bullous myringitis(inflamed Tympanic membrane), cold
autoimmune hemolytic anemia from anti-IgM antibodies.

What is the most common


cause of community acquired
lobar pneumonia?

Atypical pneumonia, myocarditis, granulomatous hepatitis.


Associated with dairy farmers and vetrinarians.

What are signs and


symptoms of infection with
Bacillus Anthracis?

Strep pneumoniae. Rapid onset, productive cough and signs of


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

What are signs and


symptoms of Actinomyces
infection?

Normal flora in tonsils and adenoids. Can produce draining sinuses


in the jaw, chest cavity and abdomen. Pus contains yellow specks
(sulfur granules) which contain the bacteria.

What are signs/symptoms of


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

What are signs and


symptoms of Nocardia
infection?

What are signs and


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

Granulomatous microabscesses in the lungs. Often disseminates


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

What are signs and


symptoms of infection with
Legionella Pneumophila?

Pneumonia associated with high fever, dry cough, flu like


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

What are signs and


symptoms of infection with
Yersinia Pestis?

The plague!!! Macrophages cannot kill bacteria due to protection by


V and W antigens so you get really sick. Bubonic causes infected
lymph node which enlarge and mat together and drain to the
surface (buboes). Pneumonic and septicemic are just what they
sound like. Treat with gentamicin and doxycycline (pneumonic) or
gentamicin and streptomycin (bubonic)

What are signs and


symptoms of infection with
Cryptococcus Neoformans?

Granulomatous inflammation with caseation. Acquired from pigeon


feces.

What are signs and


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

Aspergilloma-fungus ball that develops in a prior cavitary lesion


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

What are signs and


symptoms of infection with
Coccidoides Immitis?

What are signs and


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

What are signs and


symptoms of infection with
Pneumocystis Jiroveci?

What are the common


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

Contracted by inhaling arthrospores in dust in arid areas (increased


after earthquakes). Causes flu-like symptoms and erythema
nodosum and granulomatous inflammation of the lungs with
caseous necrosis.
Most common systemic fungal infection, endemic in Ohio and
Mississippi river valleys. Causes granulomatous inflammation with
caseous necrosis, simulating TB. Produces coin lesions,
consolidations, milary spread and cavitation. Causes marked
dystrophic calcification of granulomas and multiple calcifications in
the spleen.
Male dominant disease, common in Great lakes, central and
southern US. Causes skin disease that simulates squamous cell
carcinoma and lung disease with granulomatous inflammation and
caseous necrosis.
Cysts and trophozoites attach to Type I pneumocytes. Most
common AIDS-defining infection, CD4+ count <200. Fever,
dyspnea and severe hypoxemia, diffuse intra-alveolar foamy
exudates with cup chaped cysts (under silver or Giemsa stain).
Diffuse alveolar and interstitial infiltrates.
Aspiration of oropharyngeal material. Risk factors are alcoholism,
loss of consciousness and recent dental work. Can also be a
complication of pneumonia, a result of septic embolism or from an
obstructive lung neoplasia.
Aerobic and anaerobic streptococci, staph species, prevotella,
fusobacterium

Where are most lung


abscesses due to aspiration
located?
What are clinical findings in
a lung abscess?

What is the pathophysiology


of a pulmonary
thromboembolism?

What are consequences of


pulmonary
thromboembolism?

What are clinical signs of


pulmonary
thromboembolism?
What are lab findings of
pulmonary
thromboembolism?
What is Hampton's Hump?
Define Pulmonary
Hypertension

Right side because the bronchi going to the right lobes are more
direct (straight) so it's easier to aspirate crap into there. Usually in
the upper portion of the right lower lobe, but it depends on the
position of the person when they aspirated.
Spiking fever with productive cough and foul smelling sputum.
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
the embolus determines what it will block. Large embolus blocks
major vessels (saddle embolus) while small emboli occlude
medium and small vessels.
Increase in pulmonary artery pressure, decreased flow to
pulmonary parenchyma which can cause hemorrhagic infarct, see a
red-blue, raised, wedge shaped area that extends to the pleural
surface. Fibrinous exudate on the pleural surface and hemorrhagic
pleural effusion.
Sudden increase in PA pressure which can cause right ventricular
failure, sudden onset of dyspnea and tachypnea, fever, pleuritic
chest pain, plueral friction rub, pleural effusion, expiratory
wheezing from release of TXA2 from platelets.
Respiratory alkalosis (PCO2<33mmHg), PaO2<80 mmHg,
increased A-a gradient, increased D-Dimer
Wedge shaped area of consolidation/infarction from PE
Mean pulmonary artery pressure >25 mmHg at rest or >30mmHg
with exercise.

What causes primary


pulmonary hypertension?

What causes secondary


pulmonary hypertension?
What are clinical findings of
pulmonary hypertension?
How do you treat pulmonary
hypertension?
What is Goodpasture's
Syndrome?

What are common causes of


restrictive lung disease?

What is the pathogenesis of


interstitial fibrosis?

Mutation associated with TGF-B resulting in vascular


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
recurrent PE, left to right shunting/volume overload, mitral stenosis
resulting in volume overload.
Exertional dyspnea (common), chest pain, tapering of arteries on
CXR, accentuated P2, left parasternal heave or other signs of right
ventricular hypertrophy.
Diuretics, O2, vasodilators-Ca channel blockers, prostanoids,
endothelin receptor antagonists, lung transplant
Pulmonary hemorrhage with hemoptysis often preceding renal
failure. Autoantibodies to Type IV collagen in basement membrane
of lung and glomerulus.
Chest wall disorders with normal lungs, e.g. kyphoscoliosis, pleural
disease like mesothelioma or obesity. Acute or chronic interstitial
lung diseases, e.g. ARDS, pneumoconiosis or other fibrosing
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
during inspiration. Increased elasticity to recoil on expiration is
increased.

What are clinical findings in


restrictive lung disease?

dry cough and exertional dyspnea, late inspiratory crackles in lower


lung fields, potential cor pulmonale, equal decreases on PFT's.

What is a pneumoconiosis?

Inhalation of mineral dust into the lungs leading to interstitial


fibrosis. Can be silica, asbestos, beryllium or others.

Describe Coal Worker's


Pneumoconiosis.

What is silicosis?

Describe clinical findings in


silicosis.

"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
pulmonale or large cavitating rheumatoid nodules (Caplan
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
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
pulmonale or Caplan syndrome and increased risk of lung cancer
and TB.

How do asbestos related


diseases occur?

Serpentine asbestos-interstitial fibrosis and lung cancer; amphilobe


asbestos-interstitial fibrosis, lung cancer and mesothelioma.
Deposits in respiratory bronchioles, alveolar ducts and alveoli.
Comes from insulating pipes, naval shipyards, roofing material,
ceiling tiles, old floor tiles and demolition of old buildings.

What is the pathogenesis of


asbestos related disease?

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),
malignant mesothelioma of the pleura arising from serosal cells of
the pleura. Can cause cor pulmonale or Caplan syndrome.

What is Berylliosis?

Beryllium exposure from nuclear and aerospace industry causes


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

What is Sarcoidosis?

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
symptom.

What collagen vascular


diseases cause lung disease?

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
gammopathy, and cutaneous anergy of skin antigens like Candida
(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
exertion, chronic, nonproductive cough, and late inspiratory
crackles.
Systemic Lupus causes interstitial disease in 50% of patients and
pleuritis with effusion (serositis). Rheumatoid Arthritis can cause
rheumatoid nodules (if with a pneumoconiosis, Caplan's
syndrome).

What is hypersensitivity
pneumonitis?

Extrinsic allergic alveolitis associated with exposure to known


inhaled antigen. Does not involve IgE or have eosinophilia.

What are other clinical signs


in Sarcoidosis?

What is idiopathic pulmonary


fibrosis?

What is Farmer's Lung?

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
inflammation (type IV hypersensitivity).

What is Silo Filler's Disease?

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


an immediate hypersensitivity reaction associated with dyspnea.

What is Byssinosis?

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
occurs on returning to work-Monday Morning Blues (cyanosis)

What drugs are associated


with interstitial fibrosis?
What is obstructive lung
disease?

What causes Emphysema?

Amiodarone, Bleomycin and Busulfan, Cyclophosphamide,


Methotrexate and methysergide, nitrosurea and nitrofurantoin.
Obstruction to airflow out of the lungs. Usually loss of elastic recoil
or obstruction of airways.
Permanent enlargement of all or part of the respiratory unitrespiratory bronchioles, alveolar ducts and alveoli.
Smoking is the most common cause. Also can be from Alpha-1
Antitrypsin deficiency

What is the pathogenesis of


Emphysema?

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
results in tissue destruction. Smoking produces a functional A1AT
deficiency.

What is Emphysema?

What type of Emphysema is


most common in smokers?

Fibers attach to the outside of the walls of small airways and


provide radial traction to keep the lumen open. Destruction causes
loss of radial traction and small airway collapse, especially on
expiration.
During expiration, the distal terminal bronchioles collapse
preventing egress of air. Trapped air distends parts of the
respiratory unit that have no elastic tissue. Trapped air increases
TLC and RV
Centriacinar/Centrilobular. Mostly apical segments of upper lobes,
distal terminal bronchioles and respiratory bronchioles lose elastic
tissue.

What type of Emphysema is


most common in Alpha-1
Antitrypsin deficiency?

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.
See absent alpha-1 globulin peak in serum protein electrophoresis.
Dyspnea is sever and occurs early, causes pink puffers. Frequently
coexists with chronic bronchitis.

What is the normal function


of elastic fibers in the lung?

Where is the site of


obstruction in emphysema?

What is Chronic Bronchitis?

Paraseptal emphysema-localized to the subpleura and targets


alveolar ducts and alveoli. Increased incidence of spontaneous
pneumothorax from rupture of subpleural blebs. Irregular
Emphysema-localized disease associated with scar tissue.
Productive cough for at least 3 months. Most commonly from
smoking and Cystic Fibrosis.

What is the pathogenesis of


chronic bronchitis?

Hypersecretion of mucous in bronchi, obstruction to airflow in the


terminal bronchioles, proximal to the obstruction seen in
emphysema. Causes irreversible fibrosis of terminal bronchioles.

What are 2 non-obstructive


types of Emphysema?

What changes are seen in


the bronchi with chronic
bronchitis?

What are clinical findings of


chronic bronchitis?
What is Asthma?

What is Extrinsic Asthma?


What are other chemical
mediators involved in
Extrinsic Asthma?

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
squamous metaplasia. Mucus plugs can block the exodus of CO2.
GOblet cell metaplasia is seen with hypertrophy of mucus secreting
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
wheezing and siliant rhonchi and often cor pulmonale. Also have
chronic respiratory acidosis with increased bicarb to compensate.
Episodic and reversible obstructive airway disease. Primarily
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
produces airway constriction.
Leukotriene C, D, E4 cause prolonged bronchoconstriction.
Acetylcholine causes airway muscle contraction.

What are some histologic


changes in Extrinsic Asthma?

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.
Crystalline granules in eosinophils coalesce to form Charcot-Leyden
crystals.

What is Intrinsic Asthma?

Episodic wheezing, nocturnal cough, increased AP diameter from


air trapping. Initially have respiratory alkalosis but may turn into
respiratory acidosis if bronchospasm is not relieved.
Nonimmune asthma caused by virus-induced respiratory infection,
or air pollutants.

What is Bronchiectasis?

Permanent dilation of bronchi and bronchioles due to destruction of


cartilage and elastic tissue by chronic necrotizing infections.

What are clinical findings in


Extrinsic Asthma?

What are some causes of


Bronchiectasis?
What are some clinical
findings in Bronchiectasis?

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


obstruction (bronchogenic carcinoma), Primary ciliary dyskinesia
(absent dynein arm in cilia aka Kartagener's Syndrome), Allergic
Bronchopulmonary Aspergillosis.
Cough productive of massive amounts of sputum, hemoptysis,
digital clubbing, cor pulmonale, crowded bronchial markings that
extend to lung periphery.

What is Cystic Fibrosis?

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
dehydrated body secretions which are thick and easily infected.

What are clinical findings in


CF?

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


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

What are risk factors for lung


cancer?

Smoking, Radon gas (uranium mining), asbestos, metal exposurechromium, cadmium, beryllium, arsenic- secondhand smoke,
ionizing radiation, air pollution, prior TB

What are some features of


adenocarcinoma?

Most common tumor, weakest smoking association, tends to be


peripherally located bc filters in cigarettes remove large
carcinogens leaving the small ones that can move peripherally.

What are some features of


squamous cell carcinoma?
What are common sites for
metastasis?
Which cancers are most
commonly responsible for
lung metastasis?

