CPR II - First Aid Flashcards
A 62 year old male comes to see you complaining of dyspnea. Labs show that his PAO2 (alveolar) is 30mmHg greater than his PaO2 (arterial). What portions of this patient’s respiratory system does not contribute to this lab value?
The large airways (nose, pharynx, trachea, bronchi, bronchioles and terminal bronchioles) do not participate in gas exchange and are considered anatomic dead space. Only the respiratory bronchioles, alveolar ducts and alveoli participate in gas exchange.
You are examining histological sections of the respiratory tract of a patient and get the three sections back as seen below. How can you tell where you are at in the respiratory tract by the characteristics seen in these images?
The top image is a section from a main bronchus. Note the presence of cartilage. You would see PCC and goblet cells in a more high power view. The middle image is from a bronchiole. Note the discrete amount of smooth muscle and absence of cartilage. In a more high power view you would see PCC, Clara cells and an absence of goblet cells. The bottom image is from a respiratory bronchiole. Note the absence of cilia, presence of cuboidal cells, simple squamous epithelium and dust cells (alveolar macrophages).
A 59 year old male with a history of smoking comes to see you in your clinic complaining of shortness of breath. His FEV1 is 50% the expected value and FVC is 70% the expected value. You do a chest x-ray to make sure the patient does not have lung cancer, and he does not. You determine that he may have emphysema. At what point during his respiratory cycle is he most likely to have alveolar collapse?
Collapsing pressure = 2(surface tension)/radius. As the radius decreases and surface tension increases the tendency to collapses becomes greater. During the respiratory cycle, the radius decreases during expiration. Thus, this patient will have most alveolar collapse during expiration.
An expecting mother feels like she is going into labor early. She rushes to the hospital and the doctor wants to run a test to make sure the baby’s lungs are developed enough to be able to breath after birth. What is he testing for and what makes the newborn have difficulty breathing if this test comes back abnormal? At how many weeks gestation will this test likely come back as normal?
L (lecithin) : S (sphingomyelin) ratio >2.0. Lecithin is the main component of lung surfactant and will be at increased levels when the fetal lungs are mature (usually week 35). Surfactant production usually begins around week 26. A insufficient amount of surfactant will increase surface tension in the alveoli. Our collapsing pressure equation of 2(surface tension)/radius tells us that as surface tension increases the alveoli will be more likely to collapse.
A 44 year old female comes to the ED with fever, chills, sweats, dyspnea and pleuritic chest pain. Her WBC is elevated and she is admitted to the hospital for treatment of pneumonia. A few hours later you go to check on her and she can hardly breath at all. You determine that she has acute respiratory distress syndrome (ARDS). The activity of what cell will largely determine if this patient recovers or will suffer from restrictive lung disease for the rest of her life?
Type 2 pneumocyte. These not only secrete surfactant in the alveoli, they are also the stem cells of the alveoli that proliferate when the lungs are damaged.
What cells line the majority of the alveolar spaces?
Type 1 pneumoctyes. Theses are simple squamous epithelial cells that allow for optimal gas diffusion in these spaces.
What cells found in the termnial bronchioles are nonciliated, columnar cells that secrete a component of surfactant and degrade toxins?
Clara cells
A 77 year old male presents to the ED with increasing dyspnea and chest pain after a long plane ride. History reveals current prostate cancer and DVTs. Chest x-ray reveals decreased prominence of blood vessel markings on the left lung. If this patient is currently having a pulmonary embolism, where in relation to the bronchus would you look on a CT scan? What if vascular markings were decreased on the patient’s right side?
The left pulmonary artery is being occluded in this patient. That artery runs superior to the left main bronchus. If it were the right pulmonary artery, you would look anterior to the right main bronchus.
At what level does the Vena Cava perforate the diaphragm? Esophagus and Vagus Nerve? Aorta, Thoracic Duct and Azygos Vein?
“I 8 10 eggs at 12” I=IVC @ T8. eggs = Esophagus @ T10. at = Aorta @ T12.
You are sitting on beltway waiting for traffic to move. It’s been an hour now and you are beyond frustrated. You are just staring at the car infront of you thinking of absolutely nothing. What muscles are you using to breath at this point?
At this point you would be breathing “quietly”. With quiet inspiration you use the diaphragm and expiration is passive.
You are sitting on the beltway after getting into an accident because a car cut you off. You are fuming. What muscles are you using at this point?
You would probably be doing “labored” breathing. With inspiration you would use the external intercostals, scalenes and SCM. With expiration you would use the rectus abdominis, internal/external obliques, transversus abdominis and internal intercostals.
What lung volume measurements are indicated by the different colors seen in the image below. What does each value mean?
Blue = inspiratory reserve volume (IRV: additional air you can breath in after a normal inspiration). Yellow = tidal volume (TV: air that moves into each lung with a normal quiet inspiration, usually = 500 mL). Green = expiratory reserve volume (ERV: additional air that can be expelled after a normal exhalation). Purple = residual volume (RV: air left in lung after a maximum expiration). Blue + Yellow = Inspiratory capacity (IC: max amount of air you can hold in your lungs). Green + Purple = Functional Residual Capacity (FRC: volume left in lungs after a normal inspiration). Blue + Yellow + Green = Vital Capacity (VC: maximum volume of gas you can expire after a full inspiration). Blue + Yellow + Green + Purple = Total Lung Capacity (TLC: volume present in lungs after a maximum inspiration).
What is an easy way to remember the order from top to bottom in a lung volume graph?
“LITER”: L = lung. I = IRV. T = TV. E = ERV. R = RV. Also remember that a capacity is the sum of 2 or more volumes.
A patient comes to your clinic suffering from emphysema. You want to determine the amount of physiologic dead space in his lungs from his disease. What values do you need to know in order to do this? Where would you expect to find the most dead space where there shouldn’t be dead space?
The equation for physiologic dead space is shown below. You can remember this by the pneumonic Taco, Paco, PEco, Paco (the order of the variables) Vt = tidal volume, PaCO2 = arterial PCO2, PECO2 = expired air PCO2. As far as this patient goes, most emphysema related to smoking will manifest in the upper lungs and will present as dead space.
What is the transmural pressure in the lung-chest wall system at the functional residual capacity (FRC)?
The tendency of the lungs is to collapse (pull in) and the tendency of the chest wall is to expand (pull out). At FRC, you have just quietly exhaled and the inward pull of the lung is balanced with the outward pull of the chest, making transmural pressure (the difference in pressure between the lung and chest wall) = 0 because both systems are at atmospheric pressure.
What part of our respiratory anatomy prevents us from having a pneumothorax every time we exhale?
The negative intrapleural pressure. At FRC (normal exhale) both alveolar and airway pressures = 0 and the only thing keeping that lung from collapsing is the negative intrapleural pressure.
What happens to pulmonary compliance as we age?
As we get older, we lose the elastic recoil in our lungs and the ability to get air out decreases. This increases compliance because we hold more air. This same finding exists in patients with emphysema.
What happens to pulmonary compliance with pneumonia?
Compliance decreases. The increased fluid in the alveoli puts more pressure on the alveoli and increases elastic recoil making it more difficult to hold more air. This also happens with fibrosis of the lung.
What property of hemoglobin contributes to the dissociation curve seen below?
Hemoglobin exhibits positive cooperativity and negative allostery. This means that as O2 binds to the hemoglobin subunits (2 alphas and 2 betas), hemoglobin affinity for O2 increases (300x). This is what causes the rapid ascent of the dissociation curve as pO2 increases.
You hop on the treadmill for the first time in a few months because you feel like a fat turd. You’re also a fat nerd and want to measure your blood O2% as you run. As you first start running, your O2% goes up. Excluding any lung physiology, what could contribute to this finding?
As you exercise your muscle cells work harder and produce CO2, 2,3-BPG, H+, Cl- and your temperature increases. All of these factors actually favor the T (taut) form of hemoglobin over the R (relaxed) form. This pushes the oxyhemoglobin dissociation curve to the right, causing an increase in the unloading of O2 by hemoglobin. “C-BEAT” = Cl, BPG, Acid/Altitude, Exercise, Temperature
Why do babies have hemoglobin with a higher affinity for O2 than adults?
The fetus has a different hemoglobin (2 alphas and 2 gammas) that has a lower affinity for 2,3-BPG. This results in an increased tendency for hemoglobin to exist in the R form, a higher affinity for O2 and the oxyhemoglobin curve shifts to the left.
If you are sitting quietly in church, where are the two forms of hemoglobin most likely to be found in your body?
R (relaxed) = respiratory system. T (taut) = tissues.
