MSTP Questions Flashcards
You’ve been following a patient since yesterday for an infection. Preliminary lab results have come back showing that the patient is infected with a Gram (-) bacteria. Today, when you check on the patient, temp is 101 degrees F, HR is 104, RR is 24. Which of the following bacterial component most likely led to the patient’s vital signs? A. O antigen B. Core polysaccharide C. Lipid A D. Peptidoglycan
Answer: C. Lipid A Explanation: This question is asking “which part of LPS is toxic (leading to an inflammatory response) to humans?” This patient’s vital signs (fever, high heart rate and high respiratory rate) is consistent with SIRS criteria indicating an inflammatory response. Because you know the bacteria is Gram (-), you know that LPS is present. Lipid A (also known as endotoxin) is the component of LPS that is toxic to humans and can lead to fever at low concentration but shock at high concentration. If I had asked which component prevents clearance by complement the answer would have been (A) O antigen. Peptidoglycan makes up the cell wall and is thick in Gram (+) bacteria and thin in Gram (-) bacteria. If I had asked about a Gram (+) bacteria and asked “what gives the bacteria the darker staining color?” the answer would have been (D) peptidoglycan Lecture: 65a Introduction to Medical Microbiology Learning Objective: 4. Describe the consequences of lipopolysaccharide (endotoxin) for the human host.
You are treating a patient for Staph aureus infection with Penicillin. On day 2, the patient is not getting better so you switch to treating with Vancomycin and the patient improves tremendously. What is the most likely description of the bacterial strain infecting this patient? A. The bacteria has mutated Penicillin Binding Proteins B. The bacteria has altered its amino acid sequence of the peptides making up peptidoglycan C. The bacteria synthesizes beta-lactamase D. A or C E. A or B F. All of the above
Answer: D. A or C Explanation: This question is asking “what’s the mechanism of action of bacterial resistance to penicillin?” Bacteria can alter their penicillin binding proteins to prevent penicillin from acting on them, or they can produce beta-lactamase that chews up the penicillin drug. If the patient had been resistant to vancomycin instead and improved on penicillin, the answer would be (B), since vancomycin binds to the D-ala D-ala sequence on the peptide of peptidoglycan. Bacteria can prevent vancomycin binding by changing the sequence to D-ala D-lactate. Lecture: 65a Introduction to Medical Microbiology Learning Objective: Identify the unique structure of bacterial cell walls/envelopes, and how the differences in envelope structure distinguish Gram-positive from Gram-negative bacteria. (MKS1a)
You have a patient with breast cancer who is found to have metastasis to her lymph nodes (shown by biopsy) and other organs. What is the likely path that those cancer cells took through the lymph node (starting at the lymphatic vessels) to reach the blood to disseminate to other organs?
Answer: lymphatic vessels –> cortical afferent lymphatics –> subcapsular sinus –> trabecular sinus –> medullary sinus –> efferent lymphatics –> lymphatic vessels –> thoracic duct –> veins at the root of the neck (bloodstream) OR Lymphatic vessels –> cortical afferent lymphatics –> subcapsular sinus –> deep cortex endothelial venules (blood stream) Lecture:66a Cells and Tissues of the Immune System Learning Objective: 5. Describe the major histological features of lymph nodules, lymph nodes, the spleen, and the thymus gland, and their functional significance.
You have a trauma patient admitted to the hospital who undergoes splenectomy for a ruptured spleen due to failure of non-operative treatment. He should receive vaccines against what 3 pathogens before leaving the hospital?