2nd most common tumor, greatest smoking association. Tends to


be centrally located (mainstem bronchus)
Hilar lymph nodes (most common), adrenal glands, liver, brain,
bone

Primary breast cancer, colon cancer and renal cell carcinoma.

Where in the lung do tumors


commonly metastasize?

Parenchyma, pleura and pleural space (pleural effusions),


lymphatics (causes severe dyspnea)

What are common findings


in primary lung cancer?

Cough, weight loss, chest pain, hemoptysis, dyspnea, superior


vena cava syndrome

What is a Pancoast tumor?


What are some
paraneoplastic changes
associated with lung
cancers?

Superior sulcus tumor. Usually a primary squamous cancer located


at the extreme apex of the lung. Causes desctruction of superior
cervical sympathetic ganglion producing Horner's syndrome.
Digital clubbing from reactive periosteal changes in underlying
bone. Muscle weakness (Eaton Lambert Syndrome). Ectopic
hormone secretion (ACTH)

What are the common


causes of mediastinal
masses?

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,
malignant lymphomas (anterior mediastinum, usually nodular
sclerosing Hodgkin's in a woman), teratomas-usually benign, in
anterior mediastinum.

What are some symptoms of


Thymoma?

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
hypogammaglobulinemia, RBC aplasia and increased incidence of
other autoimmune diseases.

What is the etiology of


pleural effusions?
Describe a transudate
Describe an exudate

Increased hydrostatic pressure in visceral pleura (CHF), decreased


oncotic pressure (nephrotic syndrome), obstruction of lymphatic
drainage from pleura (lung cancer), increased vessel permeability
of pleural capillaries (pulmonary infarction, pneumonia),
metastasis to the pleura (metastatic breast cancer).
Ultrafiltrate of plasma from disturbances in Starling pressures
(CHF, nephrotic syndrome)

Describe Pseudochylous fluid

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
many chylomicrons
Turbid, milky appearance from increased inflammation with
necrotic debris. Most often from rheumatoid lung disease.

How do you distinguish


between exudate and
transudate?

Ratio of pleural fluid protein and LDH to serum protein and LDH.
PF protein/serum protein <0.5 is transudate, >0.5 is exudate. PF
LDH/serum LDH <0.6 is transudate, >0.6 is exudate. PF LDH
<200 U/L is transudate, >200 U/L is exudate

How does a spontaneous


pneumothorax happen?

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.
Loss of negative intrapleural pressure causes collapse of lung.
Sudden onset of dyspnea with pleuritic chest pain.

Describe Chylous fluid

What is the pathogenesis of


a Tension Pneumothorax?

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
mediastinal structures to deviate to contralateral side. Can cause
compromised venous return to the heart.

Reproductive
What vein drains the ovaries/testes?
What is the lymphatic drainage of the
Ovaries/Testes?
Where does lymph from the
vagina/vulva/scrotum drain to?
What does the suspensory ligament of
the ovaries connect?
What does the Cardinal ligament
connect?
What does the Round ligament of the
uterus connect?
What is the round ligament of the
uterus derive from?
What does the Broad Ligament
connects?
What does the Ligament of the ovary
connect?
What does the Genital Tubercle
become?
What does the Urogenital Fold
become?
What does the labioscrotal swelling
become?
What is the pathway of sperm during
ejaculation?

What is the autonomic innervation


causing an erection?
What is the autonomic innervation
causing Sperm Emission?
What is the autonomic innervation
causing Ejaculation?
What are the different parts of the
sperm?
Where do the different parts of the
sperm come from?
What is the function of
spermatogonia?

Left Gonadal vein to the left renal vein to the IVC. Right ovary/testis drains to right gonadal vein straight to
the IVC.
Ovary/Testis drains to the para-aortic lymph nodes.
Distal 1/3 of the vagina/vulva/scrotum drains to the superficial lymph nodes. Proximal 2/3 of vagina/uterus
drains to the obturator, external iliac and hypogastric lymph nodes
Connects ovaries to the lateral pelvic wall and contains the ovarian vessels.
Connects the cervix to the side wall of the pelvis and contains the uterine vessels.
Contains the Uterine fundus to the labia majora but carries no structures.
Derivative of the Gubernaculum. Travels through the round inguinal canal.
Connects the uterus, fallopian tubes, and ovaries to the pelvic side wall. Contains the ovaries, fallopian
tubes, and round ligaments of the uterus.
Connects the ovary to the uterus and does not contain any structures.
Becomes the Glans Penis or Clitoris
Becomes the shaft of the penis or the labia minora
Scrotum and Labia majora
(SEVEN UP) Seminiferous tubules to epididymis to vas deferens to ejaculatory ducts (nothing) to urethra to
the penis
Erection-Parasympathetic nervous system (pelvic nerve). Nitric oxide increases cGMP which causes smooth
muscle relaxation which causes vasodilation and is proerectile. Also Norepinephrine causes an increase in
Calcium which causes smooth muscle contraction which causes vasoconstriction and is antierectile.

Sympathetic nervous system via the hypogastric nerve


Visceral and somatic via the pudendal nerve
Acrosome, head, nucleus, neck, middle piece, tail
Acrosome-Golgi apparatus, Flagellum/Tail-Centrioles, Middle Piece-contains the mitochondria, Head and
nucleus come from the nucleus.
Maintain the germ pool and produce primary spermatocytes

What is the function of Sertoli Cells?


What is the function of Leydig Cells?
What is the composition of Semen?
Describe the general process of
spermatogenesis

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
hormone.
Secrete testosterone
Seminal Vesicle Products(fructose, ascorbic acid, prostaglandins, phosphorylcholine, flavins), Prostate
Products (Zinc, citrate acid, phospholipids, acid phosphatase, fibrinolysin), Sperm

What is spermiogenesis?

Spermatogenesis begins at puberty with spermatogonia. Full development takes 2 months. Occurs in
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
spermatozoa

Describe the process of


spermatogenesis.

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

Describe the hormonal regulation of


Spermatogenesis.

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
from the Sertoli cells feeds back and downregulates FSH release. Testosterone from Leydig cells feeds back
and downregulates LH production and GnRH release.

What are the common Androgens?


What are the functions of Testosterone
in development?
What is the function of
Dihydrotestosterone in development?
How is testosterone converted to
DHT?
What are the sources of Estrogen in a
woman?
What is the function of Estrogen in
development?

Testosterone (Testes), Dihydrotestosterone (Converted peripherally) and Androstendione (Adrenal)


Differentiation of the Epididymis, Vas deferens and seminal vesicles. Growth spurt of the penis, the seminal
vesicles, sperm, muscle, and red blood cell growth. Deepening of voice, closing of epiphyseal plates (via
estrogen converted from testosterone) and Libido.
In early differentiation it causes development of the penis, scrotum and prostate. In later/pubertal
development it causes prostate growth and sebaceous gland activity.
5 Alpha reductase converts Testosterone to DHT.
Ovary makes 17 Beta estradiol, Placenta makes estriol and blood/peripheral tissues can aromatize androgens
to estrogen.
Development of genitalia (external) and breast, and female fat distribution.

What are the typical functions of


estrogen beyond development?
How much do estrogens increase in
pregnancy?

Describe the hormonal regulation of


estrogen.
What is the source of Progesterone?
What does elevation of progesterone
indicate?

What is the function of Progesterone?

What happens during the


proliferative/follicular phase of a
woman's cycle?
When is follicular growth fastest?
What stimulates endometrial
proliferation?
What
What
What
What
What

maintains the endometrium?


defines Oligomenorrhea?
defines Polymenorrhea?
defines Metorrhagia?
defines Menometrorrhagia?

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.
Stimulates prolactin secretion but blocks its action at the breast. Increases transport of proteins, Steroid
hormone binding globulin synthesis, increases HDL and decreases LDL.
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
estrogen. LH acts on the Theca cells to upregulate Desmolase which convert cholesterol to androstendione.
The androstendione goes to the granulosa cells to be converted to estrogen.
Corpus Luteum, placenta, adrenal cortex and testes (in men obviously)
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
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
surge. About 1 week before ovulation, one follicle becomes dominant meaning that it becomes more
responsive to FSH. The follicle secretes lots of inhibin which downregulates FSH and causes atresia of the
other follicles.
2nd week of the proliferative phase.
Estrogen
Progesterone
Cycle greater than 35 days
Cycle less than 21 days
Frequent but irregular menstruation
Heavy, irregular menstruation

Describe the hormonal changes during


a woman's cycle (see Reproductive
Attachment 1).

Describe the maturation of the Follicle


(see Reproductive Attachment 2).

What happens to the follicle during


ovulation?
What hormonal changes are seen
during ovulation?
What is Mittelschmerz?
When does oogenesis begin and when
is it completed?

What is the process of oogenesis?


Where does Fertilization most
commonly happen?
When does implantation into the wall
of the uterus typically occur?
How is lactation induces after labor?
How is milk production maintained
after birth?
What is the role of Prolactin in the
female?

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
FSH then drop. Estrogen increases again but Progesterone increases a lot throughout the whole phase thus
maintaining the lining of the endometrium. Everything drops when entering the menstrual phase which
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
has both internal and external layers. It becomes a mature follicle when the vesicles form a single antrum.
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
remainder of the cycle or the beginning of pregnancy. The corpus luteum then degenerates to form the
corpus albicans and eventually becomes fibrotic.
Increased estrogen, increased GnRH and increased GnRH receptors on anterior pituitary, estrogen surge
precedes LH surge. Increased temperature from increased progesterone.
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
Meiosis I is arrested in Prophase for years until ovulation. Meiosis II arrests in metaphase until fertilization.
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
that degenerates.
Most commonly happens in the upper end of the Fallopian tube (the ampulla). Typically within a day after
ovulation.
6 days after fertilization. The trophoblast secretes Beta-HCG which is detectable in the blood 1 week after
conception and in urine (home test) 2 weeks after conception.
The decrease in maternal steroids induces lactation.
Suckling increases nerve stimulation which increases oxytocin and prolactin production thus maintaining milk
production.
PRL induces and maintains lactation and decreases reproductive function.

What is the role of Oxytocin in the


female?
Where is hCG made?

What is the function of hCG?


How is pregnancy detected?
What changes in hCG are there in
pathologic states?
What hormonal changes are seen in
menopause?
What is the main source of Estrogen
after menopause?
What are some symptoms of
menopause?

What is Klinefelter's Syndrome?


How does Klinefelter's Syndrome
cause infertility?

What is Turner's Syndrome?


Describe a double Y male
What hormonal changes would you
see with a defective androgen
receptor?
What hormonal changes would you
see with a Testosterone-secreting
tumor, or exogenous steroids
What hormonal changes would you
see with primary hypogonadism?
What hormonal changes would you
see with Hypogonadotropic
hypogonadism?
What is pseudohermaphroditism?

Helps with milk letdown and may be involved with uterine contractions.
Syncytiotrophoblast of the placenta.
Maintains corpus luteum (thus progesterone) for the first trimester by acting LH. The Placenta synthesizes its
own estriol and progesterone during the 2nd and 3rd trimester and the corpus luteum degenerates.
hCG is used to detect pregnancy because it appears early in the urine.
hCG is elevated in Hydatidiform moles, Choriocarcinoma, Gestational trophoblastic tumors (and other tumors
I think)
Decreased Estrogen production due to age linked decline in follicles. Significantly increased FSH, increased
LH, increased GnRH. Average age of onset is 51, earlier in smokers. Usually preceded by a few years of
irregular periods.
Estrone from peripheral conversion of androgens. Increased androgens can cause hirsutism (that's why your
grandma has a mustache)
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
distribution. May cause developmental delay. Usually a Barr body is present (inactive X chromosome)
Dysgenesis of seminiferous tubules causes decreased inhibin which leads to increased FSH. Abnormal Leydig
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
amenorrhea.
47 (XYY). Phenotypically normal, very tall, severe acne, antisocial behavior in 1-2%, normal fertility.

Increased testosterone and increased LH (female phenotype I think)

Increased testosterone but decreased LH from negative feedback

Decreased testosterone and increased LH from gonadal failure and lack of feedback.

Decreased testosterone and decreased LH from pituitary failure not stimulating the gonads.
Disagreement between the phenotypic (external genitalia) and gonadal (testes vs ovaries) sex.

What is a female
pseudohermaphrodite?
What is a male pseudohermaphrodite?
What is a true hermaphrodite?

What is Androgen Insensitivity


Syndrome?

What is 5 alpha reductase deficiency?

What is a Hyaditiform Mole?

What is a complete Hyaditiform Mole?