You are working the night shift in the ED and a patient comes to see you who is cyanotic. His O2% is 75%. Apparently he had just come from a rib eating contest and won before these symptoms began. What may be causing this patient’s O2% to be so low? How could you treat him?
Nitrites are used to cure meat, but ingestion of too many of them will cause oxidation of Fe2+ to Fe3+ in hemoglobin (forming methemoglobin). Methemoglobin does not bind O2 as readily and will cause hypoxemia. You can treat this patient by giving him methylene blue which will reduce Fe3+ back to Fe2+.
When might you consider giving a patient nitrites to save their life?
Cyanide poisoning. Cyanide disables cytochrome oxidase in the ETC. Giving the patient nitrites will convert hemoglobin to methemoglobin which will sequester cyanide and save cytochrome oxidase. You could also give the patient thiosulfate which will bind cyanide and be excreted renally.
Why should you never burn charcoal indoors?
Production of CO. Hemoglobin has a 200x greater affinity for CO than O2. Also, when carboxyhemoglobin forms, the hemoglobin dissociation curve shifts left and less oxygen is delivered to the tissues in addition to less oxygen binding to the hemoglobin.
Why does myoglobin have the dissociation curve shown below?
It is monomeric and can only bind one oxygen at a time. It lacks the cooperativity and negative allostery hemoglobin has.
A 12 year old female comes to the ED after being stung by a bee. Her airways are beginning to close and she is becoming hypoxic. What causes the amount of O2 that diffuses across the avleolar wall to decrease in this patient?
With anaphylactic shock you get bronchoconstriction and a decrease in the alveolar area. Volume of gas that diffuses = A/T * Dk(P1-P2) where A=area, T=thickness, Dk(P1-P2) = difference in partial pressures. As you can see, a decrease in area = a decrease in diffusion.
A patient comes to see you 4 weeks after having ARDS. You take is O2% and it is around 80% saturation. Why is oxygen diffusion limited in this patient?
Volume of gas that diffuses = A/T * Dk(P1-P2) where A=area, T=thickness, Dk(P1-P2) = difference in partial pressures. As you can see, an increase in wall thickness results in a decrease in diffusion across the wall.
What is the relationship between PO2 and PCO2 in the pulmonary and systemic systems?
In the pulmonary system, a decrease in PO2 and increase in PCO2 causes hypoxic vasoconstriction. In the systemic system, the same pressures cause vasodilation.
A 72 year old male with a history of emphysema comes to see you with distended neck veins, hepatomegaly and peripheral edema. What is the likely cause of these physical exam findings?
Years of hypoxia in the lung and pulmonary vasoconstriction causing increased workload on the right heart and right heart failure. This condition is called Cor Pulmonale.
A patient comes to see you in clinic complaining of increased shortness of breath over the past few years. Lab values show an A-a gradient of 35 mmHg. What is causing this patient to feel short of breath?
O2 diffusion is limited across the alveolar wall. The A-a gradient is the PAO2 (alveolar) - the PaO2 (arterial). Any value > 15 mmHg makes you worry because there is such a higher pO2 in the alveoli than in the arteries.
Why is O2 diffusion across the capillary wall slightly limited during exercise?
The flow of blood has increased and blood is at the alveolar space for a shorter period of time, allowing for less time for the gas to equilibrate between the alveoli and the blood.
A 21 year old female presents to your clinic with distended neck veins and peripheral edema. She complains of severe dyspnea when exercising. What genetic mutation may be causing her symptoms?
BMPR2 inactivating mutation. This gene normally functions to inhibit vascular smooth muscle proliferation. When mutated, smooth muscle proliferates in the pulmonary arteries and causes arteriosclerosis, medial hypertrophy and intimal fibrosis. Ultimately this will lead to right ventricular hypertrophy and heart failure (cor pulmonale).
Why are COPD, mitral stenosis, recurrent thromboemboli, autoimmune disease, left to right shunt, sleep apnea and living at a high altitude all risk factors for pulmonary hypertension?
COPD destroys lung tissue and decreases ventilation, causing pulmonary vasoconstriction. Mitral stenosis causes increased resistant to pulmonary flow and thus increased pulmonary pressure. Recurrent thromboemboli cause narrowing of vessels in the pulmonary vascular bed. Autoimmune disease causes inflammation, fibrosis, medial hypertrophy and increased pulmonary pressure. Left to right shunting of blood causes increased flow and shear stress through the pulmonary vessels which causes endothelial injury, thickening of the vessel wall in increased pulmonary pressure. Sleep apnea and high altitude living cause decreased O2 levels and pulmonary vasoconstriction.
An 80 year old male comes to see you because you suspect he is in right-sided heart failure. You send him to the cath lab and find that the pressure in his pulmonary artery is 30mmHg and the pressure in his left atrium is 10mmHg. If his cardiac output is 2L/min, what is the resistance in his pulmonary vasculature?
Pulmonary Vascular Resistance = (P(artery) - P(atrium))/CO. 10.
A 33 year old woman comes to your clinic after suffering a pulmonary embolism 3 weeks ago. Recovery is going well and you have put her on Warfarin. At the visit her INR level is 3.5. What is happening to the resistance in her blood vessels as a result of warfarin therapy?
As viscosity (n) goes down so does resistance. Note that as vessel length decreases and radius increases resistance will also decrease.
A 91 year old male comes to see you complaining of dyspnea. He has no history of smoking and you want to analyze the oxygen content in his arterial blood to see if he is hypoxic. Labs come back and PaO2 is 90 (80-100 is normal) with 95% O2 saturation in his blood. What factor is left that could cause this man to have decreased O2 content in his blood?
Decreased hemoglobin levels. The equation for O2 content = (O2 binding capacity * O2% saturation) + dissolved O2 in the blood. Dissolved O2 in the blood and O2% saturation are determined by PaO2, which was normal in this patient. That only leaves the option of decreased O2 binding capacity in this patient. Normally O2 binding capacity is 20.1 mL/dL of blood. This is because normally hemoglobin can bind 1.34mL O2 per gram of hemoglobin and a normal hemoglobin level is 15g/dL (15*1.34=20.1).
Two patients come to see you in the pulmonary clinic, one with COPD and the other with fibrotic lung disease. You decide to run a pulmonary function test on both of them to see how they are doing. In what ways will their respective tests differ?
In restrictive lung disease, TLC is decreased but there is no obstruction to flow and the FEV1:FVC ratio will remain the same. In obstructive lung disease, TLC is increased, but there is obstruction to flow and there will be a decreased FEV1:FVC ratio.
A 66 year old male comes to see you in clinic complaining of severe dyspnea. He has a 50 pack year history of smoking and a diagnosis of emphysema. If the pressures seen below are that of a normal lung, how would the pressures in this patient differ?
This patient has decreased elastic recoil in this lungs due to alveolar destruction. This creates a problem during forced expiration because the alveoli can no longer generate enough pressure to counter the positive pressure coming from the chest wall and pleural space at the EPP (equal pressure point), this causes the unsupported airways to collapse.
You are working the night shift in labor and delivery when a mother gives birth to a new child. Shortly after the delivery the child becomes cyanotic. Analysis of the child’s heart and lungs reveals no abnormalities; however, blood work reveals decreased O2 content due to decreased oxygen binding capacity. The mother reveals a family history of similar blood disorders. What would you predict the level of deoxygenated hemoglobin to be in this baby?
In thalassemia, patients have a defect in the formation of hemoglobin. This results in increased levels of deoxyhemoglobin. Cyanosis usually results when deoxyhemoglobin levels are greater than 5g/dL.
A 68 year old female comes to see you for a regular check up. She was diagnosed with CHF 6 years ago. Physical exam reveals cyanosis in the extremities. Why might you want to put this patient on iron supplementation?
Oxygen delivery to the tissues = Cardiac Output * Oxygen content of blood. She already has heart failure, so you want to maximize the oxygen content of her blood to minimize hypoxia. Oxygen content of blood is determined by hemoglobin levels, PaO2 and O2% saturation. Iron supplementation will aid in keeping hemoglobin levels up and prevent anemia.
What is the alveolar gas equation and what can it normally be approximated to?
PAO2 = alveolar O2 mmHg, PIO2 = inspired O2 mmHg, PaCO2 = arterial CO2 mmHg, R = CO2 produced/O2 consumed. This equation can normally be approximated to PAO2=150-(PaCO2/0.8).
You are preparing to deploy to the high mountains of Afghanistan and the company commander wants you to make sure individuals at high risk for hypoxia and taken care of before they leave. What medical conditions would you look for as red flags in these soldiers?
