Infection And Immunity Section2 Atz Vcu Med

Front 1

What are the 6 steps in viral multiplication?

Back 1

1- adsorption: binds to specific molecule on host cell

2- penetration

3- uncoating

4-synthesis

5-assembly

6- release- by exocytosis or cell lysis

Front 2

What do most DNA viruses use for early transcription?

Back 2

DNA-dependent RNA polymerase like RNA polymerase 2

Front 3

What are the inductor sites for the mucosal immune system?

Back 3

NALT-tonsils and adenoids

BALT

GALT-peyers patches, solitary lymphoid nodules, appendix

Front 4

What are the effector sites of the gut associated lymphoid tissue?

Back 4

the lamina propria and the epithelium

Front 5

What type of immune cells are in the gastrointestinal effector sites?

Back 5

the lamina propria contains pretty much activated immune cells of all sorts

-the epithelium contains CD8 cells

Front 6

What is the relevance of inductive and effector sites?

Back 6

If an immune cell is activated in an inductive site it is tagged with a certain integrin that acts as a homing beacon that signal it to go to the corresponding effector site

Front 7

What are the receptors that mucosal epithelial cells have to interact with bacteria?

Back 7

TLR's and NOD's. These then activate NFkB and that activates a wide array of pro-inflammatory mediators

Front 8

What determines if a bacteria in the gut will stimulate a dendritic cell to attack?

Back 8

Invasive bacteria will stimulate the dendritic cells to mature and induce inflammation.

Front 9

When an immune complex is co-crosslinked on a B cell what is the response?

Back 9

If it's a naive cell it's inhibitory, but if its a memory B cell it's activated to become a plasma cell

Front 10

What is the Original Antigenic Sin?

Back 10

It is where a pathogen is highly variable so the immune response becomes less and less effective, like the flu virus

Front 11

What are the roles of gamma:delta T cells, specifically the population with the V-gamma9:Vdelta2 T-cell receptor?

Back 11

This population of T-cells can recognize unique phosphoantigens, circulate directly to the infected tissue, and can also kill infected cells

Front 12

What are the roles of gamma:delta T cells, specifically the population with the V-gamma:Vdelta1 T-cell receptor?

Back 12

This population is found mainly in the gut and they react with a stress induced protein called MIC which can activate them and also activate NK cells

Front 13

What are some examples of inhibitory receptors on an NK cell ?

Back 13

NKG2A and KIR

Front 14

What is the activated receptor that all NK cells have and what does it bind to on an infected cell?

Back 14

NKG2D which binds to MIC on the infected cell

Front 15

Where does the majority of the damage from a viral infection come from?

Back 15

The host immune response which results in inflammatory cytokines and T cells tearing shi$ up

Front 16

What are the main causes of fever, fatigue, and drowsiness that you get with many acute viral infections?

Back 16

It's from the effects that IL-1, IL-6, IFN, and TNF have on the CNS

Front 17

What is the vaccine for smallpox?

Back 17

vaccinia

Front 18

What is the leading cause of infectious blindness?

Back 18

Keratitis from a recurrent infection of HSV

Front 19

At what age should you get the Varicella Zoster Shingles vaccine?

Back 19

over 50

Front 20

Which viral infection could cause Bells Palsy?

Back 20

Varicella Zoster Virus

Front 21

What is the reservoir for CMV latency?

Back 21

Myeloid cells like monocytes and macrophages throughout the body and it reactivates upon immunosuppression

Front 22

Let's say you had a transplant and the donor had a latent CMV infection that was transmitted with the organ and you get a primary CMV infection. When would you have the majority of complications of CMV after a transplant?

Back 22

Within the first 6 months

Front 23

What are some of the complications of getting a transplant that has CMV infection?

Back 23

Pneumonitis, hepatitis, and ulcers

Front 24

Which virus causes the severe fever and rash called Roseola infantum?

Back 24

herpes virus 6, which infects T cells and is probably latent in T cells

Front 25

What cancers are associated with Epstein-Barr infections?