46 (XX). Ovaries are present but the external genitalia are virilized or ambiguous. It's due to excessive or
inappropriate androgen exposure during early gestation. Usually congenital adrenal hyperpasia or exogenous
androgen administration.
46 (XY). Testes are present but external genitalia are female or ambiguous. The most common reason is
androgen insensitivity syndrome aka testicular feminization.
(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
the labia majora and must be surgically removed to prevent malignancy. Increased testosterone (although
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
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
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
Beta-hCG.

What characteristics are seen in a


complete mole?
What characteristics are seen in a
partial mole?
What are some common causes of
recurrent miscarriages?
What is pre-eclampsia?
What is eclampsia?
What are some risk factors for preeclampsia?
What is the pathogenesis of Preeclampsia?
What is HELLP Syndrome?
What are some clinical features of
Pre-eclampsia?

Karyotype is 46,XX or 46, XY. Massively increased hCG, increased uterine size, 2% convert to
adenocarcinoma, no fetal parts, 2 sperm +empty egg, 15-20% form malignant trophoblastic disease.
Karyotype is 69,XXY, slightly increased hCG, no change in uterine size, rare for it to convert to
choriocarcinoma, 2 sperm+1 egg, risk of malignancy is less than 5%
during the 1st weeks- low progesterone levels (no response to Beta-hCG, 1st trimester-chromosomal
abnormalities, 2nd trimester-bicornate uterus
Combination of hypertension, proteinuria and edema.
Pre-eclampsia + Seizures

How do you treat Pre-Eclampsia or


Eclampsia?

Delivery of the fetus as soon as it's viable. Otherwise bed rest, salt restriction, and monitoring/treatment of
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.
Increase in risk with smoking, hypertension and cocaine use.

What is Abruptio Placentae?

Pre-existing hypertension, diabetes, chronic renal disease and autoimmune disorders.


Caused by placental ischemia due to impaired vasodilation or spiral arteries, resulting in increased vascular
tone. May be an issue with implantation.
Hemolysis, Elevated LFT's, Low Platelets from Pre-eclampsia
Headache, blurred vision, abdominal pain, edema of the face and extremities, altered mentation,
hyperreflexia. Lab findings include thrombocytopenia and hyperuricemia.

What is Placenta Acreta?


What is Placenta Increta?

What is Placenta Percreta?


What is Placenta Previa?

What is an Ectopic Pregnancy?


What is the problem with retained
placental tissue?
What are some risk factors associated
with ectopic pregnancy?
What is Polyhydramnios?

What is Oligohydramnios?
What is Potter's Syndrome?
Describe Dysplasia and Carcinoma in
Situ of the cervix.
What virus is associated with Cervical
dysplasia?
What risk factors are associated with
cervical dysplasia?
Describe invasice carcinoma of the
cervix
What is a Koilocyte?

What is Endometriosis?
How does Endometriosis manifest
clinically?

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
the entirety of the myometrium.
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
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
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
sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
May cause postpartum hemorrhage.
History of infertility, Salpingitis/PID, ruptured appendix (at any point), prior tubal surgery or any lower
abdominal surgery, endometriosis.
Greater than 1.5-2 Liters of amniotic fluid. Associated with esophageal and duodenal atresia, causing
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
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,
pulmonary hypoplasia and cranial anomalies.
Disordered epithelial growth. Begins at the basal layer of the squamo-columnar junction and extends
outward. Classified as CIN I, CIN II or CIN III (Carcinoma in Situ), depending on the extent of the dysplasia.
HPV 16 and 18
Multiple sexual partners, smoking, early sexual intercourse, HIV infection
Pretty much the cervical cancer gone really nasty. Often squamous cell carcinoma. Papsmear can catch
cervical dysplasia (koilocytes) before it becomes invasive carcinoma. Lateral invasion can block ureters
causinf renal failure.
Cervical cell infected with HPV that is undergoing dysplasia. See large nuclei and large ring of cytoplasm.
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
else want to puke right now? Often in the ovary or on the peritoneum.
Severe menstrual-related pain.

What are possible complications of


Endometriosis?
What is Adenomyosis?
What is Endometrial Hyperplasia?
How does Endometrial Hyperplasia
manifest clinically and what are some
risk factors?

Often causes infertility, possibly due to retrograde mentrual flow or ascending infection.
Endometrium within the myometrium
Abnormal endometrial gland proliferaton usually caused by excess estrogen stimulation. Associated with
increased risk for endometrial carcinoma.

What is Endometrial Carcinoma?

Postmenopausal vaginal bleeding. Risk factors are anovulatory cycles, hormone replacement therapy,
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.
The more it's invaded the myometrium, the worse the prognosis.

Describe a Leiomyoma?

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
smooth muscle bundles (doesn't become Leiomyosarcoma). See attachment 4 for a picture.

What is a Leiomyosarcoma?
What is the epidemiology of
gynecologic tumors?

What is premature Ovarian failure?


what are the most common causes of
anovulation?

What is Polycystic Ovarian Syndrome?


What hormonal changes do you see in
PCOS?
What is a Follicular Cyst?
What is a Corpus Luteum cyst?
What is a Theca Lutein Cyst?

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
cervix and bleed (yuck!). More common in middle aged women and African American women.
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
puberty but before age 40. See decreased estrogen but increased LH and FSH b/c no feedback.
Polycystic ovarian syndrome, obesity, Asherman's Syndrome (adhesions), HPO axis abnormalities, premature
ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, Cushing Syndrome and adrenal
insufficiency
Increased LH production leading to anovulation, hyperandrogenism due to deranged steroid synthesis by
theca cells. Enlarged bilateral cystic ovaries manifest clinically with amenorrhea, infertility, obesity and
hirsutism. Associated with insulin resistance, increased risk of endometrial cancer. Treatment is weight loss,
OCP, gonadotropin analogs, clomiphene or surgery.
Increased LH and FSH and increased Testosterone.
Distention of a ruptured Grafian Follicle. May be associated with hyperestrinism and endometrial hyperplasia.
Hemorrhage into persistent corpus luteum. Commonly regresses spontaneously.
Commonly bilateral or multiple cysts. Due to gonadotropin stimulation. Associated with choriocarcinoma and
moles.

What is a Chocolate Cyst?


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

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

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

What is a serous cystadenoma?

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

What is a serous cystadenocarcinoma?

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

What is a Mucinous Cystadenoma?


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

Multilobular cyst lined by mucus-secreting epithelium. Benign. Intestine-like tissue.


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

What is a Granulosa Cell Tumor?

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

What is a teratoma?

What is a Krukenberg tumor?


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

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

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

What is a Fibroadenoma of the breast?


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

an invasive Lobular tumor?


a medullary tumor of the

Small, mobile, firm mass with sharp edges. Most common tumor in those <25 years. See increasing siza
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
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
decade. Some may become malignant.
Common postmenopause. Arise from mammary duct epithelium or lobular glands. Overexpression of
estrogen/progesterone receptors on erb-B2 (HER-2 and EGF Receptor) is common. Affects therapy and
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
live birth, obesity (adipose tissue serves as a major source of estrogen in post-menopausal women by
converting androstenedione to estrone).
Malignant tumor of the breast that fills the ductal lumen. Arises from ductal hyperplasia. Early malignancy
without basement membrane penetration.
Worst and most invasive ductal carcinoma but also most common. Forms firm, fibrous, rock hard masses
with sharp margins and small, glandular duct like cells.
Malignant breast tumor, often multiple and often bilateral. See an orderly row of cells.
Malignant tumor with a good prognosis. See fleshy, cellular, lymphatic infiltrate.

a comedocarcinoma of the
an inflammatory tumor of the

What is Paget's disease?

What is Fibrocystic disease?

What are the histologic subtypes of


Fibrocystic disease?
What is acute mastitis?
What is Fat Necrosis?

What is Gynecomastia?

Subtype of DCIS. See ductal caseous necrosis.


Nasty, malignant tumor with a 50% 5 year survival. See dermal lymphatic invasion by breast carcinoma.
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.
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
carcinomas.
Fibrosis-hyperplasia of breast stroma. Cystic-fluid filled, blue dome. Ductal dilation. Sclerosing adenosisincreases acini and intralobular fibrosis. Associated with calcifications. Epithelial hyperplasia-increase in
number of epithelial cell layers in terminal duct lobule. Increases risk of carcinoma with atypical cells.
Occurs in women >30 years of age.
Breast abscess. During breast feeding. Increases risk of bacterial infection through cracks in the nipple.
Staph Aureus is the most common pathogen.
A benign, painless lump. Forms as a result of injury to breast tissue. Up to 50% of patients may not report
trauma.
Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter's syndrome or drugs
(estrogen, marijuana, heroin, psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol,
Ketoconazole).

What is the order of structures in the


breast starting at the nipple?

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

What tumors occur at each of these


structures?
How does prostatitis present?

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

What are causes of acute prostatitis?


What are causes of chronic
prostatitis?

What is Benign Prostatic Hyperplasia


(BPH)?
How do you treat BPH?

What is Prostatic adenocarcinoma?

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

What is a Seminoma?

What is an embryonal carcinoma?


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

Usually bacterial, especially E. Coli


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

What is a Leydig Cell Tumor?


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

is
is
is
is

a
a
a
a

tunica vaginalis lesion?


Variocele?
Hydrocele?
spermatocele?

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

What is Bowen's Disease?


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

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

When does Blastocyst hatching occur?


What is the Zona Pellucida?

When the blastocyst enters the endometrial cavity, about 5 days after fertilization.
Non-cellular, porous layer of glycoproteins around the oocyte.

What proteins characterize


preimplantation of the embryo?
What are the three stages of
implantation?
What is the Decidua Basalis?
What is the Decidua Capsularis?
What is the Decidua Paritalis?
What happens to RBC and Plasma
volume and mass in pregnancy?

Early pregnancy factor, Platelet activating factor, human Chorionic Gonadotropin, Matrix Metalloproteinases
and Inhibitors of Matrix Metalloproteinases, Heparin binding-EGF like growth factor receptors

What happens to GFR and Creatinine


Clearance during pregnancy?
Why does respiratory alkalosis happen
during pregnancy?
Why do women get dyspnea during
pregnancy?

Apposition, Adhesion and Invasion


Decidua that forms underneath the embryo
Capsule of decidua over the embryo
Other decidua lining the uterine cavity
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
urea results in serum creatinine and urea that are really low. Thus normal creatinine and urea are
problematic.
Estrogen and progesterone both stimulate the respiratory center. Greater tidal volume and increased
respiration rate also cause increased minute ventilation, thus more CO2 is blown off. Thus respiratory
alkalosis from decreased PaCO2
May be due to decreased CO2 stimulating the respiratory center and causing subjective shortness of breath.

Why are Thyroxin and Cortisol


increased in pregnancy?
What defines menopause?
What are the physiologic causes of
menopause?
What are non-physiologic causes of
menopause?
What is the average age of
menopause and how is age at
menopause determined?

What are some clinical findings in


menopause?
What are some labroratory findings in
menopause?
What are some treatment options for
symptomatic menopause?
What are risks of long term hormone
replacement?
What is Hirsutism?
What is virilization?
What are male secondary sex
characteristics?
What causes virilization or hirsutism?

What are some causes of virilization


and hirsutism?

What is Polycystic Ovarian Syndrome?


What are clinical findings in polycystic
ovarian syndrome?

hCG simulates TSH since they share the same alpha subunit. Thus it stimulates T4 secretion during the first
10 weeks. Estrogen promotes growth of the pituitary and the thyroid and synthesis of thyroid binding
globulin. Thus T4 and cortisol are increased but free T4 and cortisol are the same.
No menses for one year after age 40.
Waxing and waning of estrogen levels from decreased ovarian function. Depletion of granulosa and thecal
cells. Lack of response to gonadotropins. Increased LH stimulates androgen production in stromal cells
(thus hirsutism)
Surgical removal or radiation of ovaries. Turner syndrome. Family history of early menopause and left
handedness (seriously???)
Average age is 51. The age at which it's determined is genetically determined, but smokers reach
menopause early and peri-menopause is mid-to late 40's.
Secondary amenorrhea, hot flushes, night sweats, atrophic vaginitis with pruritis, burning, bleeding and
dyspareunia. Also see mood swings, anxiety, depression, insomnia, decreased libido, urinary incontinence,
headaches, tiredness, lethargy, and osteoporosis with increased risk of Colle's and vertebral fractures.
Increase in LH and FSH from a drop in estrogen (LH) and progesterone (FSH)
Estrogen replacement, progestins added if the uterus is still present to prevent endometrial adenocarcinoma.
Thromboembolism, Coronary heart disease, stroke, slightly increased risk for breast cancer, increased risk for
dementia in women over 65.
Excess hair in normal hair-bearing areas.
Hirsutism plus 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
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
sertoli-leydig cell tumor, adrenal tumors producing Cushing syndrome, decreased steroid hormone binding
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
accumulating and producing subcortical cysts that then enlarge the ovaries.
Menstrual irregularities, mostly oligomenorrhea and often hirsutism, infertility or obesity.