Hypoxemia from hypoventilation (sleep apnea), V/Q mismatch (asthma, emphysema), diffusion limitation (sarcoidosis, scleroderma) and right to left shunts. Hypoxia from decreased cardiac output (CHF) and decreased O2 delivery (anemia). Ischemia from decreased blood flow (arteriosclerosis, decreased venous return).
You hop on the treadmill for a nice morning jog. What is happening to the V/Q ratio in the apex of your lung at this point?
It is approaching 1. Normally it is around 3 because there is less perfusion to the apex due to gravity. However, as you begin to exercise, capillaries dilate and you get increased pulmonary blood flow (Q) to the apex.
You are working in the free clinic in downtown D.C. and are participating in a fee Tb screening for the homeless population. This includes a free chest radiograph. When looking at the radiographs of these patients, where is the most likely place you will see Tb and why?
The apex of the lung. This is a high O2 environment and M. Tb thrives in areas with high O2 content.
A patient comes into the ED and is having a severe asthma attack. The first year medical student runs to get the O2 tank because this patient’s O2 saturation is down. The attending physical tells her to not grab the O2 tank, but the EPI pen. Why did he tell her to not grab the O2 tank?
Asthma is a result of bronchoconstriction, decreasing ventilation to the lungs. This decreases the V/Q ratio and causes shunt. Giving the patient 100% O2 will not help at this point because there is airway obstruction. You first need to give the EPI so beta-2 stimulation can open the airway and increase the V/Q ratio, decreasing shunt.
A patient comes to the ED suffering from a pulmonary embolism. His O2 sats are low and the first year medical student runs to grab the EPI pen, but the attending physician tells him to grab the O2 tank instead. Why did he tell her to grab the O2 tank instead of the EPI pen?
PE caused blockade to flow, decreasing flow in the lungs. This increases the V/Q ratio and creates physiologic dead space. Further dilating the patient’s lungs will not help because they are already fully dilated. Giving the patient 100% oxygen will help improve oxygen saturation and is needed due to decreased flow.
Your med school class is really nerdy and decided to dress up as the CO2 transport system for halloween. You happen to be CO2. You go to the blood vessel dance. When are you most likely to dance with an RBC, when are you most likely to leave the dance and who is controlling when you do both of these things?
H+ is the great controller. In the venous system, you have increased formation of H+ which causes O2 dissociation from Hb at the peripheral tissues (Bohr effect). Hb binds and buffers the increased [H+], pushing the equilibrium of CO2 towards bicarbonate formation (90%). CO2 can now also bind the taut Hb to form caraminohemoglobin (5%). The other 5% of CO2 just dissolves in the blood. As you move to the lungs, increased [O2] causes Hb to change to the R state, unload H+ and push the bicarbonate equilibrium back towards CO2 formation (Haldane effect). The new Hb R state also causes unloading of CO2 at the lungs.
It’s finally here, the day you check hiking Mount Everest off of your bucket list. A few days prior your doctor started you on a medication that should help you survive the low PO2 at that elevation. What does this medication do and when won’t you need it anymore?
When you first start hiking, the decreased PO2 causes a decrease in release of CO2 at the alveoli, more bicarbonate formation and respiratory alkalosis. Acetazolamide causes increased renal excretion of bicarbonate to mitigate respiratory alkalosis. It takes a number of months to adjust to the decreased PO2.
You are on a humanitarian mission with a native tribe in the Andes mountains of South America. You notice a higher than normal incidence of patients with symptoms of right-sided heart failure. None of them smoke and they all have very good dietary habits. What could be the cause of this finding?
When people live at high altitudes for long periods of time they have increased hematocrit and hemoglobin levels due to secretion of erythropoietin. This increases blood viscosity. Although 2,3-BPG causes the hemoglobin dissociation curve to shift right and release more O2 at the tissues, there is still chronic vasoconstriction due to decreased PO2 in the lungs. This combination of vasoconstriction and viscosity increases pressure on the right side of the heart and can cause heart failure.
What organelle are you most likely to see an increase in when living at higher altitudes for extended periods of time?
Mitochondria. This is to keep up with oxidative phosphorylation in the absence of sufficient oxygen levels.
A 62 year old female comes to see you complaining of a non-productive cough and generalized malaise for the past 2 or 3 months. Her WBC is elevated and you decide to do a blood culture and an x-ray. Her CXR is shown below and lab results show bacteria that do not gram stain well. What is your differential diagnosis in this patient? How would you further narrow your diagnosis?
She demonstrates symptoms of atypical pneumonia. The bacteria that do not gram stain well and cause atypical pneumonia are Mycobacteria, Mycoplasma, Legionella and Chlamydia. You would further narrow your diagnosis with specific stains and agars for each of these: MYCOBACTERIA: stain = Ziel-Neelsen acid-fast agar = Lowenstein-Jensen if M. Tb, Eaton’s if M. pneumoniae. MYCOPLASMA: agar = Eaton’s. LEGIONELLA: stain = silver, agar = charcoal w/iron & cystein. CHLAMYDIA: stain = Giemsa, look for inclusion bodies.
A 9 year old male comes to see you in clinic a week after he already saw you for a viral infection. He complains of persistent fever but now has difficulty swallowing and a hoarse voice. After looking at his throat (seen below) you take a throat swab and send it to the lab for culture. What medium will you request the lab cultures your sample on? What other symptoms may manifest as a result of infection by this bacteria?
Chocolate agar. This patient has symptoms of H. influenzae B, which commonly infects children after a viral infection and causes epiglottitis. The gram negative rod must have factors V(NAD+) and X(hematin) in order to grow in culture. H. influenzae infection also manifests in meningitis, otitis media and pneumonia.
You are doing rounds and see a patient who has been in the hospital for the past three months recovering from severe burns when he was in a house fire. A few days ago nurses found a number of infections in his wounds. You culture one of the infections and send it to the lab. What results would you expect to see on this patient’s plated culture?
A gram negative rod, non-lactose fermenting, oxidase positive bacteria that produces pyocyanin (green pigment) on MacConky’s agar. The bacteria will also have a grape-like odor.
A 20 year old male comes to see you in the clinic who has had a low-grade fever, non-productive cough and generalized malaise for the past four months. He has a history of cystic fibrosis. What drugs do you give this patient and what serious complications is he at risk for if this is not resolved?
Patient’s with cystic fibrosis have a tendency to colonize pseudomonas. Pseudomonas is a biofilm-forming bacteria and you will need to treat the patient with surfactant to break it up and antibiotic to kill it, typically an aminoglycoside (gentamycin or streptomycin) with an extended-spectrum penicillin (piperacillin or ticarcillin). If the patient is not treated, he is at risk for shock (endotoxin) and mass cell death (exotoxin A, which inactivates EF-2).
A 15 year old lifeguard comes to the clinic complaining of ear pain. You determine that he has a bacterial ear infection. Lab results reveal a gram-negative rod, non-lactose fermenting, oxidase positive bacteria that produces a green biofilm when plated. What other infections is this bacteria associated with? What would you use to treat this patient?
PSEUDOmonas: Pneumonia, Sepsis, External otitis, UTI, Drugs, Diabetes & Osteomyelitis. An aminoglycoside (gentamycin or streptomycin) with an extended-spectrum penicillin (ticarcillin or piperacillin).
A patient presents to your clinic complaining of a productive cough and pleuritic chest pain. His chest radiograph is shown below. He has been living in the dorms and no one else has caught what he has. How might you narrow your diagnosis with a biopsy of this lesion?
Histoplasmosis can often mimic the granuloma formation seen in Tb and on his CXR. Biopsy of the lesion and growth on Sabouraud’s agar in the lab would likely confirm such a fungal infection.
A 19 year old male Army recruit comes to see you in clinic complaining of low-grade fever and a non-productive cough. He is the 50th person who has come to see you with similar symptoms this month. You decide you should do a culture to investigate the culprit of this outbreak. His biopsy is shown below. What is your diagnosis and what about this microbe makes it infectious? What would you treat this patient with?
Chlamydia pneumoniae is the second most common cause of walking pneumonia and is spread via respiratory droplets, hence the outbreak. The bug goes through two phases: reticulate body (replicative non-infectious form) and the elementary body (Infectious form) that can be seen on this Giemsa stain. Note Chlamydia is inside the host cells because it cannot make it’s own ATP. Chlamydia is treated with a macrolide (azithromycin one-time treatment) or a tetracycline (doxycycline).
A 61 year old veterinarian comes to the clinic complaining of fevers, myalgias and a headache. History reveals that he is in contact with birds at the zoo. You prescribe him azithromycin and his symptoms go away in less than a week. What is your diagnosis?