Answer: (1) Neisseria meningitidis (2) Streptococcus pneumoniae (3) Haemophilus influenzae Explanation: The spleen is important in clearing encapsulated pathogens because the capsule resists phagocytosis (a mechanism relied upon by antigen presenting cells) and complement activation. After a splenectomy, this patient is at a higher risk for developing infections with N. meningitidis, S. pneumoniae, and H. influenza (among others but these are the most common), all of which have vaccines available to prevent infection. Sickle cell patients have functional asplenia due to damage caused by sickled red blood cells, so they should be treated similarly. Lecture: 67a Bacterial Structure and Function Learning Objective: 1. Compare and contrast the structure and function of capsules, flagella, and pili. (MKS1a, 1b)
You’re in a research lab and you want to overexpress a gene in E. coli. In order to do so, you subject the bacterial cells to a high voltage to make them competent and add a plasmid carrying your gene in solution. The bacterial cells then take up this plasmid and express your gene of interest. What is this process called? A. Transformation B. Transduction C. Conjugation
Answer: A. Transformation Explanation: Transformation is the uptake of DNA by competent bacterial cells. If the question had described the introduction of a virus that infects bacteria (bacteriophage) that injected DNA into your bacterial cells, then the answer would have been B. transduction. If the question had described co-culturing two bacterial strains and one developing a new feature or gene from the other, the answer would have been C. conjugation, which requires cell-to-cell contact to allow transfer of genetic material. Lecture: 68a Bacterial Physiology and Genetics Learning Objective: 5. Identify and describe the different mechanisms involved in genetic exchange in bacteria: transformation, transduction, and conjugation. (MKS1a, 1b)
You attend a back to school potluck dinner. Many brought dishes such as egg salad, chicken salad, and veggie dip. A few hours into the event you notice a large clearing of people who seem to be rushing home because they suddenly feel ‘sick.’ When you use the bathroom you hear several people vomiting in the stalls around you. What is the most likely cause of this sudden outbreak? a. Staph aureus toxic shock syndrome toxin 1 b. Staph aureus enterotoxins c. Staph aureus exfoliative toxin d. Streptococcal pyrogenic exotoxins e. Strep pyogenes M protein
Answer: B. Staph aureus enterotoxins Explanation: Staph aureus enterotoxin causes food poisoning that is especially known for its rapid onset. It acts on the neural receptors of the GI tract to stimulate the vomiting center, causing vomiting within 2-5 hours. Its characteristic in mayonnaise based dishes (egg salad, chicken salad, veggie dip) and would account for a large number of people who shared the same food suddenly feeling sick. If the vignette had been a young girl who started her period 2 days ago who presented with fever, hypotension and increased Creatinine or liver enzymes (indicating organ failure), the best answer would have been (A) Staph aureus toxic shock syndrome toxin 1. Strains producing this toxin often colonize the vagina and is associated with tampon use, especially when changed infrequently. Alternatively, consider a young child who had conjunctivitis 1 week ago who now presents with a rash. On physical exam, skin seems to be peeling off almost like after a sunburn at the site of the rash. In this case, the best answer would have been (C) Staph aureus exfoliative toxin. If instead, a patient presented with a widespread, erythematous (red) rash that spared the face, the answer would have been (D) Streptococcal pyrogenic exotoxins which are responsible for causing the rash of Scarlet Fever. A patient who presented with mitral regurgitation after an episode of streptococcal pharyngitis (strep throat) for which they didn’t receive antibiotics would be consistent with answer (E) Strep pyogenes M protein, as M protein can lead to Rheumatic Fever due to molecular mimicry with myosin of the heart. Lecture: 69a Gram Positive Bacteria I Learning Objective: 2. Identify and describe the pathogenesis, characteristics (presenting signs and symptoms), diagnosis, treatment, and prevention of the diseases caused by staphylococci, streptococci, and enterococci. (MKS 1d, 1e, 1f)
A child comes into your clinic with a fever and sore throat. On physical exam, you notice grey exudate around oropharynx (back of the throat). Which of the following is the mechanism of the toxin that caused this? A. ADP ribosylation of Elongation Factor 2 B. Increasing intracellular cAMP C. Cleaving MAPK D. Polymerizing actin