What are some lab findings in PCOS?

What is the treatment in PCOS?


What is Menorrhagia?

What is Dysmenorrhea?
What is the treatment for Primary
Dysmenorrhea?
What is the treatment for secondart
Dysmenorrhea?
What is dysfunctional uterine
bleeding?
What are some types of dysfunctional
uterine bleeding?
What is most common cause of
irregular bleeding?
What causes anovulatory
dysfunctional uterine bleeding?

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. LHreleasing hormone analogs inhibit ovarian androgen production.
Loss of blood >80 mL per period. It's likely if sheets are stained despite heavy protection. Excessive
passage of clots indicates that plasmin does not have enough time to dissolve clot.
Painful menses, occuring in approximately 50% of women. Primary type occurs in ovulatory cycles due to
increased prostaglandin PGF-2alpha. See increased uterine contractions from increased prostaglandins. The
secondary type is from endometriosis, adenomyosis, leiomyomas, or cervical stenosis.
NSAID's, OCP, nifedipine, magnesium sulfate
Essentially deal with the underlying disease.
Abnormal uterine bleeding that is unrelated to an anatomic cause. Note that this is a diagnosis of exclusion.
Menorrhagia, Hypomenorrhea, Metrorrhagia, Menometrorrhagia, Oligomenorrhea, Polymenorrhea

What is Primary Amenorrhea?


What is Secondary Amenorrhea?

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

What are some causes of


amenorrhea?

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

What are causes of abnormal vaginal


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

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

What causes ovulatory dysfunctional


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

Anovulatory dysfunctional uterine bleeding, Von Willebrand's disease

What are some causes of abnormal


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

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

Anovulatory dysfunctional uterine bleeding, endometrial hyperplasia, cancer.


Entirely covered by the chorionic plate. The chorionic villi vessels converge with the umbillical cord.
Chorion is covered with amnion
Contains cotyledons covered by decidua basalis.

Where do the chorionic villi project?


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

Into the intervillous space


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

How should you treat a placental


infection even if culture is negative?
What is Funisitis?
What is Placentitis?
What is chorioamnionitis?
What complications might arise from
chorioamnionitis?
What is Placenta Previa?

Treat prophylactically with IV Ampicillin+Erythromycin followed by PO amoxicillin and erythromycin. If


culture positive you can give IV penicillin or ampicillin
Infection of the umbillical cord
Infection of the placenta
Infection of the fetal membranes

How does Placenta Previa present?


How do you diagnose Placenta Previa?

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

Neonatal sepsis and meningitis. Treat with Cefoxitin or Ticaricillin-Clavulanate


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

What is Abruptio Placentae?


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

What is Velamentous insertion?


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

What is a complete Hyaditiform Mole?


Which type of Mole has an increased
risk of Choriocarcinoma?

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

Twin Twin Transfusion syndrome.


Toxemia of pregnancy
First pregnancy, more common in women <20 years and >35 years, history of previous preeclampsia,
positive family history, multiple gestations, african american, thrombocytosis, obesity
Abnormal placentation causing mechanical or functional obstruction of the spiral arteries. The abnormal
trophoblastic tissue invades the spiral arteries. Imbalance favors vasoconstriction over vasodilation
(decreased PGE2 and NO, increased TXA2, Ang II and increased sensitivity to Ang II)
Premature aging of the placenta, multiple placental infarctions, spiral arteries show atherosclerosis
Hypertension, proteinuria from leaky capillaries (increased inflammation), dependent pitting edema from loss
of albumin, weight gain, seizures in eclampsia, swollen endothelial cells in glomerular capillaries producing
oliguria.
Right upper quadrant pain and hepatomegaly, periportal necrosis with increased transaminases, HELLP
syndrome
Benign tumor of the chorionic villus from an empty egg and 2 sperm or an egg and 2 sperm.
The entire placenta is neoplastic. Dilated swollen villi without fetal blood vessels. No embryo is present.
Ovum 46, XX, lacking maternal chromosomes. The chromosomesare derived from the father, either 2 sperm
or duplicated 23X sperm in the ovum
Complete mole. Presents with painless vaginal bleeding in fourth, fifth month of pregnancy. Causes severe
vomiting, pre-eclampsia, uterus that is too large for gestational age, increased hCG for gestational age, and
snowstorm appearance on ultrasound.

What is a partial Hyaditiform Mole?


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

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

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

Swallowed and recycled by the fetus.


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

What can increase surfactant


production in the fetus?

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

Where is estriol made in pregnancy?

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

What is Polyhydramnios?

What part of estriol synthesis does the


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

Fetal adrenal cortex converts pregnenolone from the placenta to DHEA-S.


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

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

What hormones affect lactation?


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

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

What is sclerosing adenosis?

Fibrocystic change
Superficial thromboplebitis of veins overlying the breast, presenting as a palpable, painful cord.
Most common painful breast mass in women <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
menstrual cycle but have no malignant potential
Proliferation of small ductules/acini in the lobule-pattern is often confused with infiltrating ductal cancer.
Often contains microcalcifications.

What is Ductal Hyperplasia?

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

What is Fibrocystic change?

What is Mammary duct


ectasia/plasma cell mastitis?

What is traumatic fat necrosis?

What is a Fibroadenoma of the breast?

What is a Phyllodes tumor?


What is an Intraductal Papilloma?

Main ducts fill up with debris causing dilation, rupture and inflammation. Results in greenish-brown nipple
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
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
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 leaflike extensions.
Most common cause of bloody nipple discharge in women <50. Develops in the lactiferous ducts or sinuses.
No increased risk for cancer.

What are risk factors for breast


cancer?
What are some genetic markers for
breast cancer?
What decreases risk for breast
cancer?
What are clinical findings in breast
cancer?

Prolonged estrogen stimulation, genetic susceptibility, especially if first generation relatives. Prolonged
estrogen stimulation from either early menarche or late menopause or nulliparity.

What is the primary screening test for


breast cancer?
Where do microcalcifications most
commonly occur?
How is estrogen and progesterone
receptor expression related to
prognosis?
What is a Ductal Carcinom in Situ
(DCIS)?

Mammography-detects 80-90% of non-palpable breast masses. Does not distinguish benign from malignant
lesions. Can identify microcalcifications and spiculated masses with or without microcalcification.
Ductal carcinoma in situ, and sclerosing adenosis. Five or more microcalcifications that are punctate,
microlinear or branching all suggest malignancy

BRCA 1 and BRCA 2, Li-Fraumeni, RAS oncogene, ERBB2, RB suppressor gene


Breast feeding, moderate or vigorous physical training, healthy body weight.
Painless mass in the breast, usually the upper outer quadrant. Skin or nipple retraction, painless axillary
lymphadenopathy, hepatomegaly and bone pain if there are metastases.

What is inflammatory carcinoma of


the breast?

ER/PR expression generally confers a good prognosis whereas ERB2/NEU has a poor prognosis if amplified.
Nonpalpable mass. Forms a cribiform pattern (seive like) or comodo like pattern (necrotic center).
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
identifiable on mammography. Lobules are distended with bland neoplastic cells. Usually ER/PR positive.
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
causing induration.
Extension of DCIS into the lactiferrous ducts and skin of the nipple producing a rash with or without nipple
retraction. Palpable mass often present, see Paget's cells as well.
Invasive tumor associated with BRCA1 mutations. Bluky, soft tumor with large cells and a lymphoid infiltrate.
Most are ER/PR negative.
Invasive tumor that presents with erythematous breast with dimpling of the skin like an orange peel from
fixed opening of the sweat glands. Plugs of tumor block the lumen of dermal lymphatics causing localized
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?


What is a Colloid (Mucinous)
Carcinoma?

Invasive mass that develops in terminal ductules. Increased incidence of cancer in the opposite breast.

What is a Lobular Carcinoma in Situ


(LCIS)?

What is Infiltrating Ductal Carcinoma?


What is Paget's disease?
What is Medullary Carcinoma of the
breast?

What is Gynecomastia?

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
elderly.

What causes pathologic


gynecomastia?
What is the most common cause of
Bartholin gland abscesses?
What is Lichen Sclerosis?
What is Lichen Simplex Chronicus?
What is a Papillary Hidradenoma?
What is Vulvar Intraepithelial
Neoplasia?
What are risk factors for squamous
cell carcinoma of the vulva?
What is extramammary Paget's
disease?
What is Malignant melanoma of the
vulva?
What type of lesion results from
infection with Calymmatobacterium
Granulomatis?
What types of lesions result from
infection with Candida Albicans?

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
activity like DES or digoxin, or androgen blocking drugs like spironolactone or flutamide or that decrease
androgen production like leuprolide. These all increase estrogen.
Infection with Neisseria Gonorrhea
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
Squamous Cell Carcinoma.
Benign tumor of the apocrine sweat gland. Causes painful nodule on the labia majora.
Dysplasia of the vulva, ranging from mild to carcinoma in situ. Strong association with HPV 16 and high risk
of developing squamous cell carcinoma

HPV 16, smoking, immunodeficiency.


Red, crusted vulvar lesion. Intraepithelial adenocarcinoma derived from primitive epithelial progenitor cells.
Malignant Paget cells contain mucin which is Periodic Acid Schiff positive. Spreads along the epithelium but
rarely invades the dermis.
Melanoma cells, histologically similar to Paget cells except these are PAS negative.

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

What type of lesion results form


infection with Chlamydia Trachomatis?
What types of lesions result from
infection with Chlamydia Trachomatis
subspecies?

Yeast and pseudohyphae which should be part of the normal vaginal flora. Causes vaginitis, pruritic vaginitis
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),
proctitis and bartholin gland abscesses (in females obviously). Can also cause conjunctivitis and pneumonia
in a newborn.
Lymphogranuloma venerum, papules with no ulceration, inguinal lymphadenitis with granulomatous
microabscesses and draining sinuses. Lymphedema of the scrotum or vulva and possibly rectal strictures in
women

What types of lesions are seen with


infection by Gardnerella Vaginalis?

Gram negative rod that causes bacterial vaginosis. Most common vaginitis which presents with malodorous
discharge. Organisms adhere to the squamous epithelium forming clue cells.

What types of lesions result from


infection with Hemophilus Ducreyi?

Gram negative rod that causes Chancroid. Male dominant disease, often correlated with HIV. Causes painful
genital warts and perianal ulcers with suppurative inguinal nodes which main have draining sinuses.

What types of lesions result from


infection with HSV-2?

STD with the virus remaining latent in the sensory ganglia. Causes recurrent vesicles that ulcerate on the
vulva, penis, cervix and perianal area. See multinucleated squamous cells on Tzanck prep

What types of lesions result from


infection with HPV?
How do you treat HPV?
What types of lesions result from
infection with Neisseria Gonorrhoeae?
What are signs of disseminated
Gonococcemia?

What types of lesions result from


infection with Treponema Pallidum?
What are the non-specific screening
tests for Syphillis?
What are the confirmatory tests for
Syphillis?
What is the Jarisch-Herxheimer
reaction?

Types 6 and 11 associated with Condyloma Acuminata (warts)-fernlike or flat lesions in the genital area.
Types 16 and 18 associated with dysplasia and squamous cell carcinoma. See koilocytes in squamous
epithelium. Cells have wrinkled, pyknotic nuclei surrounded by a clear halo.
Vaccine! Topical podophyllin, alpha-IFN injections and imiquimod cream
Gram negative diplococcus that infects glandular transitional epithelium in sites similar to Chalmydia. Causes
prululent lesions and urethritis. Can cause ectopic pregnancy, male sterility, disseminated gonococcemia,
septic arthritis, and Fitz Hugh Curtis.
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
and soles along with generalized lymphadenopathy, condylomata lata (flat lesions) and alopecia. Tertiary
syphillis presents with neurosyphillis, aortitis and gummas.
RPR or VDRL. Titers should decrease after treatment.
FTA-ABS which is positive with or without treatment
Intensification of rash in primary or secondary syphillis after proteins are released from the dead organisms
following penicillin treatment

what types of lesion results from


infection with Trichamonas Vaginalis?
What is Rokitansky-Kuster Hauser
Syndrome?

Flagellated protozoan with jerky motility which produces vaginitis, cervicitis and urethritis. Causes a
strawberry colored cervix and fiery red vaginal mucosa with greenish, frothy discahrge.

What is a Gartner's Duct cyst?