Chlamydia psittaci. It is typically zoonotic and causes atypical pneumonia in humans.
You are in Mexico working at a humanitarian health center. A 19 year old male comes to the clinic with fever, night sweats, weight loss and hemoptysis. His chest x-ray is shown below and labs reveal that he is positive for the PPD test. What are the main factors contributing to the virulence of the organism infecting this patient?
M. tuberculosis expresses high levels of cord factor. This inhibits macrophage maturation and induces TNF-alpha secretion which is key in formation of the granuloma. Surface lipids on M. tuberculosis (sulfatides) inhibit phagolysosomal fusion and allow M. tuberculosis to survive inside the macrophage. As a side note, it also survives extracellularly.
A 31 year old medical from France student joined the Navy so he could pay his bills. When he was having his physical done, he had a positive PPD and the US military wanted to treat him with combination anti-biotic therapy for the next 9 months. CXR was negative for any pulmonary lesions and the patient was asymptomatic. Should he take the meds?
No. It is likely he was vaccinated with BCG for M. Tb which is common in Europe.
A 40 year old female comes to see you complaining of fever, night sweats, weight loss and hemoptysis. She has a history of HIV. Her chest x-ray is shown below. What might you see if you took a biopsy of this patient’s lung tissue and what is concerning about her history and chest x-ray?
This patient demonstrates symptoms of miliary tuberculosis. Biopsy would reveal acid-fast organisms seen below. Miliary Tb often indicates hematogenous dissemination to other organs and she may manifest symptoms in the CNS (tuberculoma or meningitis), vertebral bodies (Pott’s disease), lymphadenitis, renal and GI systems.
A 43 year old male with AIDS complains of fever, chills, night-sweats and a productive cough. History only reveals recent purchase of a hot tub. His chest x ray is shown below. Treatment with isoniazid does not relieve his symptoms but azithromycin does. What is your diagnosis?
M. avium-intracellulare is capable of causing systemic and pulmonary symptoms (note cavitary lesion on right upper lung in x-ray). It is like M. Tb, but does not resolve with isoniazid. People with AIDS are highly susceptible and it can be found in hot tubs.
A patient comes in for a regular check up. He was previously diagnosed with tuberculosis. His chest x-ray is seen below. What would put this patient at risk for possible reactivation of Tb?
Anything that makes him immunocompromised. Dormant tubercle bacilli may remain in the tubercle seen on his radiograph and can spread when the immune system wanes.
A 77 year old male comes to see you in clinic complaining of fever, chills, night sweats, a productive cough and GI irritation. He works as a journeyman in the sewer business. Labs reveal hyponatremia (low sodium). Sputum culture reveals a gram negative rod that grows on charcoal yeast extract. What is your diagnosis and how do you treat this patient?
Legionella pneumophila infection. Legionella is commonly found in water, presents with low sodium and cultures in charcoal yeast extract due to presence of iron and cysteine. This patient would be treated with macrolides (azithromycin or erythromycin) or a quinolone.
A 52 year old female presents with fever, dyspnea, sweats, chills, myalgias and a productive cough with red currant jelly sputum. She has a long history of alcohol abuse and diabetes. Her chest radiograph is shown below. What would you expect to see in the lab if you cultured a sample from the abscess seen in her lung?
Klebsiella is a normal intestinal flora that can cause pneumonia and abscess formation in patients at risk for aspiration (alcoholics and diabetics). In lab culture, you would expect to see a gram negative rod and a fast lactose fermenter which is urease-positive.
You take your new baby to the doctor and he says she needs to get her immunizations. One of them is the Hib vaccine. You ask the doc why that one is so dang expensive. What does he tell you?
H. influenzae type B is an encapsulated bacteria. Kids’ immune systems are not great at T-dependent recognition of carbohydrates. So, they complexed the carbohydrate on the capsule with a protein that kids’ immune systems can recognize. That is an expensive process.
Aside from being encapsulate, how are H. influenzae and strep pneumoniae good at evading the immune system in the respiratory tract?
They make IgA protease which allows them to colonize respiratory mucosa (mostly defended by IgA antibodies).
Why are patient’s diagnosed with rheumatic fever at risk for shock?
Strep pyogenes (group A strep) produces exotoxin A which is a super antigen (permanently binding MHC II and TCR) which causes mass release of IFN-gamma and IL-2, leading to shock.
A 32 year old female presents with a high fever, myalgias, rusty-colored sputum and dyspnea. Her lower right lung is dull to percussion and her chest x-ray is shown below. What bug is the most common culprit of this patient’s condition? What would you expect to see on a sputum culture?
Strep pneumoniae is the most common cause of community acquired bacterial “MOPS”: meningitis, otitis media (kids), pneumonia and sinusitis. Culture reveals a lancet-shaped, gram-positive, catalase negative, alpha-hemolytic diplococci that is optichin sensitive.
A 55 year old male presents with pneumonia. Sputum culture is shown below and it is determined the bacteria are catalase negative and alpha-hemolytic. What test would help you determine if this patient is at risk for endocarditis or not? What would you prescribe to this patient?
These are gram-positive, alpha-hemolytic diplococci. All you need to do at this point is test optochin sensitivity. If it is not sensitive, you have strep viridans and the patient is at risk for subacute endocarditis. If it is sensitive, you have strep pneumoniae.
A 9 year old female comes to see you with a sore throat and you do a throat swab. Labs come back with a positive ASO titer. What would this patient’s swab culture look like and what further complications is she at risk for?
An elevated ASO titer indicates recent strep pyogenes (group A) infection. You would see a gram positive, catalase-negative, beta-hemolytic and bacitracin sensitive cocci. Patients with group A strep are at risk for: cellulitis, impetigo, necrotizing fasciitis, scarlet fever, rheumatic fever (anti-M protein antibodies), acute glomerulonephritis (anti-M protein antibodies) and TSS (exotoxin A).
A 7 year old female comes to the doctor with a severe dry cough that “whoops” on inspiration. Throat swab and culture reveals a gram negative coccoid rod. What is the mechanism of damage caused by this microbe?
Bordetella pertussis lands in the respiratory tract and secretes pertussis toxin. This toxin is an ADP ribosylating A-B toxin (B=binding to cell surface and A=active component disables Gi, increases cAMP levels, evades immune response and destroys cilia)
A patient comes to see you a few weeks after a strep throat infection with chest pain. You assess the patient to see if he may meet the criteria for acute rheumatic fever. What are the criteria?
JONES criteria = Joints (polyarthritis), Myocarditis, Nodules (Osltler & Janeway), Erythema marginatum and Syndenham’s chorea
A 68 year old male presents with mild chest pain. He is also battling colon cancer. What is the mostly likely offending agent in this patient?
Strep bovis. This colonizes in the gut, can cause bacteremia and endocarditis.
You are working in an overseas clinic and see a patient with a grayish-white membrane in his pharynx, bull neck, myocarditis and arrhythmias. His health is deteriorating rapidly and you do a blood culture to see what is going on. What will you most likely seen culture and what is the mechanism of damage by this pathogen?
The grayish-white membrane (pseudomembranous pharyngitis) and bull neck (lymphadenopathy) is indicative of corynebacterium diphtheriae. These show up as club shaped (coryne) black colonies on cysteine-tellurite agar. They stain as gram positive rods with metachromatic (blue and red) granules. A beta-prophage gets into the bacteria and encodes the exotoxin which inhibits cellular protein synthesis via ADP-ribosylation of EF-2.
You are working for the national Indian health service and do a two week trip to Texas. You come across a group of people that eat armadillos regularly. You also note many of them have collapsed noses, lumpy earlobes and do not have eyebrows. Do you think this is a special ethnic characteristic of this group? Do you shake hands with these people? How would you treat them?
This is Hansen’s disease caused by mycobacterium leprae. The characteristics seen in these patients are Leonine facies, typical of lepromatous m. leprae. This type is contagious so you wouldn’t shake hands. Additionally, the bacterium like cooler temperatures and cause loss of sensation in the glove and stocking areas, so they probably wouldn’t feel the handshake anyways. You would treat these patients with dapsone, rifampin and clofazimine for 2-5 years.
A 55 year old armadillo trainer presents to your clinic with a few hairless skin plaques on the lower left side of his back. Biopsy of the lesion is shown below. What causes this condition to progress to the more serious condition?
This patient has tuberculoid leprosy. This is characterized by high cell-mediated and Th1 immunity. When cell-mediated immunity wanes and Th1 humoral immunity takes over, it spreads and progresses to lepromatous leprosy.