Back 25

African Burkitts lymphoma

Hodgkins Lymphoma

Asian nasopharyngeal carcinoma

Front 26

Who is typically infected with Kaposi's sarcoma, and what does it cause?

Back 26

AIDS and transplant patients, as well as older dudes form the mediterranean

Causes skin lesions in most, and causes B-cell lymphoma in AIDS patients

Front 27

What is unique about the pox virus?

Back 27

It is brick shaped, and it is the only DNA virus that can replicate in the cytoplasm

Front 28

how does acyclovir work?

Back 28

it blocks viral DNA polymerase

Front 29

What is the name of the genital warts that you get from HPV and what strain do you get it from?

Back 29

They're called condyloma acuminatum, and they come from strains 6 and 11

Front 30

What are the warts that are associated with cancer and the strains involved?

Back 30

The condyloma planum, and it is strains 16 and 18

Front 31

Which antibody would you not see in a chronic hepatitis infection?

Back 31

anti-HBs

Front 32

What time period indicates that hepatitis is still acute?

Back 32

>6 months

Front 33

What is another virus other than HIV that uses reverse transciptase?

Back 33

Hepatitis B

Front 34

If someone is infected with Hepatitis D what else must they be infected with? Is hep D bad?

Back 34

hepatitis B

Hep D usually has a more serious prognosis and can lead to rapid liver failure and chronic active hepatitis and cirrhosis

Front 35

What are the two vaccines for polio? Which one is injected? Why is the oral vaccine better?

Back 35

Salk (injected) and the Sabin (live-attenuated)

The oral vaccine is better because it protects from GI infection, although both protect from CNS infection

Front 36

Although hepatitis E is mainly in developing countries and doesn't usually progress to a chronic state, to whom can the infection be life-threatening?

Back 36

prEgnant women

Front 37

What are some of the problems of congenital rubella?

Back 37

heart disease, cataracts, hepatitis, CNS damage, and deafness

Front 38

Is there hope for someone infected with hepatitis C?

Back 38

yes, antivirals have a 90% cure rate

Front 39

Whats different about when you can give a vaccine for rabies?

Back 39

You can give it after exposure since the incubation period is fairly long

Front 40

Of the 3 types of orthomyxovirus which two are significant human pathogens, and of those two which one has a bunch of subtypes?

Back 40

influenza types A and B are the human pathogens, and A is the one with 16 H and 9 N subtypes. B doesn't have an animal reservoir so it doesn't have a bunch of different H and N antigens

Front 41

What is the pathogenesis in a flu infection?

Back 41

the destruction of respiratory cells by T-cells, which can lead to serious pneumonia

Front 42

What percentage of the US population gets the flu every year, and how many die?

Back 42

5-20% catch the flu, and 36,000 die

Front 43

What is the disease you can get from cannibalism?

Back 43

Kuru, a prion infection

Front 44

What are the two types of creutzfeldt-jakob disease?

Back 44

Theres the variant type which you get from eating contaminated beef, and the normal type which is from an inherited germ line mutation of the PrP gene or something else

Front 45

What type of prion diseases are inherited?

Back 45

(CJD) Creutzfeldt-Jakob disease, (GSS) Gerstmann-Straussler-Schneiker disease and (FFI) Fatal familial insomnia

Front 46

What parts of the brain are affected by Creutzfeldt-Jakob disease?

Back 46

The cerebrum and the thalamus

Front 47

What parts of the brain are affected by Gerstmann-Straussler-Schneiker disease?

Back 47

the spinal cord and cerebellum

Front 48

What parts of the brain are affected by Kuru?

Back 48

the cerebellum

Front 49

What parts of the brain are affected by Fatal familial insomnia?

Back 49

The same as CJD, the cerebrum and thalamus

Front 50

What parts of the brain are affected by variant Creutzfeldt-Jakob disease that you get from eating contaminated meat?

Back 50

The thalamus and cerebellum

Front 51

How do prions cause disease?

Back 51

When they come in contact with other proteins they cause a alternative folding pattern that contains lots of beta-pleated sheets which makes the protein insoluble leading to deposits in the brain and rapid degeneration of neurons

Front 52

How does Trypanosoma brucei change its antigens so much?