What is a Rhabdomyoma?
What is an Embryonal
Rhabdomyosarcoma?

Remnant of the Wolffian/mesonephric duct which presents as a cyst on the lateral wall of the vagina.
Benign tumor of skeletal muscle in the vagina (can also be on the tongue or heart)

What is clear cell adenocarcinoma of


the vagina?

Adenocarcinoma of the vaginal wall (pretty self explanatory). Occurs in women with DES exposure since DES
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
the vagina

What is Vaginal Adenosis?

Absence of the upper vagina and uterus resulting in primary amenorrhea

Necrotic, grape like mass protruding from the vagina, most often in girls <5 years

What are some other DES related


abnormalities?
What is vaginal squamous cell
carcinoma?
What does the cervix actually consist
of?
What lines the exocervix?
What lines endocervical glands?
How does the endocervical epithelium
transform into the exocervical
epithelium?
What is the pathogenesis of a
Nabothian cyst?
What is acute cervicitis?
What are clinical findings in acute
cervicitis?
What causes chronic cervicitis?
What is follicular cervicitis?
What is the purpose of a Cervical Pap
test?
What do superficial squamous cells
indicate on Pap?
What do intermediate squamous cells
on Pap indicate?
What do parabasal cells on Pap
indicate?
What types of cells are seen on Pap
from a non-pregnant and pregnant
woman?
What is a Cervical Polyp?
Describe Cervical Intraepithelial
Neoplasia, CIN
What is CIN I?
What is CIN II?
What is CIN III?
What is the epidemiology of cervical
cancer?
What are clinical findings in cervical
cancer?

Abnormally shaped uterus that thwarts implantation (T shape). Cervical incompetence which can cause
recurrent miscarriage.
It's what it sounds like. That said, primary SCC is associated with HPV 16. Most of these are actually
extensions of cervical SCC into the vagina.
Endocervix and exocervix. The exocervix begins at the cervical os
squamous epithelium
Mucus secreting columnar cells
Endocervical epithelium migrates down to the exocervix where exposure to the acid pH of the vagina causes
squamous metaplasia. This area is called the transformation zone and is the most likely location for
squamous dysplasia and cancer.
Metaplastic squamous cells block endocervical gland orifices resulting in obstruction to outflow of mucus.
This is a normal finding however.
Acute inflammation is often present in the transformation zone, however pathologic acute inflammation may
be due to infection-Chlamydia, Neisseria, Trichomonas, Candida, HSV, HPV.
Vaginal discharge, pelvic pain, dyspareunia, pain on palpation (chandelier sign), easy bleeding and
erythematous or exudative cervical os.
Essentially persistence of acute cervicitis
Pronounced lymphoid infiltrate with germinal centers caused by Chlamydia Trachomatis.
Screening test for squamous dysplasia and cancer. Evaluate the hormone status of the patient.
Adequate estrogen
Adequate progesterone
Lack of estrogen and progesterone.
Non-pregnant: 70% superficial, 30% intermediate squamous cells. Pregnant: 100% intermediate squamous
cells from progesterone effect.
Non-neoplastic polyp that protrudes from the cervical os. Arises from the endocervix, most commonly in
perimenopausal or multigravida women.
Most cases associated with HPV which produces koilocytes in squamous cells. Associated with early age of
sexual intercourse, multipe high-risk partners, high risk HPV types, smoking, OCP's and immunodeficiency.
Mild dysplasia involving the lower third of the epithelium
Moderate dysplasia involving the lower 2/3 of the epithelium
Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium
Least common GYN cancer with higher incidence in developing countries. Most are squamous cell carcinomas
with the same risk factors as CIN
Abnormal vaginal bleeding, often post coital, malodorous discharge

What are some characteristics of


cervical cancer?
What is the sequence to menarche?
When does ovulation occur?
What mediates the secretory phase of
the cycle?

What changes occur after fertilization?


What initiates menses?
What are the functions of FSH?

What are the functions of LH?


What hormonal changes are seen in
pregnancy?
What is in Oral Contraceptive Pills and
how do they work?
Where does Estradiol come from?
Where does Estrone come from?
Where does Estriol come from?
Where does androstendione come
from in a woman?
Where does DHEA come from in a
woman?
Where does testosterone come from
in a woman?
What is Sex Hormone Binding
Globulin?
What does SHBG have a greater
affinity for?

What is acute endometritis?

Cancer often extends down into the vagna and out into the lateral wall of the cervix and vagina. May
infiltrate the bladder wall and obstruct the uterus causing postrenal azotemia and possibly death. May
metastasize distantly, e.g. to the lungs.
Breast budding (Thelarche), growth spurt, pubic hair, axillary hair, menarche (mean age is 12.8 years).
Between days 14 and 16
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
exaggerated secretory phase in pregnancy called the Arias-Stella phenomenon.
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
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
LH isn't doing these things directly but it uprgulates necessary enzymes)
Human chorionic gonadotropin-synthesized in the syncytiotrophoblast lining the chorionic villus. hCG acts as
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
arrests the proliferative phase and cause gland atrophy and also inhibit LH directly. OCP's also render the
cervical mucus hostile to sperm and alter Fallopian tube motility.
Aromatized testosterone in granulosa cells. Primary estrogen in non-pregnant women.
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
maternal liver.
Equal derivation from ovaries and adrenal cortex
Almost exclusively from the adrenal cortex
derived from conversion of androstenedione to testosterone in the ovaries and adrenal glands. Can be
converted to DHT peripherally.
Binding protein for both estrogen and testosterone, mostly synthesized in the liver. Androgens, obesity and
hypothyroidism all decrease SHBG
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
or miscarriage. Group B strep, staph a, bacteroides, C. trachomatis, N. Gonorrhoeae, E Coli.

What are clinical findings in acute


endometritis?
What causes chronic endometritis?
What is the key histologic finding in
chronic endometritis?
What is Adenomyosis?
What are clinical findings in
adenomyosis?

What is Endometriosis?
What are clinical findings in
Endometriosis?
What is an endometrial polyp?
What are clinical findings of an
endometrial polyp?
What is a Hyatid Cyst of Morgagni?

Fever, uterine tenderness, prululent or foul vaginal discharge and abdominal pain.
Retained placenta, gonorrhea, IUD (with infection)
Like all chronic inflammatory conditions, you see plasma cells
Invagination of the stratum basalis into the myometrium. See glands and stroma thickening in the
myometrium and general enlargement of the uterus.
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
tubes and intestines.
Dysmenorrhea, abnormal bleeding, painful stooling during menses, intestinal obstruction and bleeding during
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
carcinoma but it can protrude through the cervix into the vagina.
Common cause of menorrhagia, spotting in between periods or after menopause

What is pelvic inflammatory disease?

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,
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


(SIN)?

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

What is ectopic pregnancy?


What are risk factors for ectopic
pregnancy?

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


ectopic pregnancy?
How do you diagnose ectopic
pregnancy?
What is Oophoritis?

What is stromal hyperthecosis?

What are risk factors for Ovarian


cancer?

How can ovarian tumors be classified?

What are some clinical findings in


Ovarian tumors?
What is a common tumor marker of
malignant ovarian tumors?

What is a Serous Ovarian tumor?

Sudden onset of lower abdominal pain and tenderness, usually about 6 weeks after LMP, adnexal tenderness,
peritoneal signs, abnormal uterine bleeding, hypovolemic shock as a result of intraperitoneal hemorrhage.
Beta hCG is a good screening test but a positive hCG doesn't mean that there is an ectopic pregnancy.
Vaginal ultrasound showing an amniotic sac is confirmatory.
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
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
syndrome (dysgerminoma), Peutz-Jeghers syndrome (sex cord tumors with annular tubules), history of
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,
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,
malignant pleural effusion, torsion and infarction (cystic teratomas), signs of hyperestrinism in estrogen
secreting tumors or virilization in androgen secreting 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
and has psammoma bodies and dystrophic calcification.

What is a cystic teratoma?

Cysts lined by mucus-secreting cells (like endocervical cells). Cause large multi-nucleated tumors. Seeding
of tumor produces pseudomyxoma peritonei. A mucinous cystadenoma is benign and may be associated with
Brenner tumors. A mucinous cystadenocarcinoma is malignant.
Malignant tumor associated with endometrial carcinoma. Commonly bilateral
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
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.

What is a Mucinous tumor of the


ovary?
What is an endometroid tumor?
What is a Brenner tumor?

What is a Gonadoblastoma?
What is a Krukenberg tumor?

Malignant tumor with a mixture of germ cells (dysgerminoma) and sex-cord stromal cells. Associated with
abnormal sexual development. May calcify
Metastasis to the ovary. Contains signet ring cells from hematogenous spread of gastric cancer.

Renal
What does the urinary system
derive from?
How many sets of kidneys are
there?
What is the pronephros?

Intermediate mesoderm of the posterior wall of the abdominal


cavity.
Three sets of kidneys-pronephros, mesonephros and
metanephros
First kidney. Nonfunctional and disappears by week 4

What are the collecting ducts


of the kidney derived from?

Forms after the pronephros and forms the mesonephric/Wolffian


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

What adult structure does the


Allantois become?

Allantois goes to Urachus and becomes the Median umbilical


ligament. Don't confuse this with the medial umbilical ligament
which is a remnant of the umbilical artery.

What is Potter's Sequence?

Malformation of the Ureteric Bud which results in bilateral renal


agenesis. Results in oligohydramnios/Potter's syndrome

What is the mesonephros?


What is the metanephros?
What is the excretory system
of the kidneys derived from?

What are the limb deformities


in Potter's Syndrome?
What are the facial deformities
in Potter's Syndrome?
Why does Pulmonary
Hypoplasia result from Potter's
Syndrome?

Clubfoot, flipper hands, hyperextensible joints, and compressed


thorax
Sloping forehead, flattened nose, recessed chin, low floppy
ears. Results from compression of the fetus against the wall of
the the amniotic sac.
Fetal lungs mature through swallowing of amnion which allows
the lungs to expand. Thus decreased amnion causes decreased
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?

Wat causes a pelvic kidney?


How do pelvic kidneys
present?

What is a Horseshoe kidney?


What is the most common
presentation of horseshoe
kidney?
What is required for definitive
diagnosis of Horseshoe
kidney?

Urinary bladder and urethra


During development, the embryologic kidneys must ascend and
pass under the umbilical arteries. If a kidney can't pass, it
remains in the pelvis
Obstructive hydronephrosis and vesicoureteric reflux. May have
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
inferior mesenteric artery. Associated with Turner's
Most are asymptomatic but can present with UTI followed by
obstructive hematuria or abdominal pain. Predisposes to
nephrolithiasis
IV pyelogram shows rotated calyces but doesn't show the
isthmus. Need a Dimercaptosuccinic Acid Scan (DMSA)

What is the origin and


insertion, innervation, blood
supply and action of the Psoas
major muscle?
What is the origin and
insertion, innervation, blood
supply and action of the Psoas
minor muscle?
What is the origin and
insertion, innervation, blood
supply and action of the
Iliacus muscle?

Origin-vertebral column (T12-L5), insertion-lesser trochanter of


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

What is the origin and


insertion, innervation, blood
supply and action of the
Quadratus Lumborum muscle?

Origin-Transverse process of L3-5, insertion-lower border of the


12th rib. Innervation-Ventral branches of T12 and L1-4.
Action-extends and laterally flexes vertebral column.

Which structures are


retroperitoneal?
Where are the kidneys
located?
Where do the ureters pass in
relation to the uterine artery
or vas deferens?
What is the arterial supply to
the kidneys?
What is the venous return
from the kidneys?
What is unique about the Left
Renal Vein?
What are the structures of the
Renal filtration system in the
order in which filtrate would
pass through?
What is the direction of
urinary drainage out of the
kidneys?
What types of epithelium line
the Urethra?

What are the anatomic


divisions of the male urethra?

What are the anatomic


divisions of the female
urethra?

Pancreas (except tail), Duodenum (second, third and fourth


parts), ascending and descending colon, aorta, IVC, rectum,
adrenal glands, and since this is the renal section-the kidneys!!!
Located at T12-L3 on the left and slightly lower on the right,
embedded in Gerota's Fascia.
Water goes under the bridge. Pass across the bifurcation of the
common iliac and pass under the uterine arteries or vas
deferens and then join the bladder on the posteroinferior side.
Renal arteries which branch off the abdominal aorta
Renal veins drain into the IVC
It also drains blood from the left gonad and is longer than the
right renal vein since it must cross the IVC
Glomerulus surrounded by Bowman's capsule then proximal
convoluted tubule the the straight portion of the proximal
tubule, then thick descending, the Loop of Henle, then thick
ascending limb, then the distal collecting tubule followed by the
collecting duct.
Renal pyramids to the renal papillae to the minor calyces to the
major calyces
Transitional epithelium as it exits the bladder, then stratified
columnar epithelium followed by stratified squamous
epithelium.
Prostatic, Membranous (surrounded by striated muscle forming
the voluntary external urethral sphincter), Bulbous then
Pendulous (surrounded by Littre's glands. Does that mean it
swings like a pendulum? Just wondering
Much shorter so not really divided. Lined by stratified
squamous and pseudostratified columnar epithelium. At the
mid-portion it's surrounded by the striated muscle of the
voluntary external urethral sphincter. Also surrounded by
Littre's glands

What comprises a Renal


Corpuscle?