Answer: A. ADP ribosylation of Elongation Factor 2 Explanation: Corynebacterium diptheriae’s AB exotoxin causes necrosis of pharyngeal epithelial cells (which forms the grey exudate composed of cell debris in the oropharynx) by (A) ADP-ribosylating Elongation Factor 2 and inhibiting protein synthesis in those cells. Bacillus anthracis’s Edema Factor has adenylate cyclase activity that leads to (B) increased intracellular cAMP. Here you would have a patient who presents with dry cough and hemorrhagic mediastinitis, quickly followed by shortness of breath and hypotension with death quickly following. Bacillus anthracis’s Lethal Factor is a protease that (C) cleaves MAPK and causes tissue necrosis. Here you would have a patient who presents with a painless ulcer and necrotic eschar. Listeria monocytogenes’s protein ActA (D) polymerizes actin to move from cell to cell within the host, allowing it to evade the humoral immune response (antibodies can’t see it if it’s inside a host cell). Here you may have seen an elderly patient presenting with neck stiffness consistent with meningitis after eating unpasteurized milk or cheese. Lecture: 71a Gram Positive Bacteria II Learning Objective: 1. Describe the properties and virulence determinants of the Gram-positive bacilli. (MKS1b)
Which of the following distinguishes Clostridium tetani from Clostridium botulinum? A. C. tetani is spore forming B. C. tetani cleaves SNARE proteins C. C. tetani is an obligate anerobe D. C. tetani has an AB toxin E. C. tetani causes spastic paralysis
Answer: E. C. tetani causes spastic paralysis Explanation: This question is designed to draw your attention to the similarities between C. tetani and C. botulinum. Both are spore forming, obligate anaerobes. Both have AB toxins that cleave SNARE proteins, thus preventing the release of neurotransmitters. BUT C. tetani’s toxin cleaves SNARE proteins of Renshaw cells that release GABA and Glycine, 2 inhibitory neurotransmitters, thus it leads to a spastic paralysis. Whereas, C. botulinum cleaves SNARE proteins in motor neurons that release Ach, which is responsible for generating muscle contractions, thus it leads to a flaccid paralysis. Lecture: 72a Gram Positive Bacteria III and Gram Negative Bacteria I Learning Objective: 1. Describe the properties and virulence determinants of anaerobic bacteria, and members of the Actinomycetes and the Enterobacteriaceae. (MKS1b)
A child comes in with bloody diarrhea and decreased platelet count after a “hamburger” eating contest at school. What is the most likely mechanism of the toxin that caused this? A. Increased cAMP B. Increased cGMP C. Inhibits 60S ribosome subunit
Answer: C. Inhibits 60S ribosome subunit Explanation: Enterohemorrhagic E. coli (EHEC) causes bloody diarrhea and hemolytic uremic syndrome (decreased platelet count, RBC lysis, and kidney (glomerular) damage) mediated by Shiga-like toxin, which inhibits the 60 S ribosome subunit. If instead the patient had watery diarrhea after drinking cocktails in Mexico, you’d be thinking (A) increased cAMP, which is mediated by Heat Labile Toxin or (B) increased cGMP which is mediated by Heat Stable Toxin, both of which are toxins of Enterotoxigenic E. coli (ETEC). ETEC causes Traveler’s Diarrhea. Lecture: 72a Gram Positive Bacteria III and Gram Negative Bacteria I
Fill in the diagram of lymph flow below the best you can. (Hint: A, B and C represent the common path on which all lymph converges to reach the blood stream)
Explanation: If you can fill out this diagram, you have pretty well captured Dr. Cochard’s lecture. Don’t be discouraged if you didn’t fill this out completely. Use it as a study guide as you go back through Dr. Cochard’s lecture. This question is designed to be a tool just as much as a gauge of understanding.
Lecture: 70a Anatomy of the Lymphatic System
Learning Objective: 6. Identify the general route of lymph flow from any particular organ or region to blood in the veins of the neck, or identify lymph nodes that are directly downstream. With this knowledge, you can predict where cancer or infectious agents might spread if they enter lymphatic vessels.
Under each item in the top column, write the items of the bottom column that belong. (There will be multiple items under each top column item and many bottom column items will be used more than once). Hint: it may be helpful to write this on a piece of paper in front of you before flipping the card
Innate Immunity
Adaptive Immunity
Cell Mediated Immunity
Humoral Immunity
Protein recognition only
Lymphocyte
NK cells
T cells
B cells
T cells
B cells
Plasma cells
NK cells
Neutrophils
CD 19
CD56
CD3
CD4 (bonus: which MHC does this associate with?)
CD8 (bonus: which MHC does this associate with?)