Back 52

It uses gene conversion to constantly change the dominant surface glycoprotein

Front 53

What cytokine might be useful to treat leprosy?

Back 53

IFN-gamma, because it stimulates a TH-1 response and inhibits the TH-2 response. Also useful in leishmaniasis

Front 54

The transcription factor T-bet is needed for what cell line to be stimulated and what is the protective role of that cell line?

Back 54

The TH-1 cell line which protects against intracellular pathogens

Front 55

The transcription factor Gata-3 is needed for what cell line to be stimulated and what is the protective role of that cell line?

Back 55

The TH-2 cell line which protects against parasitic infections

Front 56

The transcription factor ROR-gamma t is needed for what cell line to be stimulated and what is the protective role of that cell line?

Back 56

The TH-17 cell line which protects against extracellular bacteria

Front 57

The transcription factor FoxP3 is needed for what cell line to be stimulated and what is the protective role of that cell line?

Back 57

The T-Reg cell line which is important for protecting against autoimmunity, but if theres too much T-Reg it can result in cancer

Front 58

How does CMV fool natural killer cells?

Back 58

It produces a MHC class I homolog since normal Class I inhibits the killing response

Front 59

How does interferon stop viral replication within a host cell?

Back 59

Interferon up regulates Pkr (protein kinase RNA) which is activated by binding to viral intermediate dsRNA, and once activated it phosphorylates translation initiation factor eIF2-alpha which shuts down translation and stops viral replication

Front 60

How does EBV Burkitt's lymphoma avoid being broken down?

Back 60

It only expresses EBNA-1 which is resistant to proteosomal degradation

Front 61

In someone with a antibody deficiency, such as X-linked agammaglobulinemia, which type of bacteria would they not be able to clear out of their system?

Back 61

extracellular, so they need monthly injections of antibodies

Front 62

what are some examples of adjuvants?

Back 62

there are particulate adjuvants like alum, and emulsifying adjuvants like MF59, and some even mimic the ligand that are specific for TLRs

Front 63

What are two markers that correlate with increased rate of T-cell loss and progression to AIDS?

Back 63

increased expression of HLA-DR and CD-38

Front 64

The severity of HIV-associated Neurologic Disease is strongly associated with the density of what?

Back 64

activated CNS macrophages which tells you there are most likely microglial cells and T-cells that are activated and all producing neurotoxic mediators like IL-6, TNF, and HIV proteins tat, GP120

Front 65

If you measure the viral load of HIV in a patient what can it tell you? What does the viral load not include?

Back 65

It can tell you about disease progression and treatment but it doesn't include any virus that may be latent

Front 66

If someone infected with HIV has less than a 500 CD4 count you can knock them out super easy, I'm talking TKO with PVC. What diseases are they susceptible to?

Back 66

Thrush, Kaposi's sarcoma, Oral hairy lekoplakia

Pneumonia that bacterial, Varicella zoster, Consumption (pulmonary TB)

Front 67

If someone with HIV has a CD4 count less than 200 they become a PRO at watching the PNEU HISTOry of COCCS show on TB channel 200. So what disease are they susceptible to?

Back 67

PML, Histoplasmosis, coccidomycosis, extrapulmonary TB, and PJP

Front 68

If you suspected someone of having a pneumocystis jiroveci pneumonia what would their signs be?

Back 68

Typically associated with CD4<200. Has hypoxia, increased LDH, dry cough, fever, dyspnea, and diffuse chest x-ray.

Front 69

If you suspected your patient of having toxoplasmosis how would you diagnose it?

Back 69

Do an MRI on the brain and there should be more than 2 enhancing lesions

Front 70

What treatment decreases the number of opportunistic infections is HIV patients?

Back 70

HAART aka cART

Highly Active AntiRetroviral Therapy

combination AntiRetroviral Therapy

Front 71

What would make you initiate HAART treatment on a patient?

Back 71

They have a history that makes you think AIDS

CD4 <350

pregnant

Front 72

What do most HIV patients die of now that we have antiretroviral treatment?