What is the glomerulus?

What is Bowman's capsule?


What is special about the
visceral layer of Bowman's
capsule?

Is the basement membrane of


the Glomerulus charged?
Describe the histology of the
Proximal Convoluted Tubule

Describe the histology of the


Loop of Henle
Describe the histology of the
Distal Convoluted Tubule
Describe the histology of the
collecting tubule
Describe the histology of the
Collecting Ducts
What doe Juxtamedullary
nephrons do?

Primary filtering component, comprised of the glomerulus and


Bowman's capsule
Collection of dilated capillaries with a fenestrated endothelium,
which emerge from the afferent arteriole and drain into the
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
convoluted tubules.
Specialized filtration lining that is made of Podocytes resting on
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
impenetrable to things like albumin that are also negatively
charged.
Lined by simple cuboidal epithelium with a microvilli brush
border. Interdigitations between the cells prevent loss of fluid
and solutes
Specialized system for absorption and secretion of electrolytes.
Consists of the thick descending, thin descending, thin
ascending and thick ascending loops (see more about transport
later)

Lined by simple cuboidal epithelium without a brush border


Lined by simple cuboidal epithelium. Transports urine from the
functional nephron to the hilum
Lined by columnar epithelium
Exceptionally long Loops of Henle allow them to set up a
hypertonic gradient in the kidney, regulating the production of
concentrated urine

What are Juxtaglomerular


cells?

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
blood pressure, decreases sodium delivery to the distal tubule
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
hormones.
Specialized myoepithelial cells located on the afferent arterioles
which act as baroreceptors. Monitor BP and maintain GFR
through Renin release

What are extraglomerular


mesangial cells?

Contractile cells with receptors for angiotensin II and natriuretic


factor allowing them to regulate glomerular flow.

What is the Juxtaglomerular


Apparatus?

What is the Macula Densa?

What types of cells line the


bladder?
Walk through a Darrow-Yannet
Diagram (see following
questions as well)
What are clinical implications
of Water deprivation?
What are the clinical
implications of Diarrhea?
What are the clinical
implications of Adrenal
Insufficiency?

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


Smooth muscle in 3 layers arranged in multiple dimensions
which evevntually become three distinct layers at the bladder's
neck. Innermost is the involuntary sphincter.
Diagram shows volume of ICF and ECF in the body. Osmolarity
should be equal between ICF and ECF. Normovolemia is 42
liters total with 28L in the ICF. See Attachment 1 and walk
through the diagram.
ICF decreased, ECF increased, osm increased. Technically
volume contraction and hypotonic but water more contracted
that solute.
No change in ICF, ECF decreased, no change in osm.
Essenitally volume and solute contraction but equal contraction.
ICF increased, ECF decreased, Osm decreased. Volume and
solute contracted because not holding onto water and salt

What are the clinical


implications of Infusion of
isotonic NaCl?
What are the clinical
implications of high NaCl
intake?
What are the clinical
implications of SIADH?

ICF unchanged, ECF increased, osm unchanged. Giving


increasing amounts of fluid and solute so volume expansion.

What is Renal Clearance?

ICF decreased, ECF increased, osm increased. Volume


expansion but solute pulls water into ECF
ICF increased, ECF increased, osm decreased. Holding onto
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
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


GFR?
How are Creatinine Clearance
and GFR related?

Inulin can be used because it is freely filtered and neither


reabsorbed nor secreted. GFR=Uinulin *V/Pinulin = Cinulin
Creatinine Clearance is an approximate measure of GFR.
Slightly overestimates GFR because there is moderate secretion
of creatinine by the renal tubules.

What is the Clearance ratio


(with Inulin)?

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


that clearance is less than inulin so either not filtered or filtered
and reabsorbed. >1 means that clearance is more than inulin
so filtered and excreted/activelly pumped.

What forms the Glomerular


Filtration Barrier?
How can you estimate
Effective Renal Plasma Flow
(ERPF)?

Fenestrated capillary endothelium. Glomerular basement


membrane-composed of type IV and V collagen, laminin,
heparan sulfate. Three layers-Lamina rara interna, lamina
densa and lamina rara externa. Epithelial layer consists of
podocytes which help form a barrier.
Estimate using PAH clearance because it's filtered and actively
secreted in the proximal tubule-thus all PAH is excreted.
ERPF=UPAH *V/PPAH = CPAH

How do you estimate Renal


Blood Flow?

What is Dopamine's effect on


the nephron?

RBF=RPF/(1-Hct). Note that ERPF underestimates RPF by


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
tubule in response to an increase in BP resulting in decreased
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?
How does constriction of the
ureter affect RPF, GFR and
Filtration Fraction?

No change in RPF, increased GFR and increased filtration fraction

No change in RPF, decreased GFR, decreased filtration fraction

Describe autoregulation of
blood flow in the kidneys

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
sensed by the macula densa. This results in constriction of the
afferent arteriole, attenuating RBF.

What is Filtration Fraction?

Fraction of plasma filtered across the membrane of the


glomerular capillaries. FF=GFR/RPF. Normal FF is about 20%

What is Filtered Load?


What is Free Water Clearance?
Where does free water
clearance occur?
How does ADH affect Ch2o?
How can you calculate
Excretion rate?
How can you calculate
Reabsorption?
How can you calculate
Secretion?

How is glucose reabsorbed


and how does it go wrong?

How are amino acids cleared?


What is Hartnup's Disease?

Define the Nephron.


How do tubules of the nephron
maintain low intracellular Na
and the Na gradient across the
tube?

GFR * Plasma concentration.


Ability to dilute urine. Free water (Ch2o)= V-Cosm
(Cosm=Uosm*V/Posm)
Thick ascending limb and early distal tubule. NaCl is
reabsorbed without reabsorption/permeability to H2O.
ADH causes retention of free water so Ch2o<0. Concentrated
urine
Excretion rate= V*Ux
Reabsorption=Filtered-Excreted
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
overwhelmed. At 350 mg/dL, all transporters are fully
saturated so clinical glucosuria develops
Shouldn't be cleared. Na dependent transporters in the
proximal tubules reabsorb amino acids with multiple carrier
systems.
Deficiency of neutral amino acid (tryptophan) transporter.
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
urine.

Na/K ATPase on the basolateral membrane maintains the Na


gradient from the lumen to the cell.

Describe transport across the


luminal and basolateral side of
the Proximal Tubule (see
attachment 2).
How is bicarb
regulated/excreted in the
Proximal tubule?
How do Angiotensin II and
Atrial Natriuretic Peptide act
on the Proximal tubule?
How does Parathyroid
hormone affect
excretion/absorption?

Describe transport across the


Loop of Henle.

Describe transport across the


distal convoluted tubule.
Describe transport across the
late distal tubule and
collecting ducts.
How does Aldosterone affect
the collecting ducts?
How does ADH affect the
collecting tubules?

The proximal tubule is the major site of reabsorption, based on


the transmembrane Na gradient. Reabsorbs all filtered glucose
and amino acids via cotransport with Na. Reabsorbs most
bicarb, sodium, chloride and water. Isotonic absorption.
Generates and secretes ammonia which buffers secreted H. Na
and H are exchanged, Cl is absorbed in exchange for bicarb.
CO2 and H2O cross the membrane and are made into bicarb by
carbonic anhydrase. That is excreted and then made into CO2
and H2O again.

Ang II stimulates Na reabsorption which ANP blocks Na


reabsorption.
PTH inhibits Na/Phosphate cotransport resulting in phosphate
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
into the lumen creating a positive charge in the lumen. It's
impermeable to H2O so it dilutes urine.
Impermeable to water and urea. Early distal tubule actively
reabsorbs Na and Cl making urine hypotonic. PTH increases
Ca/Na exchange thus increasing Ca absorption.
Principle cells reabsorb Na and H2O and secrete K via the Na/K
ATPase. Intercalated cells secrete H and reabsorb K and HCO3.
Inserts more Na channels on the luminal side increasing Na
reabsorption.
Acts at V2 receptors and inserts aquaporins H2O channels into
the luminal side.

What is the Vasa Recta?

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
absorption.

What does it mean if Tubular


Fluid (TF)/Plasma (P) >1?

Solute is being reabsorbed more slowly than water or there is


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 arteriolesincreased FF to maintain GFR in low volume states. Increases
proximal tubule Na/H activity and can stimulate thirst in the
hypothalamus.
Released from the atria in response to low volume. Relaxes
vascular smooth muscle via cGMP resulting in increased GFR
and decreased renin.

What is the function of


Angiotensin II?

What is the function of ANP?

What is the function of ADH?

What is the function of


Aldosterone?

What is Erythropoietin?
What is 1, 25-(OH)2 Vitamin
D?

Regulates osmolarity and responds to low blood volume which


takes precedence over osmolarity. Increases H2O channel
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
Na gradient for Na and H2O reabsorption. Primarily regulates
blood volume.
Glycoprotein hormone that stimulates RBC production in
response to hypoxia. Released from endothelial cells of
peritubular capillaries. Epo receptors are on proerythroblasts
which mature in response.
Active Vitamin D. Proximal tubule cells convert 25-OH-Vitamin
D to the dihydroxy form. This increases intestinal reabsorption
of both calcium and phosphate.

What do prostaglandins do in
the kidney?

PTH directly acts on the kidney to increase renal calcium


reabsorption and decrease renal phosphate excretion. Also
stimulates proximal tubule cells to make 1, 25
dihydroxycholicalciferol.
Secreted by JG cells in response to increased renal arterial
pressure and increased renal sympathetic discharge (Beta 1
effect). Stimulates Angiotensin
Paracrine secretion of PGE2 vasodilates the afferent arterioles to
increase GFR. NSAIDs can cause acute renal failure by
inhibiting PGE thus preventing the arterioles to vasodilate to
maintain GFR.

Where do each of the above


hormones act on the kidney?
(this rehashes all the functions
as well)

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
aquaporins. Acts on collecting ducts. Aldosterone is secreted
in response to decreased blood volume and increased plasma K,
resulting in increased Na reabsorption and increased Kand H
secretion. Acts on collecting duct.

What causes K shift out of


cells?

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


antagonists (decreased Na/K ATPase), Acidosis or severe
exercise (K/H exchange), Hyperosmolarity, Digitalis (blocks
Na/K ATPase), Cell lysis

How does Parathyroid


Hormone affect the kidney's
endocrine function?

What is Renin?

What causes K shift into cells?

Insulin (increased Na/K ATPase), Beta Adrenergic agonists


(increased Na/K ATPase), Alkalosis (K/H exchanger), Hypoosmolarity.

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.
PCO2=1.5 (HCO3) +8 (+/-2)

What is Winter's Formula?


How much should PCO2
increase when bicarb
increases?
What is respiratory acidosis?

PCO2 increases 0.7 mmHg for every 1 mEq/L HCO3


Increased PCO2. Compensation with increased bicarb
absorption

What is respiratory alkalosis?

Decreased PCO2. Compensate with less bicarb reabsorption.

What are some causes of


Respiratory Acidosis?

Hypoventilation-Airway obstruction, acute lung disease, chronic


lung disease, opiods/narcotics, weak respiratory muscles.
MUDPILES-Methanol, Uremia, Diabetic Ketoacidosis,
Paraldehyde or Phenformin, Iron tablets or INH, Lactic Acidosis,
Ethylene glycol, Salicylates

What are some causes of


Anion Gap Metabolic Acidosis?
What are some causes of nonAnion Gap Metabolic Acidosis?
What are some causes of
Respiratory Alkalosis?
What are some causes of
Metabolic Alkalosis?

Diarrhea, Glue sniffing, Renal Tubular Acidosis, Hyperchloremia


Hyperventilation-(early) high altitude exposure, Aspirin
ingestion (early)
Diuretic use, vomiting, antacid use, hyperaldosteronism.

What is Type 1 (Distal) Renal


Tubular Acidosis?

Defect in the collecting tubule's ability to excrete H. Associated


with hypokalemia and risk for Ca containing kidney stones.