A 42 year old rancher comes to see you complaining of dyspnea, fever, malaise and a productive cough. His chest x-ray reveals right lower lobe consolidation and increased vascular markings. Inhalation of the spores of what microbe could be causing these symptoms?
Coxiella burnetii. The spores of this bacteria can be inhaled from tick feces or cattle placenta and presents as pneumonia (Q fever).
A 23 year old Army recruit presents to the clinic with a headache and a non-productive cough over the past two months. His chest x-ray is seen below. How do you decide what you are going to treat this patient with?
Note the diffuse interstitial infiltrate in the patient’s lungs typical of atypical pneumonia. Mycoplasma pneumoniae is the most common cause of atypical pneumonia. You could try to grow the bacteria on Eaton’s agar, but that would take too long. A high titer of IgM agglutinins is present in these patients and can be tested to see if they lyse RBCs. If it is determined that mycoplasma is the culprit, you would treat with a macrolide or fluorquinolone.
Why don’t mycoplasma bacterium stain well on Gram stain? What does this imply about therapies used to treat these types of infection?
They don’t have a cell wall, they use sterols for stability instead. You cannot resolve these infections with penicillins.
A 28 year old male comes to you complaining of a persistent cough and flu-like symptoms for the past three weeks. His chest x-ray somewhat resembles miliary Tb, but he tested negative on the PPD. He is a big-time spelunker from the central states. What would you expect to see if you took a sample from bronchoalveolar lavage in this patient? How would you treat him?
This is histoplasmosis. You would see macrophages filled with histoplasma yeast. This fungal infection is endemic in the middle states and present in bat droppings. You treat this with fluconazole or itraconazole for local infections of IV amphotericin B for systemic infections.
A 33 year old female from the south-central states comes to see you complaining of rapid onset of myalgia, headache, productive cough and pleuritic chest pain. She also has verrucous skin lesions and joint pain. What would you expect to see in a biopsy of this patient and how would you treat her?
This is blastomycosis, characterized by broad-based budding yeasts surrounded by neutrophils. It is endemic in the south. You would treat localized infections with fluconazole or itraconazole. You would treat systemic infections with IV amphotericin.
A bunch of nerds were out in San Joaquin Valley in California flying their model airplanes. Most of the nerds came down with pneumonia and some got meningitis. Chest x-ray showed fibrocaseous nodules in their lungs but each one of them had a negative PPD. What caused this outbreak? What would it look like under a microscope? How would you treat it?
Coccidioidomycosis lives in the ground and releases spores that can get kicked up and inhaled. It is endemic to the southwestern US. Note the spherule filled with endospores waiting to be released. You would treat localized infections with fluconazole or itraconazole. You would treat system infections with IV amphotericin.
A group of Navy sailors came back from a trip to South America with pneumonia. Chest x-rays of the sailors revealed granuloma formation, but all had negative PPD tests. What fungal infection may they have gotten on their trip? What would it look like under the microscope? How would you treat it?
Paracoccidioidomycosis. It is endemic to South America and forms a large “captain’s wheel” budding yeast. You would treat localized infections with fluconazole or itraconazole. You would treat system infections with IV amphotericin.
What pneumonia-causing mycoses are dimorphic (mold in environment and yeast inside host)?
Histoplasmosis, blastomycosis and paracoccidioidomycosis.
A 17 year old female comes to see you in clinic with a fever, lymphadenopathy and pharyngitis that has affected her over the last month. Her boyfriend had the same thing. Her peripheral blood smear is shown below. What is likely causing her condition and what more serious complications is she at risk for down the road? What test could you do to further narrow your diagnosis?
Note the atypical lymphocytes seen in the peripheral blood smear. The atypical cells seen rare reactive CTLs in response to B-cell infection by EBV. Further testing may include a mono spot test where heterophile antibodies are detected by agglutination of horse or sheep RBCs. EBV is also associated with Hodgin’s lymphoma, Burkitt’s lymphoma and nasopharyngeal carcinoma.
A 30 year old otherwise healthy male comes to see you with a runny nose and cough. You determine he has the common cold. What are the characteristics of this viruses that cause the common cold? Which is more common? Which one can be more serious?
Rhinovirus: no envelope, +ssRNA, isocahedral capsid (100+ serotypes). Coronavirus: enveloped, +ssRNA, helical capsid (also causes SARS)
A 21 year old college sophomore comes to the health clinic for his flu shot. He gets the nasal spray. What are the characteristics of the virus in the nasal spray? He came back a month later mad that he got the flu. What about this virus caused him to get the flu even though he got the vaccine?
It is a temperature-sensitive orthomyxovirus (influenza) that replicates in the nose but not in the lungs. Enveloped, -ssRNA, 8 segments, helical, comes w/RNA polymerase. The 8 RNA segments can be transferred and allow for antigenic shift, rendering the vaccine ineffective against the new strain.
What are the characteristics of the virus that causes croup in adults and bronchiolitis in babies?
Paramyxoviruses. Enveloped, -ssRNA, helical, comes w/RNA polymerase. Parainfluenza = croup. RSV = bronchiolitis in babies. Measels and mumps.
You are working at the AIDS clinic during flu season. A patient comes in and tells you his girlfriend had the flu and he is now feeling sick. What drugs can you give him to prevent serious influenza infection and why does it work?
You could give him zanamivir/oseltamivir to inhibit neuraminidase, making it impossible for the new virions to dissociate from a host cell and thus cannot spread. You could also give him amantadine/rimantadine which block the M2 channel and prevent viral disassembly.
What drugs could you use to treat a child who was infected with RSV?
Ribavirin. Inhibits synthesis of guanine nucleotides. Palivizumab is a monoclonal antibody against the F protein created by paramyxoviruses that normally causes fusion of epithelial cells.
What drug has weak activity on EBV?
Acyclovir
If you could develop a drug that would entirely inhibit viral entry into the host cell, what viral component would it target?
Hemagglutinin. It binds to sialic acid on the host cells and causes endocytosis.
Why are orthomyxoviruses so prone to antigenic drift?
RNA polymerase does not have proofreading activity.
What are the three different kidney layers that are formed during fetal development? When do they form?
Pronephros (week 4), Mesonephros (1st trimester) and Metanephros (week 5)
When and where does nephrogenesis occur in the developing fetus?
Metanephros. Weeks 32-36.
What embryonic structure functions as a kidney in utero but later contributes to the male reproductive system?
Mesonephros
What embryonic structure is derived from the caudal end of the mesonephros? What does it go on to form?
The ureteric bud. It goes on to form the collecting system (ureter, renal pelvis, calyces and collecting ducts).
What embryonic structures communicate to induce fetal development of the tubular system (glomerulus, proximal convoluted tubule, loop of Henle and distal convoluted tubule)?
Ureteric bud and the metanephric mesenchyme.
A mother goes to see her physician because she is concerned that she hasn’t felt her baby move in three days. Her baby did not make it and gross biopsy of the child’s kidney is shown below. What developmental malformation possibly caused this condition?
Failure of the uretopelvic junction to canalize is the most common site of urinary obstruction in the fetus.
A child is born with limb and facial deformities. Shortly after birth the child dies due to pulmonary hypoplasia. What are possible causes for the developmental abnormalities seen in this child?
The child presents with oligohydramnios and Potter’s Sequence. Possible causes of this is ARPKD, posterior urethral valves and bilateral renal agenesis.
While doing an ultrasound on a patient with stomach pain you image the kidneys of the patient as seen below. Where in the abdomen would you find this and what syndrome is this condition associated with?
Horseshoe kidneys are found around the inferior mesenteric artery. They are associated with Turner’s syndrome.
A mother comes to see you with her 2 year old child. He has been constipated for the past week and she is holding a radiograph in her hands. The radiograph shows an enlarged right kidney and she is scared it is cancer. Renal ultrasound of the left kidney is shown below. What is the pathogenesis behind the condition of this boy?
Multicystic dysplastic kidneys form from abnormal interaction between the ureteric bud and the metanephric mesenchyme. Consequently, this child’s right kidney has hypertrophied to compensate for a non-functional left kidney.
What strutters are labeled in the image below?
1=Macula Densa apposed to the 2=Distal convoluted tubule
What percentage of our total body weight is water? What fraction of that water is ECF? What fraction of that water is ICF? What fraction of the ECF is plasma? What fraction of the ECF is interstitial volume?
Total H20 = 60%. ECF=2/3 of total H20. ICF=1/3 of total H20. Plasma =1/4 of ECF. Interstitial Fluid = 3/4 of ECF.
How might you measure total plasma volume?
Radio-labeled albumin.
What structural change in the glomerulus is responsible for albuminuria, hypoproteinemia, generalized edema and hyperlipidemia in patients with nephrotic syndrome?