Innate immunity: Neutrophils, NK cells
Adaptive immunity: T cells, B cells, plasma cells
Cell Mediated Immunity: T cells
Humoral Immunity: B cells, plasma cells
Protein recognition only: T cells
Lymphocytes: T cells, B cells, NK cells
T cells: CD3, CD4 (associate with MHC II), CD8 (associate with MHC I)
B cells: CD19
NK cells: CD56
Explanation: Neutrophils are the “first responders” of innate immunity. NK (CD56+) cells nonspecifically kill virally infected cells or tumor cells by secreting cytotoxic proteins as part of the innate immune response. T cells (CD3+, CD4+/CD8+) recognize protein and are highly specific thus they make up the adaptive immune response; they are best at fighting against intracellular bacteria, viruses, fungi and parasites through cell mediated immunity. B cells (CD19+) and plasma cells can recognize anything through antibodies (thus they are part of humoral immunity) and are highly specific (thus part of adaptive immunity); they are best at fighting against extracellular bacteria, viruses, and toxins.
Lecture: 73a Introduction to Immunology
Learning Objective: (2) Distinguish between innate and adaptive immunity (MKS1a) (3) Describe the difference between humoral (antibody-mediated) and cell-mediated immunity (MKS1a)
All of the following are capable of presenting antigens after processing pathogens via phagocytosis/endocytosis, EXCEPT:
- Macrophages
- Dendritic Cells
- B cells
- T cells
Answer: D. T Cells
Explanation: The professional antigen presenting cells (APC’s) are macrophages, dendritic cells and B cells. They recognize pathogens by pattern recognition and process them with phagocytosis then present the antigens to T cells, which will be activated in the presence of a second signal. This serves as the link between innate and adaptive immunity.
Lecture: 74a Innate Immunity
Learning Objective: 5. Describe the connection between innate immunity and adaptive immunity (MKS1a)
Which of the following best describes the steps of phagocytic cell recruitment? Bonus if you can identify the features shown in the image below.
- Margination -> Rolling -> Adhesion -> Diapedesis -> Chemotaxis
- Adhesion -> Margination -> Rolling -> Chemotaxis -> Diapedesis
- Margination -> Adhesion -> Rolling -> Diapedesis -> Chemotaxis
Answer: A. Margination -> Rolling -> Adhesion -> Diapedesis -> Chemotaxis
Explanation: First, white blood cells move to the periphery of blood flow due to vasodilation and slowed blood flow with increased vascular permeability (Margination). Then sialyl Lewis X (A) on neutrophils binds P-selectin or E-selectin (B) (the expression of which is induced by histamine, IL-1 and TNF-alpha (C)), which allows for slow rolling of the neutrophil on the vessel wall (Rolling). Then, Integrin (D) on neutrophils (induced by C5a and leukotriene (G)) binds to ICAM/VCAM (E) (cellular adhesion molecules induced by TNF-alpha and IL-1 (F)) on endothelium. Then neutrophil migration through the endothelium (Diapedesis) occurs followed by neutrophil movement into tissue towards chemokines (Chemotaxis).
Lecture: 77a Inflammation
Learning Objective: 3. Describe the steps involved in phagocytic cell recruitment and migration into sites of inflammation (MKS1a)
You have a patient with pneumonia. Which of the following findings would lead you to believe the infection is caused by Pseudomonas?
- The patient is a smoker
- The organism is not seen on gram stain
- The patient has a history of Cystic Fibrosis
Answer: C. The patient has a history of Cystic Fibrosis
Explanation: Pseudomonas colonizes aquatic environments and causes pneumonia in patients with CF and patients who have been hospitalized for an extended period of time, especially if they were mechanically ventilated. Legionella is associated with smokers, the elderly, alcoholics and patients with COPD and is poorly visualized on gram stain and requires silver staining. (Pseudomonas is visualized on gram stain, but the gram staining is light, thus its gram negative).
Lecture: 75a Gram Negative Bacteria II
Learning Objective: 2. Identify and describe the pathogenesis, characteristics (presenting signs and symptoms), diagnosis, treatment, and prevention of the diseases caused by Gram-positive bacilli. (MKS1b, 1d, 1e, 1f)
Match the associations listed in the bottom column with the microbes listed in the top column. (Each microbe will likely have multiple answers and many items may be used for more than one microbe).