What is Type 2 (proximal)


Renal Tubular Acidosis?

Defect in proximal tubule HCO3 reabsorption. Associated with


hypokalemia and hypophosphatemic rickets.

What is Type 4 (hyperkalemic)


Renal Tubular Acidosis?

How does Aldosterone act on


the Late Distal Tubule?
How do you calculate the
anion gap?

Why does an anion gap occur?

What is a delta delta?


How do you calculate a delta
delta?
How do you interpret a delta
delta?
How much should CO2 rise in
response to increased bicarb?

What are the general functions


of the Kidneys?

Hyperaldosteronism or lack of collecting tubule response to


aldosterone causes hyperkalemia- inhibition of ammonia
excretion in proximal tubule. Leads to decreased urine pH due
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
stimulated alpha-intercalated cells to secrete more H, thus
regulating plasma HCO3 and acid-base balance.
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
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
disorder.
Change in anion gap = AG-12. Change in Bicarb = 24measured HCO3. Delta delta is ratio of the two
AG>HCO3 - Metabolic alkalosis + metabolic acidosis.
AG<HCO3 -Wide AG + non AG metabolic acidosis. Equal-wide
anion gap metabolic acidosis.
For every 10 mmol/L rise in HCO3, PCO2 should increase
6mmHg
Excretes harmful waste (urea, creatinine, uric acid, etc.),
Maintains acid-base homeostasis, Reabsorbs essential
substances, Regulates water and sodium metabolism, Maintains
vascular tone, Produces erythropoeitin, Maintains calcium
homeostasis.

What is hematuria and what


are some common causes?
What is Proteinuria?
What are diagnostic tests for
proteinuria?
What is Functional Proteinuria?
What is Orthostatic
Proteinuria?

What is Overflow proteinuria?

What is Serum BUN?


What does serum BUN depend
on?

What are some causes of


increased BUN?

What are some causes of


decreased BUN?

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
related causes-anticoagulants, cyclophosphamide (hemorrhagic
cystitis and risk for transitional cell carcinoma)
Protein >150 mg/24 hours or >30 mg/dL via dipstick.
Dipstick-detects albumin only. Sulfosalicylic acid-detects
albumin and globulins.
Protein <2g/24 hour, not associated with renal disease. Causes
are fever, exercise, CHF.
Postural-only occurs when standing. First void in the morning
has no protein but subsequent during the day does have
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
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
tubule (amount reabsorbed is flow dependent).
GFR, protein content of the diet, proximal tubule reabsorption
and the functional status of the urea cycle.
Decreased cardiac output (decreased GFR), increased protein
intake/breakdown, increased tissue catabolism (burns, surgery,
etc), acute glomerulonephritis, acute or chronic renal failure,
postrenal disease.
Increased plasma volume (pregnancy, SIADH, etc), decreased
urea synthesis (cirrhosis, Reye syndrome, fulminant liver
failure), decreased protein intake (Kwashiorkor, starvation
gluconeogenesis in kideys)

What is Prerenal Azotemia and


what are some causes?

Metabolic end product of creatine in muscle. Filtered in the


kidneys and not reabsorbed or secreted. Serum concentration
varies with age and muscle mass.
Increased serum BUN and creatinine
15. Urea is filtered and partly reabsorbed whereas Creatinine is
filtered entirely. BUN:Cr ratio depends on changes-can be
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
>15 because proportionately more Urea is reabsorbed from the
low flow rate.

What is Renal Azotemia and


what are some causes?

Increased BUN and Cr from parenchymal damage to the


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

What is Serum Creatinine?


What is Azotemia?
What is a normal Serum BUN:
Creatinine ratio?

What is Postrenal Azotemia


and what are some causes?
What is a normal Cr
Clearance?

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
decreases GFR resulting in back diffusion of urea (not Cr) into
blood and a disproportionate increase in BUN.
97-137 mL/minute. Less than 100 mL/minute is abnormal.

What are some causes of


decreased CR Clearance?

Normal pregnancy (Increased plasma volume means increased


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

What does dark yellow color


indicate in Urinalysis?

Concentrated urine, Bilirubinemia, Increased UBG, Vitamins

What does Red or Pink color


indicate in Urinalysis?

Hematuria, hemoglobinuria, myoglobinurua, drugs


(phenazopyridine), porphyria

What are some causes of


increased Cr Clearance?

What does smoky-colored


urine indicate?

Acid pH converts Hb to hematin. Common in nephritic


glomerulonephritis

What does black urine after


exposure to light indicate?

Alkaptonuria. Deficiency of homogentisate oxidase resulting in


buildup of homogentisic acid

What does clarity of the urine


indicate?

Cloudy urine with alkaline pH is normal, probably from


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

What does the specific gravity


of the urine indicate?

What does the pH of the urine


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

What does Urobilinogen


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

Urine concentration and dilution. SG>1.023 indicates urine


concentration and excludes intrinsic renal disease. Hypotonic
<1.015. Fixed SG (1.008-1.010) may indicate a lack of
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
plus strong ammonia smell indicates a urease producing
pathogen.
Increased serum glucose means glucosuria and DM. Normal
serum glucose and glucosuria can happen in normal pregnancy,
benign glucosuria
First sign of diabetic nephropathy
Acetone and acetoacetic acid. Ketonuria from DKA, starvation,
ketogenic diets, pregnancy and isopropyl alcohol poisoning
Bilirubinuria may indicate hepatitis or obstructive jaundice
Trace amounts are normal. No UBG with increased urine
bilirubin may be obstructive jaundice. Increased UBG with
absent urine bilirubin means extravascular hemolytic anemia.
Increased UBG with increased urine bilirubin means hepatitis
Hematuria from renal stone, hemoglobinuria from intravascular
hemolytic anemia, myoglobinuria from increased serum creatine
kinase and crush injuries.
Nitrites produced by nitrate reducing uropathogens.

What does Leukocyte Esterase


in the urine indicate?

Esterase in neutrophiles (pyuria). Infections from urethritis,


cystitis, pyelonephritis. Sterile pyuria-Chalmydia trachomatis
urethritis, TB, drug induced interstitial nephritis

What is a renal tubular cast?

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


glomerulonephritis. Dysmorphic RBC's-hematuria of glomerular
origin. Neutrophils-pyuria from UTI or sterile pyuria. Oval fat
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
protein leaking through the glomeruli. Proves renal origin of
the disease.
Acellular, ghost like cast containing protein. Only significant if
there is accompanying proteinuria
Nepritic type of glomerulonephritis resulting in a cast made of
RBC's
Cast of WBC's indicating acute pyelonephritis, acute
tubulointerstitial nephritis
Cast of a sloughed off renal tubule. Indicates acute tubular
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 crystalshyperuricemia from gout or massive cell destruction after
chemotherapy. Triple phosphate crystals-sign of UTI from
urease producing pathogens like Proteus. Cystine crystalshexagonal 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
controlled by renal-derived PGE2 and renin. Efferent blood flow
is controlled by ATH (vasoconstrictor)

What do cells in the urine


indicate?

What do casts indicate in the


urine?
What is a hyaline cast?
What is a RBC Cast?
What is a WBC cast?

What types of crystals can be


seen in the urine and what do
they indicate?

Describe the blood supply to


the kidney.

What is minimal change


disease?
What protein produces the
charge on the glomerular
basement membrane?

Loss of charge of the glomerular basement membrane which


produces selective proteinuria.

What do Visceral Epithelial


Cells do in the glomerulus?

Heparan Sulfate
Deposition of immunocomplexes such as in membranous
glomerulopathy. Increased synthesis of Type IV Collagen such
as in DM.
Production of the GBM. Contain podocytes and slit pores
between podocytes which serve as a distal barrier to prevent
protein loss in the urine. Podocytes fuse in nephrotic
syndrome, no matter what the cause.

What do Mesangial Cells do in


the glomerulus?

Support the glomerular capillary. Can release inflammatory


mediators and proliferate-IgA glomerulopathy has mesangial
immune complex deposits.

What do parietal epithelial


cells do in the glomerulus?

Lining cells of Bowman's capsule. Proliferation causes crescents


that encroach upon and destroy the glomerulus.

What are some causes of GBM


thickening?

What is Juvenile Polycystic


Kidney Disease?

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
flank mass. May lead to chronic renal failure.
AR disease. Bilateral cystic disease with cysts involving all
parts of the nephron in the cortex and medulla. Bilaterally
palpable kidneys.

What other types of conditions


are seen in Juvenile Polycystic
Kidney Disease?

Cysts present in liver. Associated with congenital hepatic


fibrosis which leads to portal hypertension. Also associated
with oligohydramnios and Potter's Syndrome.

What is Adult Polycystic


Kidney Disease?

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


the cysts involving all parts of the cortex and medulla. Develop
chronic renal failure a lot of the time.

What is Renal Dysplasia?

What other conditions are


associated with Adult PKD?

What is Medullary Sponge


Disease?
What is Acquired Polycystic
Kidney Disease?

What are simple retention


cysts?
What is Focal
Glomerulonephritis?
What is Diffuse
Glomerulonephritis?
What is Proliferative
Glomerulonephritis?
What is Membranous
Glomerulonephropathy?
What is Membranoproliferative
Glomerulonephritis?
What is Focal Segmental
Glomerulosclerosis?
What is Crescentic
Glomerulonephritis?
What is Primary Glomerular
Disease?
What is Secondary Glomerular
Disease?

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,
hematuria, mitral valve prolapse, and risk for developing renal
cell carcinoma.
Multiple cysts in the collecting ducts present in the medulla.
See striations in the papillary ducts of the medulla (swiss
cheese appearance). Recurrent UTI's, hematuria and renal
stones.
Most commonly caused by renal dialysis. Tubules become
obstructed by interstitial fibrosis or oxalate crystals. Small risk
for renal cell carcinoma.
Most common adult renal cyst. Derived from tubular
obstruction. May cause hematuria and may resemble renal cell
carcinoma. Needle aspiration will distinguish it from RCC
Only a few glomeruli are abnormal
All glomeruli are abnormal
>100 nuclei in affected glomeruli
Thick GBM, no proliferative change

Thick GBM, hypercellular glomeruli


Fibrosis involving only a segment of the involved glomerulus
Proliferation of the parietal cells around the glomerulus (in
Bowman's Space, thus forming a crescent)
Involves only glomeruli and no other target organs. Essentially
something like minimal change disease.
Involves glomeruli and other organs, e.g. SLE

Look at Golijan page 400 and


go through all the histology
What does a Linear pattern
indicate on
Immunofluorescence?
What does a Granular or
Lumpy Bumpy appearance
indicate on
Immunofluorescence?

What do immune complexes


look like on Electron
Microscopy?

Ya, definitely do that :-)


Antibodies line upagainst evenly distributed antigens in the
GBM. Think Goodpasture's Syndrome

Think immunocomplex deposits in the glomerulus forming


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
has passed through the GBM but is stuck in the podocytes.
Intramembranous is within the GBM and Mesangial is within the
mesangium.

How does Type III Immune


complex disease cause
glomerular disease?
How does something like
Goodpasture's Disease cause
glomerular damage?

Circulate and deposit in glomeruli or develop in situ. Immune


complexes then activate complement, procude C5a which is
chemotactic to neutrophils which attack the GBM.

How does T Cell production of


cytokines damage the GBM?
What are clinical
manifestations of glomerular
disease?

Cytokines cause the GBM to lose its negative charge. Cytokines


also damage podocytes causing them to fuse.

Describe the pathophysiology


of Nephritic Syndrome?

Anti GBM antibodies attack the glomerular basement membrane

Nephritic syndrome, nephrotic syndrome and chronic


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
sediment, especially if immune complex. RBC casts are a key
finding, and occasionally there are WBC casts.

What are some lab findings in


Nephritic syndrome?

What is IgA Nephropathy


(Berger's Disease)?
What does Berger's disease
often immitate?
What happens after a URI in
Berger's disease?

Proteinuria>150mg/day but less than 3.5 g/day. Azotemia with


BUN:Cr ratio >15 because tubular function is intact in acute
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
deposits with granular immunofluorescence. IC's activate the
alternative complement pathway.

What is Post-Streptococcal
Glomerulonephritis?

Henoch Schonlein Purpura


Episodic hematuria and hypertension following URI because of
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
pathway. See a diffuse proliferative pattern with neutrophilic
infiltrate.

How does Post-Streptococcal


Glomerulonephritis present?

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


nephritogenic strain (never produces rheumatic fever). Causes
periorbital edema from sodium retention not hypoalbuminemia,
transient, sometimes severe hypertension.

What lab tests are indicative of


Post-Strep
Glomerulonephritis?