The negatively-charged heparan sulfate basement membrane of the glomerulus is lost.
What structure of the glomerulus is responsible for filtration of particles solely based on size?
Fenestrated capillary endothelium.
What structure of the glomerulus has diaphragms?
Podocyte foot processes.
How do you calculate clearance of a solute from the blood through the urinary system?
Note that Vol = urine flow rate
After calculating renal clearance of a solute in the blood, how do you figure out if the solute is being reabsorbed or secreted by the tubular system?
If clearance > GFR, the substance has a net secretion of X. If clearance is < GFR, the substance has a net reabsorption of X.
Why is inulin a good measure of GFR?
It is freely filtered and neither reabsorbed or secreted.
What is a normal GFR?
100mL/min
Labs typically use creatinine levels to estimate GFR. Would this result in a general over or underestimation of a patient’s GFR?
Overestimation. Creatinine is moderately secreted by the tubules as well as filtered.
How can you calculate GFR from hydrostatic and oncotic pressures?
K=capillary permeability. HP = hydrostatic pressure. pi=oncotic pressure. GC=glomerular capillary. BS=Bowman’s space
Labs typically use PAH to estimate effective renal plasma flow (eRPF). Would this result in a general over or underestimation of a patient’s eRPF?
Underestimation by about 10%. 90% of PAH is both filtered by the glomerulus and secreted by the PCT, making it a good estimate of how much plasma is reaching the glomerulus per unit time.
How do you calculate effective renal plasma flow (eRPF)? How do you get renal blood flow (RBF) out of this?
In order to calculate the actual renal blood flow, you need to remember that PAH is in the plasma, which is only a portion of the blood. eRPF/(1-Hematocrit) will give you renal blood flow.
How do you calculate the amount of fluid that passes through the renal tubules in relation to the amount of fluid that reaches the kidneys? What is a normal value?
Filtration fraction= GFR/RPF. A normal filtration fraction is 20%.
How do you calculate the amount of any solute filtered into Bowman’s space per unit of time?
Filtered load = GFR * Plasma [X]
What happens to the filtration fraction in response to prostaglandins acting on the glomerular afferent arteriole?
It remains constant because FF = GFR/RPF and RPF & GFR both increase in response to prostaglandins.
Why is it not a good idea to prescribe NSAIDs to a patient with renal failure?
They inhibit prostaglandin action at the afferent arteriole and decrease the RPF (renal plasma flow) and GFR.
What happens to the filtration fraction in response to angiotensin II acting on the glomerular efferent arteriole.
It increases because FF = GFR/RPF and GFR increases and RPF decreases in response to angiotensin II.
Why is it a bad idea to prescribe an ACE inhibitor to a patient with arteriolosclerosis of the afferent arteriole?
Constriction of the efferent arteriole may be the last regulatory mechanism the glomerulus has in its pocket.
What happens to filtration fraction in response to a decrease in plasma protein levels? What about an increase?
Decrease: no change in RPF w/ an increase in GFR = increased FF. Increase: no change in RPF w/ a decrease in GFR = decreased FF.
Why do pregnant women sometimes present with glucosuria?
The normal threshold (~160mg/dL) and transport maximum (~350mg/dL) are decreased during pregnancy.
How is glucose reabsorbed in the kidney?
Na+/Glucose cotransporters completely reabsorb glucose at the proximal convoluted tubule.
How are amino acids reabsorbed in the kidney?
Na+-dependent transporters in the proximal convoluted tubule.
What is Hartnup’s disease?
Pellagra due to a deficiency in the tryptophan amino acid transporter in the PCT.
What things are reabsorbed by the proximal convoluted tubule?
Glucose, amino acids, bicarbonate, Na+, Cl+, PO4 and H2O
What is the tonicity of the fluid in the proximal convoluted tubule?
Isotonic. It is absorbing electrolytes and water.
How does the kidney buffer the H+ that is secreted at the proximal convoluted tubule?
Generation and secretion of ammonia at the PCT
How does PTH affect exchange at the PCT?
Na+/PO4 transport is inhibited and more PO4 is excreted.
How does angiotensin II affect exchange at the PCT?
Na+/H+ exchange is stimulated. This increases Na+, H2O and HCO3 reabsorption.
How does angiotensin II contraction alkalosis?
It stimulates the Na+/H+ exchange and more H+ is sent out in the urine.
What percentage of filtered Na+ is reabsorbed at the PCT?
65-80%
What portion of the nephron is responsible for hyper concentrating the urine?
Thin descending loop of Henle. Water is passively reabsorbed here due to medullary hypertonicity.
What things are reabsorbed by the thick ascending loop of Henle?
Active reabsorption of Na+, K+ and Cl-. Paracellular transport of Mg2+ and Ca2+
Where does urine become less concentrated in the nephron?
At the thick ascending loop of Henle. This tube is impermeable to water and allows ions to escape.
How much sodium is reabsorbed at the thick ascending loop of Henle?
10-20% of what was filtered.
What is reabsorbed at the distal convoluted tubule?
Na+, Cl-
How much sodium is reabsorbed at the distal convoluted tubule?
5-10% of what was filtered.
How does PTH affect the distal convoluted tubule?
It increases Ca2+/Na+ exchange, increasing Ca2+ reabsorption.
What is reabsorbed and secreted at the collecting tubules?
Na+ and Cl- are reabsorbed in exchange for K+ and H+ secretion
How does aldosterone affect the collecting tubules?
Activation of the mineralocorticoid receptor increases Na+ channels on the lumenal side.
How does ADH affect the collecting tubules?
Activation of V2 receptor increases aquaporin channels on the lumenal side.
How much sodium is reabsorbed at the collecting tubules?
3-5%
How does the ratio of [tubular solute]:[plasma solute] change as you move down the proximal convoluted tubule for Cl-, urea, Creatinine, Amino Acids, HCO3, Glucose and Na+?
*
What happens to tubular concentration as you move down the proximal convoluted tubule?
It increases because water is reabsorbed but it is not.
Why does the juxtaglomerular apparatus think he’s so special?
He is Mr. Smooth Muscle that can secrete renin in response to decreased BP in the afferent arteriole, decreased [NaCl] sensed by the macula densa and beta-1 stimulation.
After angiotensin I is converted to angiotensin II by ACE in the lungs, what tissues does angiotensin II go on to make contact with?
Vascular smooth muscle (AT1 receptors), Efferent glomerular arteriole, Adrenal gland, Posterior pituitary gland, Proximal convoluted tubule and the Hypothalamus.
How does angiotensin II maintain GFR when you are dehydrated?
Constriction of the efferent glomerular arteriole decreases renal blood flow, increases filtration fraction and thus maintains GFR.
What are the major causes of conjunctivitis?
Mostly Adenovirus, some H. influenzae (bacterial pink-eye)
What are the major causes of otitis media?
Strep pneumoniae, H. influenzae and Moraxella catarrhali
What are the major causes of pharyngitis?
Rhinovirus, Adenovirus, EBV and streptococcus pyogenes
What is the major cause of epiglottitis?
H. influenzae type B
What is the major cause of acute onset pneumonia with cough, fever, malaise and chills?
Strep pneumoniae
What is the major cause of acute onset pneumonia with cough, fever, malaise and chills in babies?
RSV
What are the major causes of acute onset pneumonia with cough, fever, malaise and chills in the elderly?
Strep pneumoniae and influenza
What is the major cause of acute onset pneumonia with cough, fever, malaise and chills after having the flu?
Staph aureus
What are the major causes of acute onset pneumonia with cough, fever, malaise and chills in young adults?
Adenovirus serotypes 4 & 7
What is the major cause of acute onset pneumonia with cough, fever, malaise and chills accompanied by nausea and diarrhea?
Legionella
What are the major causes of atypical pneumonia with gradual onset, a persistent cough, malaise and fatigue?
Mycoplasma pneumoniae (90%) and chlamydia (10%)
What are the major causes of atypical pneumonia with gradual onset, a persistent cough, malaise and fatigue accompanied with GI symptoms?
Legionella
What are the major causes of atypical pneumonia with gradual onset, a persistent cough, malaise and fatigue with weight loss and night sweats?
Endemic mycoses and mybobacterium tuberculosis
What are the major causes of atypical pneumonia with gradual onset, a persistent cough, malaise and fatigue with hemoptysis?
Mycobacterium Tb.
What respiratory infections are toxin-mediated?
Corynebacterium diphtheriae (diphtheria toxin) and Mycoplasma (CARDS)
How does diphtheria toxin work?
It is ADP-ribosylating EF-2 toxin. This stops protein synthesis and causes cell death in the oropharynx.