Back 72

Cancer, cardiovascular disease (CVD), and liver disease so it's important for physicians to screen for these things now

Front 73

What prophylaxis should you give an HIV patient with a CD4 count of <200, and prior pneumocystis pneumonia and thrush? When can you stop giving it to them?

Back 73

Bactrim, which is trimethroprim and sulfamethoxazole

You can stop when they are on effective HAART and their CD4 count is >200 and HIV viral load is <50 for 6 months

Front 74

If an HIV patient has a high CD4 count but has Hepatitis B should you start them on HAART?

Back 74

Yes, it is recommended regardless of CD4 count

Front 75

What are the pathogenic intestinal protozoa?

Back 75

Entamoeba histolytica (ameba)

Balatidium coli (ciliate)

Giardia lamblia (flagellate)

Cryptosporidium parvum (sporozoan)

Hint: intestinal Protozoa like to Eat Bile and GI Crunchies

Front 76

How would you acquire a Entamoeba histolytic infection, what are the symptoms, and how would you diagnose it?

Back 76

You get it from food or water contaminated with cysts and you can get amoebic dysentery with bloody diarrhea and hepatic amebiasis which leads to hepatomegaly and liver abscesses and flask shape ulcers in intestine. Diagnosis made by finding the cysts in feces

Front 77

What are the symptoms of Giardiasis?

Back 77

Fatty stools b/c it messes with fat absorption and fat soluble vitamin absorption, villous atrophy from it attaching to the villi, and pretty much lactose intolerant symptoms

Front 78

What happens in the course of a Cryptosporidium infection from ingestion to ejection?

Back 78

you ingest the cyst which will attach to the brush border and release sporozoites which are INTRACELLULAR PARASITES, and they enter the epithelial cells, divide, and the organism is passed in the feces. If your normal it's a short bought of diarrhea, if you have HIV it's very severe diarrhea with dehydration and electrolyte imbalance

Front 79

If a patient has diarrhea and you see a ciliated parasite in the stool what is it?

Back 79

Balantidium coli

Front 80

What are the symptoms of trichomonas?

Back 80

In females you have a yellow discharge and burning with a persistent vaginitis,

in males it's mostly asymptomatic

Front 81

What is "Blackwater Fever" and what causes it?

Back 81

it is a hemoglobinuria caused by malaria

Front 82

What can happen in an immunocompromised patient who gets Toxoplasmosis from their cat or uncooked meat?

Back 82

The bug disseminates to the tissues via blood and it divides in macrophages and disrupts them causing a focal area of necrosis. If antibodies are present it induces encystment in the muscles and when the host become immune incompetent again the bug comes out and can cause cerebral toxoplasmosis

Front 83

What are the symptoms of congenital toxoplasmosis?

Back 83

It can cause hydrocephaly, chorioretinitis, and calcification of the brain, or if it's a latent infection with late manifestations it can cause ocular toxoplasmosis or mental retardation

Front 84

What transfers Babesia microti and what does Babesiosis cause?

Back 84

Transferred by the ixodes tick and it infects RBC's causing them to lyse leading to anemia

Hint: Beware the Babes of Ixodes! They're really vampires, no pigment and they suck your blood!

Front 85

What transmits Leishmania and where in the human body does it replicate and what does it cause?

Back 85

Transmitted by Sand Flies and replicates in macrophages causing mucocutaneous and cutaneous lesions that extensively involve the face and nose are secondarily infected with bacteria leaving disfiguring scars

Front 86

What species causes cutaneous Leichmaniasis?

Back 86

Leishmania tropica

Front 87

What species causes mucocutaneous Leichmaniasis?

Back 87

Leishmania brasiliensis

Front 88

What species causes visceral Leishmaniasis, and what is it?

Back 88

Leichmania donovani,it is a chronic and potentially fatal infection of the liver, spleen, lymph nodes and bone marrow It can give the patient a swollen abdomen.

Hint: Don Kala Azar will cut you viscerally if you mention his big belly

Front 89

Where do you mainly see Leishmania infections?