Increased DNAase B titers. ASO is degraded by oil in the skin


and is thus not increased. Streptozyme test is positive (antiDNAase B, ASO, anti-AH and anti-NAD antibodies).

What is Diffuse Proliferative


Glomerulonephritis?

Most common type of glomerular disease in SLE.


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

What does the serum ANA test


look like in Diffuse Proliferative
Glomerulonephritis?

Serum ANA has a rim pattern, corresponding to the presence of


anti-ds DNA antibodies

How do you treat Diffuse


Proliferative
Glomerulonephritis?

What is Rapidly progressive


Crescentic Glomerulonephritis?

Corticosteroids and Cyclophosphamide


Clinical syndrome that may be either primary or secondary
disease. See a rapid loss of renal function that progresses to
acute renal failure within weeks. May or may not be associated
with crescent formation.

Which diseases are associated


with Rapidly Progressive
Crescentic Glomerulonephritis?

Goodpasture's syndrome, microscopic polyarteritis (p-ANCA),


Wegener's granulomatosis (c-ANCA)

What HLA type is common in


Goodpasture's syndrome?

80% are HLA-BR2 positive

How do you treat


Goodpasture's syndrome?

What is Nephrotic Syndrome?

What are the key findings in


nephrotic syndrome?
What type f kidney disease
does Diabetic Glomerulopathy
cause?

Plasma exchange to remove antibodies, immunosuppressive


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
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
loss). Hypogammaglobulinemia from protein loss. Fatty casts
with maltese crosses and oval fat bodies.
Nephrotic syndrome with Nodular Glomerulosclerosis
(Kimmelstiel-Wilson disease). Risk factors are poor glycemic
control, hypertension and high correlation with coexisting
diabetic retinopathy.

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

Nonenzymatic glycosylation of the GBM, also affecting the


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

What lab values are significant


in Diabetic Glomerulopathy?

Microalbuminuria

What is the pathogenesis of


Diabetic Glomerulopathy?

Are there any other diseases


of the kidney associated with
Diabetic Glomerulopathy?

What is Alport's Syndrome?

Renal papillary necrosis and acute or chronic pyelonephritis


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

What is Thin Basement


Membrane Disease?

Benign familial hematuria. AD disorder with extremely thin


basement membranes in the setting of normal renal functin.
See mild proteinuria and persistent microscopic hematuria

What is renal amyloidosis?

What are the common causes


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

What is ischemic Acute


Tubular Necrosis?

What segments of the nephron


are damaged in ischemic ATN?

What is Nephrotoxic Acute


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

What is Acute Renal Failure?

Rapidly progressive glomerulonephritis, focal segmental


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

Shrunken kidenys with glomerular sclerosis and tubular atrophy

Most often caused by prerenal azotemia due to hypovolemia.


Ischemia damages endothelial cells decreasing vasodilators and
increasing vasoconstrictors, thus worsening the situation and
further decreasing GFR. Ischemia also damages tubular cells
which then detach into the lumen, cause obstruction and
produce pigmented renal tubular cell casts. The casts further
obstruct the lumen increasing tubular pressure, decreasing GFR
and pushing fluid into the interstitium resulting in oliguria.
Straight segment of the Proximal tubule (part of the degree
most susceptible to hypoxia), Medullary segment of the thick
ascending limb (location of the NK2C transporter), and the
Tubular basement membrane (interferes with renal tubular cell
regeneration)
ATN from nephrotoxic substances. Aminoglycosides are most
common, radiocontrast agents and heavy metal poisoning are
also causes. Most commonly see oliguria, occasionally polyuria.
This primarily damages proximal tubule while the tubular
basement membrane is intact. Also see pigmented renal
tubular cell casts, hyperkalemia and anion gap metabolic
acidosis, increased BUN and Cr with ratio of BUN:Cr <15. Often
have issues with hypokalemia in the diuresis phase.
10% of ICU patients, 40% iatrogenic, 20% of patients with
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
ATN.

What are some causes of


Acute Renal Failure?
What is RPGN?

Postrenal obstruction, vascular disease (malignant htn), RPGN,


drugs, DIC, urate nephropathy.
Rapidly progressive glomerular nephritis

What are common causes of


acute pyelonephritis?

Treat prerenal azotemia-volume expansion if hypovolemic to


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

How does vesicoureteral reflux


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

Intravesical portion of the ureter is not compressed during


micturition so urine refluxes up. Causes ascending infection
into the renal pelvis and parenchyma.
Urine output <400 mL/day or less than 20 mL/hr.
Prerenal azotemia, acute glomerulonephritis, acute tubular
necrosis/renal azotemia, and postural azotemia.
Urine osm <350 mOsm/kg indicates poor concentrating ability
and thus tubular dysfunction

How do you treat Acute Renal


Failure?

What is Tubulointerstitial
Nephritis?

How do you calculate a FENa?


What does a FENa less than
1% indicate?
What does a FENa greater
than 2% indicate?

FENa = (Una * PCr)/(PNa * Ucr) *100


Sodium filtration closely mimics creatinine filtration. FENa less
than 1% means good tubular function
Tubular dysfunction. Good predictor of ATN

What can UNa tell you about


tubular function?

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


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

How do you distinguish


postrenal azotemia from ATN?

ATN usually presents with pigmented tubular casts. In


postrenal azotemia, the sediment is usually normal.

What should you suspect if


there is staph a. cultured in
the urine?
What are gross and
microscopic findings in
pyelonephritis?

Hematogenous spread of the infection to the kidneys.


Grayish white areas of abscess formation in the cortex and
medulla. Microabscesses form in the tubular lumens and
interstitium.

What are the clinical and lab


findings in pyelonephritis?
What are complications of
Acute Pyelonephritis?

Clinical-spiking fever, flank pain, frequency and dysuria. LabWBC casts, pyuria, bacteruria, hematuria
Chronic Pyelonephritis, Perinephric Abscess, Renal Papillary
necrosis, septicemia with endotoxic shock

What are pathological findings


in Chroninc Pyelonephritis?
What pathological findings are
seen in obstructive Chronic
Pyelonephritis?

U shaped cortical scars overlying a blunt calyx, visible on IV


pyelogram.

What are microscopic findings


of Chronic Pyelonephritis?

Uniform dilation of the calyces and diffuse thinning of cortical


tissue.
Chromic inflammation with scarring of the glomeruli. Tubular
atrophy-tubules contain eosinophilic material resembling thyroid
tissue (thyroidization)

What can reflux nephropathy


cause in children?

Hypertension

What drugs are associated


with acute drug induced ATN?

What is the pathogenesis of


Drug induced ATN?

Penicillin esp. methicillin. Rifampin, sulfonamides, NSAIDs,


diuretics
Combination of Type I and IV hypersensitivity. Abrupt onset of
fever, oliguria and rash that resolves with withdrawal of the
drug. Causes tubular disease with a BUN:Cr <15, eosinophilia
and eosinophiluria

What is Analgesic Nephritis?

Chronic drug induced Tubulointerstitial nephritis. Chronic use of


Acetominophen with Aspirin because Acetominophen causes
free radical damage while aspirin inhibits renal synthesis of
PGE2 leaving AT II unopposed.

What is Urate Nephropathy?


How does lead poisoning
cause Urate Nephropathy?

Renal papillary necrosis-sloughing of renal papillae producing


gross hematuria, proteinuria and colicky flank pain. Ring defect
where papillae used to reside. Hypertension, CRF and Renal
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
chemo), lead poisoning or gout.
Decreased excretion of uric acid from the lead. Also direct toxic
effects cause TIN

What is seen microscopically


in Urate Nephropathy resulting
from lead poisoning?

Nuclear acid-fast inclusions in the proximal tubule

What are complications of


Analgesic Nephritis?

How does Multiple Myeloma


cause renal disease?
What are hematologic findings
in Chronic Renal Failure?

What is Renal Osteodystrophy?

What are some complications


of Renal Osteodystrophy?

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
may be converted to amyloid and cause primary amyloidosis
resulting in nephrotic syndrome.
Normocytic anemia with low corrected reticulocyte count. Due
to decreased Erythropoietin production. Also see qualitative
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
cysts caused brown discoloration.
Osteomalacia from decreased mineralization of the osteoid.
Osteoporosis from loss of organic bone mass and minerals
(often due to chronic metabolic acidosis because excess H is
buffered by bone minerals).

What are some cardiovascular


findings in Chronic Renal
Failure?
What are some other clinical
consequences of Chronic Renal
Failure?

Hypertension from salt retention, hemorrhagic fibrinous


pericarditis, CHF and accelerated atherosclerosis.
Hemorrhagic gastritis and uremic frost (urea crystals deposit on
the skin). Also hyperkalemia and anion-gap metabolic acidosis.

Why does renal failure cause


hypocalcemia?

Hypovitaminosis D from decreased 1-Alpha Hydroxylase and


thus decreased reabsorption of calcium from the small
intestines. Also hyperphosphatemia from decreased renal
excretion drives calcium into bone and soft tissue.

Why is there increased Serum


Cystatin C?
What is seen on urinalysis in
Chronic Kidney Failure?

Cystatin in a Cysteine protease inhibitor produces by the


nucleus of all cells. It should be filtered by the glomerulus but
not secreted so it's a good marker of renal function.
Fixed specific gravity because no concentrating ability, free
water clearance is 0, waxy/broad casts are present.

Why do you give ACE


inhibitors in kidney disease?

What is benign
nephrosclerosis?

What is Malignany
Hypertension?

What microscopic changes are


seen in Malignant
Hypertension?
What are clinical findings in
Malignant Hypertension?

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
sclerosis. See small kidneys with a finely granular cortical
surface.
Sudden onset of accelerated hypertension with end organ
damage. Risk factors are pre-existing BNS, Hemolytic Uremic
syndrome, thrombotic thrombocytopenic purpura and systemic
sclerosis
Fibrinoid necrosis and necrotizing arteriolotis and glomerulitis
with pinpoint hemorrhages on the cortical surface. Also
hyperplastic arteriolosclerosis (onion skin lesions) with smooth
muscle hyperplasia and reduplication of the basement
membrane.
Hypertensive encephalopathy-cerebral edema, papilledema,
retinopathy with flame hemorhages and potential for an
intracerebral bleed.

What causes Renal infarction?


What is the gross and
microscopic appearance of a
renal infarction?

What is Diffuse cortical


necrosis?
What are some causes of
Hydronephrosis?
What are some clinical
findings of hydronephrosis?

What causes Urolithiasis?

What is a calcium stone?


What is a Magnesium
Ammonium Phosphate stone?
How do you treat a calcium
stone?
How do you treat a Uric Acid
stone?
How do you treat a struvite
stone?

Embolization from thrombi in the left heart, atheroembolic renal


disease, vasculitis especially polyarteritis nodosa.
Irregular wedge-shaped pale infarct in the renal cortex. Old
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
capillaries and bilateral, diffuse, pale infarcts of the renal
cortex. See anuria in a pregnant woman followed by ARF.
Renal stones, retroperitoneal fibrosis, cervical cancer and BPH
Compression atrophy of the renal medulla and cortex and
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
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
acidosis.
Struvite stone causing a Staghorn calculus. Associated with
urease producing bugs. Urine is alkaline and smells like
ammonia.
Most pass. Can give hydrochlorothiazide which increases renal
tubule reabsorption of calcium. Cellulose phosphate binds
calcium in the intestine.
Allopurinol, increase urinary pH to make the stone soluble.
Cotreat chemo patients with allopurinol to prevent urate
nephropathy.
Surgical removal because of size. Antibiotic to eliminate urease
producer.

What is an Angiomyolipoma?
What are risks for Renal Cell
Carcinoma?

Hamartoma composed of blood vessels, smooth muscle and


adipose cells. Associated with tuberous sclerosis causing
mental retardation and multisystem hamartomas.

What is Von Hippel Lindau


disease?

Smoking, Von Hippel-Lindau, Adult PKD, obesity, asbestos and


lead exposure, and gasoline or petroleum product exposure.
AD disease with defect on chr 3. Increased VEGF causes
hemangiobalstomas of the cerebellum and retina and bilateral
renal cell carcinomas.

What are some gross and


microscopic findings in Clear
Cell renal carcinoma?

Upper pole mass with cysts and hemorrhage composed of clear


cells that contain lipids and glycogen. Tendency for renal vein
invasion and invasion into the IVC and right heart.

What are clinical signs of clear


cell renal carcinoma?
What hormonal changes are
seen in renal clear cell
carcinoma?

What is Renal Pelvic Cancer?

What is a Wilm's Tumor?


Where do Wilm's tumors come
from?
How does a Wilm's tumor
present?

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


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

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