Haemophilus influenzae
Bordetella pertussis
Brucella
Francisella tularensis
Pasteurella multocida
Dog or cat bite
Epiglottis
Facultative intracellular
Granulomas
Zoonotic
5% sheep’s blood agar
AB toxin
Increased cAMP
Otitis media
Farm animals
Rabbits
Answer:
Haemophilus influenzae: Epiglottis, Otitis media
Bordetella pertussis: AB toxin, Increased cAMP, filamentous hemagglutinin, Catarrhal phase and parosymal phase
Brucella: Farm animals, zoonotic, facultative intracellular
Francisella tularensis: Facultative intracellular, Granolomas, Zoonotic, Rabbits
Pasteurella multocida: Dog or cat bite, 5% sheep’s blood agar, zoonotic
Explanation:
Haemophilus influenzae can cause epiglottitis and otitis media
Bordetella pertussis causes whooping cough. It’s filamentous hemagglutinin attaches to the respiratory ciliated epithelium where it grows and releases AB toxin, which ribosylates Gi leading to an increase in cAMP. It includes 1-2 weeks of a catarrhal phase which involves conjunctival injection and lacrimation followed by 2wks-2mo of paroxysmal stage which involves the whooping cough with 3 mo of convalescent stage during which symptoms gradually resolve.
Brucella causes undulating fever, chills and anorexia and is transmitted by contact with farm animals, so it’s a zoonotic infection. It’s facultative intracellular and will grow in macrophages.
Francisella causes regional lymphadenopathy and granulomatous necrosis in lymph nodes. It is transmitted by direct contact with rabbits (so it’s zoonotic) or by tick bite. It’s facultative intracellular.
Pasteurella causes cellulitis after a dog or cat bite, so it is zoonotic. It grows on 5% Sheep’s blood agar and exhibits bipolar (safety pin) staining.
Lecture: 76a Gram Negative Bacteria III and Misc Bacteria
Learning Objective: 2. Identify and describe the pathogenesis, characteristics (presenting signs and symptoms), diagnosis, treatment, and prevention of the diseases caused byGram-negative bacterial pathogens, obligate intracellular bacteria, and spirochetes. (MKS1b, 1d, 1e, 1f)
You are joining the pathology lab as they perform autopsies. On one patient, you find a mass in the lung. When you look under the microscope at the specimen of the lung mass, you see caseating necrosis at the center with giant cells present. Which of these did this patient most likely have?
- Strep pneumoniae pneumonia
- Lung Cancer
- TB
- Viral pneumonia
Answer: C. TB
Explanation: This question wants you to quickly recognize a granuloma and think of its association with TB. You may also see words like “foamy macrophages,” “fibrous cuff,” “immune cells present, including monocytes, macrophages, neutrophils +/- lymphocytes” as descriptors for granuloma, but “central caseating necrosis” and “giant cells” should immediately make you think granuloma. Granuloma is a signature of TB and you would not see that with pneumonia caused by a virus or other bacterial strain. Lung cancer may present with a mass so often it’s important to distinguish a cancerous mass and granuloma on imaging (which is tricky, especially on chest X-ray). You may also see a lung granuloma with fungal causes of pneumonia and sarcoidosis.
Lecture: 78a Mycobacteria
Learning Objective: 2. Identify and describe the pathogenesis, characteristics, diagnosis, treatment, and prevention of the diseases caused by mycobacteria. (MKS1b, 1d, 1e, 1f)
Through FACS cell sorting, you identify a B cell with surface IgM and IgD. Which of the following processes has this B cell NOT gone through (identify all of the following that are correct)?
- Gene rearrangement of mu heavy chain
- Gene rearrangement of the light chain
- Clonal Deletion
- Receptor Editing
- Anergy
- Non-self Antigen Binding
- Isotype Switching
- Somatic Hypermutation
- Affinity Maturation
Answer: 3. Clonal deletion, 6. Non-self antigen binding, 7. Isotype switching, 8. Somatic Hypermutation, 9. Affinity maturation
Explanation: A B cell with surface IgM and IgD is a naïve B cell. It’s already undergone 1. Gene rearrangement of mu heavy chain to become a pre-B cell and 2. Gene rearrangement of the light chain to become an immature B cell. If it had undergone 3. Clonal deletion you wouldn’t have identified it with cell sorting (because it would have undergone apoptosis). It’s possible that this naïve B cell bound cell antigen in the lymphoid tissues and had to undergo 4. Receptor editing by VDJ recombinase so that it wouldn’t bind self. It’s also possible that this naïve B cell bound self antigen in the periphery and so underwent 5. Anergy to keep the immune system from attacking self tissues. This naïve B cell has not bound 6. non-self antigen or else it would have been costimulated by T cell CD40L to induce 7. Isotype Switching from IgM/IgD to IgA or IgG or IgE and 8. Somatic Hypermutation to generate variants that bind the non-self antigen more tightly that are then selected for their affinity by 9. Affinity Maturation. All four of these processes (binding non-self antigen, isotype switching, somatic hypermutation, and affinity maturation) convert a naïve B cell into a mature B cell with high affinity to its given antigen.