Back 89

India, the Sudan, and Brazil, with several hundred cases in the mediterranean area and a few cases in north america

Front 90

What is the cool name for visceral Leichmaniasis?

Back 90

Kala Azar- infect reticuloendothelial system and is fatal in 90% of cases

Front 91

Trypanosome brucei is transferred by what and the infection leads to what kind of symptoms and what cytokines are produces in response to it?

Back 91

Tsetse fly transmits it. Leads to neurological symptoms like tremor, paralysis, sleepiness and even coma which is why it's called the african sleeping sickness. There is production of TNF and IL-1

Front 92

What does trypanosoma cruzi cause?

Back 92

Chagas disease

Front 93

What are the infective forms of T. cruzi

Back 93

promastigotes from the Triatoma bugs feces

Front 94

What are some of the symptoms of Chaga's disease?

Back 94

Heart block, apical aneurysm, cardiomegaly, and megacolon

Front 95

What does Nagleria fowleri cause?

Back 95

PAM! primary amoebic meningoencephalitis, which causes hemorrhagic necrosis in the brain and can cause death within 3-10 days of infection

Hint; it doesn't get any fowler than PAM!

Front 96

So if you suspect a patient has PAM, how do you think it got in, and how would you diagnose it?

Back 96

It probably got in through the olfactory bulb when the patient was swimming in a freshwater lake and you would diagnose it by finding the amoeba in the CSF

Front 97

What is an amoeba that is associated with keratitis due to poor contact lens hygiene?

Back 97

Acanthamoeba

Front 98

What diseases are caused by Acanthamoebae?

Back 98

Granulomatous Amebic Encephalitis. The ameba enter the body through the nose or cuts and the blood carries it to the brain where it can cause disorientation, headaches and seizures

Also amoebic keratitis which is associated with poor contact lens hygiene.

Hint: Acan for your contacts can help you avoid keratitis and from looking GAE

Front 99

Which of the protozoa can cause a swollen eye and conjunctivitis?

Back 99

Trypanosoma cruzi

Front 100

Which tapeworm is from beef and which one is from pork? Which one causes more damage to the host?

Back 100

Taenia saginatum is the beef tapeworm, Taenia solium is the pork tapeworm they are both ingested as the larval form, and solium causes more host damage

Front 101

What happens if you eat Taenia eggs?

Back 101

It causes cysticercosis where the eggs develop into larvae in the tissue and cause all kinds of disgusting bumps on the skin and can get into the brain causing neurocysticersosis and can cause epileptic like seizures and death

Front 102

How would you get Clonorchiasis?

Back 102

You would have to be in the far east and eat fresh water fish that is infected with Clonorchis sinensis which is a trematode of the bile ducts

Front 103

Which helminth can cause cholangiocarcinoma?

Back 103

Clonorchis sinensis which is the chinese liver fluke and it also causes hyperplasia and fatty degeneration of the liver

Front 104

What is the blood fluke that is a chronic parasitic helminth? Do you find it in the US?

Back 104

Schistosomiasis. The adult worms can live in humans for 30-40 years

Not found in the US because we don't have the snail that it lives in here

Front 105

Which of the Schistosoma causes urinary tract cancer and is found in the middle east?

Back 105

Schistosoma haematobium

Front 106

How would you get infected with Schistosomiasis?

Back 106

By being in waters that are infected. There is a cercariae form of the worm that can penetrate skin

Front 107

What can happen with the liver in a Schistosoma infection?

Back 107

The worm causes the formation of granulomas which can lead to fibrosis of the liver, portal hypertension(mansoni), ascites, and dilated veins

Front 108

What are the picornaviruses? And are the genetic characteristics of picornaviruses?

Back 108

Hep A, Coxsackie, Rhinovirus, Echovirus, Entrovirus, Poliovirus

They are positive sense ssRNA

Hint: Pickled corn gives my stomach the Hep A CREEPS

Front 109

What is the cause of swimmers itch, and where do you see it (geographically)?