What agents will not gram stain in a sputum stain of a patient with respiratory illness?
Chlamydia (intracellular), influenze (too small), mycobacterium Tb (mycolic acid waxy coat), mycoplasma p. (no cell wall) and legionella p. (intracellular)
Elimination of the capsule in what bacterium will usually eliminate respiratory disease?
S. pneumoniae, H. influenzae B, Pseudomonas aeruginosa and Klebsiella pneumoniae
What virus is responsible for the common cold?
Rhinovirus and Adenovirus
What are the genomic characteristics of influenza? How do we make drugs that target these characteristics?
Segmented -ssRNA, enveloped, neuraminidase and hemagluttinin. Amantidine & Rimantidine = M2 blockade blocks virus disassembly. Relenza & Tamiflu = NA blockade blocks release of influenza A & B. Vaccine = neutralizing Ab against NA & HA
What virus is most often responsible for infant pneumonia and bronchiolitis? How do you treat it?
The paramyxovirus, RSV. You can treat it with an antiviral (Ribavirin) and passive antibody.
What about the virus that causes the common cold makes it so virulent?
Rhinovirus (member of Picornavirus family): +ssRNA (translated on entry), 99 different types, unenveloped (small & stable).
Describe the envelope of EBV?
It is a DNA virus so it replicates in the nucleus and takes nuclear membrane with it as it buds off.
How do you diagnose EBV?
Hepatosplenomegaly, atypical lymphocytes and heterophile antibodies
Where is the primary site of EBV infection? Where is it latent?
Primary = PCC & lymph nodes. Latent = B cells
What cancers is EBV linked to?
Nasopharyngeal (from PCC infection) and lymphoma (from B cell latency)
What respiratory infections are most commonly associated with unvaccinated populations?
H. influenzae, diphtheria and bordatella
What respiratory infections are most common in older people?
H. influenzae, Legionella and strep pneumoniae.
What respiratory infections are most common due to reactivation of a sequestered infection?
M. Tb, Histo, Blasto & Cocci
What respiratory infection is most often associated with cystic fibrosis?
Pseudomonas aeruginosa
What respiratory infection is most often associated with the Ohio river valley? Mississippi river valley? San Joaquin valley?
Ohio = Histo. Mississippi = Blasto. San Joaquin = Cocci.
What respiratory infection is most often associated with bird lovers?
Chlamydia psittaci
What respiratory disease has conjugate vaccines? Who gets this vaccine & why?
Hib (PRP) & Strep pneumoniae (pneumococcal PCV13). Kids get this because kids need a little push to help the T-cell response recognize the polysaccharide antigen.
What respiratory disease has a polysaccharide vaccine? Who gets this vaccine & why?
Strep pneumoniae. PPS 23 is given to older adults because they have a more developed T cell response that can identify the polysaccharide.
What respiratory diseases have a live attenuated vaccine?
Influenza, adenovirus, RSV and BCG (M. Tb)
What respiratory disease has a toxoid vaccine?
Diphtheria
Who gets killed/inactivated vaccines?
People at risk for the flu who are young children or older adults.
What respiratory pathogens are facultative intracellular organisms?
Legionella (macrophages in humans & amebas out), M. Tb and Histo.
What respiratory pathogens are obligate intracellular organisms?
Chlamydia (needs ATP from host) and all viruses
What sites are colonized by strep viridans?
Oral cavity, respiratory tract, GI and vagina
What distinguished strep viridans from other strep organisms?
Alpha-hemolytic
What is strep viridans’ role in disease?
Dental cavities & endocarditis
What are the prominent strep viridans species?
Mitis, Mutans, Oralis & Sanguinis
What organisms are associated with uncomplicated UTIs?
E. coli and staph saprophyticus
What organisms are associated with complicated UTIs?
Proteus mirabilis and enterococci
What organisms are associated with nosocomial UTIs?
Pseudomonas aeruginosa and drug resistant gram-negative rods (Serratia, Enterobacter & Klebsiella)
You culture a bacteria on MacConkey agar that does not ferment lactose, produces a green pigment, has a fruity smell and is oxidase positive. What diseases is this pathogen associated with?
Pneumonia in cystic fibrosis, opportunistic infection, otitis externa and hot tub folliculitis.
What makes Pseudomonas aeruginosa virulent?
Alginate capsule, exotoxins, proteases and LPS
What special tests are available for M. Tb detection?
PPD skin test & IGRA
What special test is available for mycoplasma pneumoniae?
Cold agglutinin (agglutinates RBCs in the cold)
What special test is available for Legionella?
Urine test
What special tests are available for EBV?
Heterophile monospot test and atypical lymphocytes on CBC.
How does the appearance of histo differ in tissue and in culture?
*
How does the appearance of blasto differ in tissue and in culture?
*
How does the appearance of cocci differ in tissue and in culture?
*
What tests do you do in differentiating gram-negative rods from one another?
Bacterial morphology, lactose and oxidase
What tests do you do in differentiating gram-positive rods from one another?
Bacterial morphology, Catalase, Coagulase, Hemolysis, Optichin, and Bacitracin
Where is the transitional epithelium lining the ureter derived from?
Ureteric bud
What structures are indicated by the arrows below?
Arterioles. Note the layers of smooth muscle surrounding the endothelium.
What structure is indicated in the image below?
Proximal convoluted tubule. Note the brush border, absence of cell borders and nuclei sitting at the bases of the cells.
What structures are indicated in the image below?
1=Vein, 2=Arteriole
What type of tubule is indicated by the arrow below?
Distal convoluted tubule. Note that it is connected to the tubule adjacent to the macula densa, which is a DCT.
What cells reside in the area indicated below. What are their functions?
Intra-glomerular mesangial cells reside between the endothelial cells & the GBM. They are phagocytes.
What cells are found in the region indicated below? What is their function?
Extra-glomerular mesangial cells. They receive signals from the macula densa that [NaCl] is low, release Ca2+ and stimulate renin release from the smooth muscle cells in the juxtaglomerular apparatus.
What structures are indicated below?
Arteriole, dark (intercalated) cells and light (principal) cells. The dark intercalated cells are involved in secretion and reabsorption of H+ and HCO3-. The principal cells are involved in sodium and water reabsorption and potassium secretion.
What structures are in the circle below?
Capillaries and thin limbs. They are really hard to differentiate from one another.
What renal structures are indicated below?
1=Thick descending limb. 2=Thick ascending limb 3=Thin limb 4=Peritubular capillary
What is the difference between GFR and clearance?
Clearance takes reabsorption of the filtered material when measuring how much has been excreted. GFR is the amount of substance the glomerulus is filtering…measured by a substance that is freely filtered and excreted but not reabsorbed.
What molecules are reabsorbed via secondary active transport?
Glucose and amino acids are both moved against their concentration gradients with Na+ cotransport. This is because the Na/K ATPase is actively maintaining a gradient for Na to flow down.
How does hyperaldosteronism result in hypokalemia?
Increased secretion of aldosterone from the adrenal gland not only upregulates Na+ channels and Na/K ATPase, it also upregulates lumenal K+ channels in the principal cells and H+ channels in the intercalated cells. This is all to create a favorable gradient for Na+ reabsorption.
A patient comes to see you in the ER after throwing up his guts all over the place. His blood pressure has dropped and labs reveal a contraction alkalosis. What is causing this to happen?
When he throws up he loses ECV. This causes renin release and formation of ATII and aldosterone. ATII increases Na+/H+ exchange at the proximal tubule and encourages reabsorption of bicarbonate. Aldosterone activates H+ ATPase that pumps H+ into the lumen and encourages formation of new bicarbonate. Both of these processes lead to contraction alkalosis.
A patient with CHF comes to see you in clinic. Labs reveal an elevated ANP. How would this lab value increase this patient’s GFR? How will ANP help him out with edema?
It stimulates smooth muscle relaxation via cGMP. This increases GFR and decreases renin release. Its net effect will be a loss of Na+ and fluid because it elicits and increased GFR with no compensatory Na+ reabsorption.
What regulatory system does ADH have true allegiance to beneath all the frills and fluffiness?
Response to low blood volume by ADH always takes precedence over osmolality
Who are the members of the group they call the Juxtaglomerular Apparatus and what do they do?
JG cells (afferent arteriole smooth muscle cells that secrete renin) and macula densa cells (NaCl sensor in distal tubule portion)
What stimulatory signals cause renin release from the JG cells?
Decreased afferent arteriole blood flow, decreased [NaCl] in distal tubule and increased beta-1 sympathetic tone.