Lecture: 79a B Cell Differentiation
Learning Objective: 1. Diagram the steps in B cell development (MKS1a).
You sit down to eat at a table with a friend. You decide to clean your area before eating to stop the spread of germs, so you apply ethanol to the table and wipe it down. Your friend thinks you are being over-cautious and insists on eating before letting you clean his area too. The next day, you go to class and you text your friend to find out he is home sick and the Urgent Care doctor told him it was likely a virus. Which characteristic can you deduce to be true of this virus?
- It’s enveloped
- It’s non-enveloped
- It’s a DNA virus
- It’s an RNA virus
Answer: A. It’s enveloped
Explanation: Since your friend got sick and you didn’t you can assume the ethanol was successful in clearing the virus from your eating area. Ethanol can dry out (dessicate) the envelopes of viruses and ‘kill’ them. Non-enveloped viruses are less sensitive to dessciation so wiping the table with ethanol may not get rid of non-enveloped viruses. You don’t have enough information to determine what type of nucleic acid this virus has.
Lecture: 80a Viral Structure and Life Cycle
Learning Objective: 1. Define, categorize and explain essential features of viruses. (MKS1b)
You are encouraging patients to get their flu shot this year. Why won’t their flu shot from last year provide immunity for this year? (Choose the answer that is most correct)
- Antigenic Drift (Point mutations in influenza glycoproteins)
- Antigenic Drift (Reassortment of influenza genome segments)
- Antigenic Shift (Point mutations in influenza glycoproteins)
- Antigenic Shift (Reassortment of influenza genome segments)
Answer: A. Antigenic Drift (Point mutations in influenza glycoproteins)
Explanation: This question wants you to remember the terms Antigenic Drift and Antigenic Shift and to remember that Antigenic Drift causes epidemics (seasonal flu) and Antigenic Shift causes pandemics (Spanish Flu, H1N1). It also wants you to remember that Antigenic Drift occurs due to point mutations and Antigenic Shift occurs to genome segment reassortment.
Lecture: 81a Respiratory Viruses
Learning Objective: 1. Distinguish antigenic drift and antigenic shift and how it impacts influenza virus epidemiology. (MKS1b).
A 32 year old patient presents with a sudden fever and headache a few days after traveling abroad. Her occipital lymph nodes are palpable. A blood smear was obtained and shown below. Which correctly describes the life cycle or pathogenesis of this parasite?
- The reduviid bug bites the host and defecates near the wound
- The tsetse fly takes up trypomastigotes from the host bloodstream, and the epimastigote form then develops in the tsetse fly gut
- Caused by an insect vector found in the Americas
- Chronic infection leads to cardiomyopathy and megacolon
- Caused by the flagellate Trypanosoma cruzi
The correct answer is B. The patient most likely has East African sleeping sickness caused by Trypanosoma brucei rhodesiense. The blood smear shows trypomastigotes. The insect vector for T. brucei is the tsetse fly.
A, C, D, and E are incorrect. Trypanosoma cruzi causes Chagas disease, and the insect vector for T. cruzi is the reduviid bug, which is found in the Americas. The reduviid bug bites the host and defecates near the bite wound or a mucous membrane. Metacyclics can then contaminate the wound, penetrate a host cell, then rupture the cell to circulate in the blood stream as trypomastigotes. Chronic infection can lead to cardiomyopathy, megacolon and megaesophagus.
Learning objective: SM 101, 102, 104, or 105. Distinguish the mechanism of transmission and clinical features of African and American trypanosomiasis. (MSK1b)