Back 109

Shistosomes form bird feces are the cause. They penetrate the skin but remain as larvae causing severe itchiness and inflammation. Seen in the U.S

Front 110

What is the most common helminth in the US?

Back 110

Enterobius vermicularis, the pin worm

Front 111

What is the lifecycle of Necator? What symptoms to they cause?

Back 111

it burrows through your skin, gets into the blood stream and goes to the lungs where you cough it up, swallow it, and then it becomes an adult worm in the intestine secreting eggs

causing pneumonitis, severe anemia, and diarrhea

Front 112

How do you get round worm/ ascariasis, and what does it cause?

Back 112

You ingest the egg, the larvae migrate through the intestine up to the lung causing mechanical damage and molt causing a hypersensitivity pneumonitis, cough it up and swallow it, developes into adult in intestine causing obstruction and it can perforate them, they can also move to the liver and gall bladder

Front 113

What does cutaneous Larva migrans look like and what causes it?

Back 113

You get it form stepping on dog or cat crap, the larvae penetrate the skin but they remain as larvae since we're abnormal hosts and they make these "creeping eruptions" in the where it looks like a squiggly scar- it's called the tissue roundworm

Front 114

What does visceral Larva migrans look like and what causes it?

Back 114

This one is ingested eggs from Toxocara canid or cati and larvae develop and can into the brain, kidney, or liver.

Front 115

Let's say a little kid has appendicitis and you do an appendectomy and find its full of worms! what could cause this and would you be ok by just treating the child?

Back 115

It's caused by Enterobius vermicularis and you need to treat the whole family b/c it's extremely contagious

Front 116

What is the causative agent of elephantitis?

Back 116

Wuchereria bancrofti

Front 117

What is the causative agent of river blindness? What are some symptoms?

Back 117

The filarial worm Onchocerca volvulus- doesn't occur in the US

Symptoms include eosinophilia, lesions caused by the worms, and chronic infection of the subcutaneous tissues and eyes in which the worms produce toxins that lead to inflammation and blindness

Front 118

For dimorphic fungi what are the temps for the different structure?

Back 118

Yeast at body temp, mold at room temp

Front 119

What are the Superficial dermatophyte fungi? What's unique about them?

Back 119

Epidermophyton, Microsporum, and Trichophyton

They are the only pathogenic fungi with human to human spread

Hint: The Superficial fighters are Epider-man, Mexi-microsporum, and Trixie Trichophyton

Front 120

What are some signs of a subcutaneous fungal mycetoma infection? What is a typical treatment?

Back 120

Dematiaceous fungi, abscesses, and granules of varying color

Often need to amputate

Front 121

What are some signs of a subcutaneous fungal chromomycosis infection?

Back 121

caused by dematiaceous fungi found in tropical areas, cauliflower-like dermatitis, and yeast-like cells

Front 122

What are the fungi that cause Deep systemic fungal infections?

Back 122

Sporothrix schenckii, Coccidoides immitis, Paracoccidoides brasialensis, Histoplasma capsulatum, and Blastomycoses dermatitides

Hint: if you want to go deep on her you have to Spear her with you Coccidoides, and let your paracoccidoides make some histoplasma that you can Blast on her dermatitides

Front 123

Most of the deep systemic fungi are found in very specific geographical areas, except which one?

Back 123

Sporothrix

Front 124

What area of the US is Histoplasma common?

Back 124

Around Mississippi and the South East

Front 125

What area of the US is Blastomyces common?

Back 125

South east and upper mid west

Front 126

What area of the US is Coccidoides common?

Back 126

Around california and texas

Front 127

What area is Paracoccidoides common?

Back 127

South and central america

Front 128

What is the morphology of deep systemic fungi and specifically what features would you see for Blastomycosis, Coccidoides, and Paracoccidoides?

Back 128

They are all dimorphic

Blastomycoses is a wide based budding yeast

Coccidoides has the spherule with endospores

Paracoccidoides is the mariner wheel

Front 129

How do you get infected by Sporothrix schenkii, what does it cause?