A patient comes to see you in clinic who has been on antibiotics for the past week and is now peeing blood. Damage to what portion of the kidney would actually decrease the amount of RBCs seen in his urine?
Interstitial cells in the peritubular capillary bed. These guys secrete erythropoietin in response to hypoxia. Decreased EPO = decreased RBC production.
What role do cells of the nephron play in serum calcium levels?
Proximal tubular cells have 1alpha-hydroxylase that converts 25-OH vitamin D to 1,25-(OH)2 Vitamin D. PTH causes increased production of 1alpha-hydroxylase in the PCT, increased reabsorption of Ca2+ in the DCT and decreased reabsorption of PO4 in the PCT.
Why are NSAIDs bad for your kidney?
They inhibit renal prostaglandin production. These prostaglandins keep the afferent arterioles vasodilated to maintain a healthy GFR.
Where in the kidney does ATII cause vasoconstriction? How does this affect the body?
Efferent arteriole. This will increase GFR and FF with a compensatory Na+ reabsorption. The net effect will be an increase in ECV.
How does the adrenal gland respond to hyperkalemia?
Osmoreceptors cause an increase in aldosterone secretion. This will promote increased K+ and H+ secretion at the collecting duct.
What are six ways that cellular K+ shifts can cause hyperkalemia?
Digoxin, Osmolarity increase, Insulin deficiency, Lysis of cells, Acidosis, Beta-adrenergic antagonist. “DO Insulin LAB”
What are four ways that cellular K+ shifts can cause hypokalemia?
Hypo-osmolarity, insulin (increases Na/K ATPase activity), Alkalosis and beta-adrendergic agonist (increases Na/K ATPase activity)
A diabetic patient comes to see you in clinic. Labs reveal a serum pH of 7.2 and HCO3- level of 10. How would you determine if a mixed acid-base disorder is going on in this patient?
Look at the pCO2 to see if it has gone down with a compensatory respiratory alkalosis. You can do this numerically with Winter’s formula: PCO2 = 1.5(HCO3) + 8 +/- 2. This will give you a predicted compensatory pCO2 level. It the predicted is far from the actualy you likely have a mixed acid-base disorder going on.
A 62 year old male comes to see you in clinic. He has a blood pH of 7.2, HCO3 of 32 and a pCO2 of 60mmHg. List 5 possible causes of this patient’s condition?
This patient has a respiratory acidosis with compensatory metabolic alkalosis. Causes for respiratory acidosis include 1) Airway obstruction 2) Acute lung disease 3) Chronic lung disease 4) Sedatives 5) Neuromuscular weakness
A 62 year old male comes to see you in clinic. He has a blood pH of 7.2, HCO3 of 10 and a pCO2 of 20. What is the next value you should check on this patient? What are possible causes of his condition?
Check the anion gap = Na - Cl - HCO3. If it is normal (~12) HARD-ASS (Hyperalimentation, Addison’s, RTA, Diarrhea, Acetazolamide, Spironolactone, Saline infusion). If it is increased MUDPILES (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicate late effects).
A 72 year old man comes to see you in clinic. He has a blood pH of 7.5, HCO3 of 10 and a pCO2 of 20. What are 2 possible causes of this patient’s condition?
This patient has a respiratory alkalosis with a compensatory metabolic acidosis. Respiratory alkalosis can be caused by hyperventilation and early effects of salicylates.
A 72 year old man comes to see you in clinic. He has a blood pH of 7.5, HCO3 of 32 and a pCO2 of 60mmH. What are 5 possible causes of this patient’s condition?
This patient has a metabolic alkalosis with a compensatory respiratory acidosis. Metabolic alkalosis can be caused by loop diuretics, hypoventilation, vomiting, antacids and hyperaldosteronism.
A patient comes to see you with right flank pain. Imaging reveals a kidney stone. Labs: urine pH 6 and hypokalemia. What type of renal tubular acidosis (RTA) does this patient have?
Type I. This is a defect in the collecting tubule’s ability to excrete H+. If the tubule cannot excrete H+, the urine pH will be high and put the patient at risk for calcium phosphate stones. Decreased H+ excretion also causes decreased K+ and Ca2+ reabsorption in the collecting duct.
A 17 year old boy comes to see you because of polydipsia over the past few years with increasing bone pain. Labs: urine pH 5, hypokalemia and hypophosphatemia. What type of RTA does this patient have?
Type II. This is a defect in the proximal tubule’s ability to reabsorb HCO3. It can be associated with Fanconi’s syndrome as seen in this patient.
How does a type 4 RTA cause a decrease in urine pH?
Hypoaldosteronism or nephrogenic diabetes insipidus causes hyperkalemia. Hyperkalemia impairs ammoniagenesis in the proximal tubule, decreases buffering capacity and decreases urine pH.
A 44 year old woman comes to the ED after a car accident. She has elevated intracranial pressure that needs to be relieved but she cannot go to surgery right now. What diuretic would you prescribe her?
Mannitol. It increases tubular osmolarity and takes fluid off. It is specifically recommended for intracranial and intraocular pressure.
A patient comes to see you in clinic with severe right flank pain. He has a history of gout. You decide to measure his urine pH and it is 5. What might you prescribe this patient to prevent him from forming stones? How might this backfire?
Acetazolamide inhibits carbonic anhydrase. This causes HCO3 to stay in the urine and raise the pH. This is great for uric acid or cystine stones because they form at low pH. However, calcium oxalate stones tend to form at a higher pH and this could backfire.
You are planning a trip to hike Mt. Everest and your physician gives you a drug to help prevent altitude sickness during your ascent. How does this drug work?
Decreased pO2 as you ascend causes hyperventilation. This will cause respiratory alkalosis that can be prevented by prophylaxis with acetazolamide, which increases urinary excretion of HCO3 by inhibiting carbonic anhydrase.
A 61 year old man comes to your clinic because he has squamous cell carcinoma of the lung. He also has hypertension and lower extremity edema. Labs reveal an elevated calcium level. What drug could you prescribe to this patient to relieve him of his hypertension, hypercalcemia and edema? What drug do you need to remind him to not take with it?
Loop diuretics inhibit the Na/K/2Cl transporter which inhibits Ca2+ paracellular transport. This will help with his hypercalcemia. Inhibiting Na+ transport will increase diuresis and relieve him of his edema. Loop diuretics also stimulate PGE release and cause vasodilation, which will help with his HTN. Finally, you should tell him to stay away from NSAIDs because they will obliterate the vasodilatory effects of the loop diuretic.
What are the side effects some patients may experience when taking a loop diuretic?
“OH DANG”. Ototoxicity, hypokalemia, dehydration, allergy, nephritis and gout.
A 61 year old man comes to your clinic because he has squamous cell carcinoma of the lung. He also has hypertension and lower extremity edema. History reveals a sulfa allergy. Labs reveal an elevated calcium level. What drug could you prescribe to this patient to relieve him of his hypertension, hypercalcemia and edema?
Ethacrynic acid. It is a loop diuretic like Furosemide, but does not have sulfa in it and can be given to people with allergies.
A patient comes to see you with CHF and hypocalcemia. What is a good diuretic that could help with these two things?
Hydrochlorothiazide. These block the Na/Cl transporter, decreasing Na reabsorption and increasing diuresis. They also increase Ca2+ paracellular transport and will help get his Ca2+ levels back up.
A 72 year old female with CHF, hyperaldosteronism and hypokalemia comes to see you because of a 5 lb weight gain in the last two days. She normally takes Furosemide. What can you give her to help her out?
You might change her Furosemide to Spironolactone or Eplerenone to target the hyperaldosteronism as the source of fluid retention. You should also prescribe the K-sparing diuretics: Amiloride or Triampterine (block CCT Na+ channels to prevent K+ displacement into urine).
What effect do most diuretics have on potassium levels?
They cause hypokalemia because of increased tubular flow and increased Na delivery to CCT (Na uptake is linked to K secretion)
What diuretics cause acidemia?
Carbonic anhydrase inhibitors and K-sparing diuretics (prevents K+ AND H+ secretion)
How does hyperkalemia cause acidemia?
Cellular uptake of K that happens in hyperkalemia happens via K/H exchangers.
What diuretics cause alkalemia? How do they do this?
Loops and thiazides. 1) Volume depresseion -> ATII -> increased Na/H exchange at PCT -> increased HCO3 formation and reabsorption. 2) Hypokalemia causes K+ exit from cells via K/H exchanger
What serum markers will help you to determine if the ACE-I you prescribed to a patient with renal failure is working?
Increased creatinine due to decreased GFR from efferent arteriole dilation. Hyperkalemia from decreased tubular flow rate.