Back 129

you get shanked by a rose or just get infected while gardening and it causes an ulcerated lesion or infectious arthritis if the joint space is inoculated

Front 130

What can an infection with blastomycosis cause?

Back 130

Pneumonia and these crazy looking skin lesions

Front 131

What does an infection with Coccidoides cause, how do you get it, and what's dangerous about it?

Back 131

It can cause fever and even have meningeal effects. You get it from breathing in spores from outdoor activity or dust storms, and it is dangerous to culture so notify the lab if you suspect it!

Front 132

What does and infection with Histoplasmosis cause, how do you get it, and who is at a greater risk, how could you diagnose it?

Back 132

Causes acute pulmonary disease, or chronic if the patient has COPD. You get it from bird and bat droppings, and HIV patients are susceptible

You can do a urine histoplasma antigen test to diagnose

Front 133

What are some sings of an allergic bronchopulmonary aspergillosis?

Back 133

Looks like asthma, you'll have infiltrates on chest x-ray and eosinophilia with increased serum IgE. Associated with Black mold

Front 134

What can invasive aspergillosis cause and what is the mechanism behind it?

Back 134

It can cause pulmonary disease and necrosis of tissue in the nose, palate, brain, and orbit through invasion of the vessels

Front 135

What are some features of zygomycosis? How do you differentiate it from a aspergillus infection?

Back 135

It causes similar symptoms to aspergillus causing ischemia and necrosis but it can be devastating within hours

Differentiate: It's always in the mold state, and the hyphae are wide and branch at weird angles

Front 136

What are some symptoms of a Cryptococcus? What is it's virulence factor?

Back 136

Sometimes a subclinical pneumonia but more that 50% have meningeal involvement and it is actually the most common cause of meningitis in HIV patients

Virulence factor is it's capsule

Front 137

What is secreted by mast cells in a type I hypersensitivity reaction?

Back 137

Tryptase, histamine (which is toxic to parasites), and TNF

Front 138

What are the lipid mediators that are mady by mast cells after activation and play an important role in late stage hypersensitivity?

Back 138

Prostaglandins (synthesis blocked by aspirin) and leukotrienes

Front 139

What mediator in eosinophils is toxic to parasites and mammalian cells and also causes histamine release from mast cells?

Back 139

Major basic protein MBP

Front 140

What are the opportunistic fungal infections?

Back 140

Aspergillosis, Cryptococcosis, zygomycosis, and candidiasis - usually not dimorphic

Front 141

What is Goodpasture's syndrome?

Back 141

It's where you have autoantibodies against the basement membranes of the kidney and lung. It is a type II hypersensitivity.

The autoantibodies go to pasture in the lung and kidney

Front 142

If you gave someone the wrong blood type what type of hypersensitivity reaction would they have?

Back 142

a type II- it involves antibodies binding to a cell duh

Front 143

When is a type III hypersensitivity reaction likely to cause the most problems?

Back 143

When you have an excess of antigen and little antibody. This forms small immune complexes which are muy peligroso since they can get lodged in the capillaries

Front 144

What are some examples of Type IV hypersensitivity? What is type IV also known as?

Back 144

PPD test (delayed type), poison ivy (contact), and celiac disease

Known as delayed type hypersensitivity

Front 145

What are the 3 types of solid organ rejection?

Back 145

hyperacute, acute, and chronic

Front 146

What are the 3 ways to develop anti-HLA antibodies?

Back 146

Pregnancy, multiple blood transfusion, and organ transplant

Front 147

What is hyper acute organ rejection?

Back 147

ABO antibodies attack an unmatched organ or pre-existing HLA class I antibodies attack. This rejection can happen before the recipient even leaves the OR- unpreventable

Front 148

What is acute organ rejection?

Back 148

recipient T-cells directly attack the organ. This can be avoided by doing a Mixed Lymphocyte Reaction in which you check if recipient lymphs proliferate when exposed to irradiated donor lymphs. This rejection develops over several days- preventable by using anti-T cell antibodies

Front 149

What is chronic organ rejection?

Back 149

This is an indirect recognition of donor HLA antigens which are from dendritic cells that are processed and presented which lead to anti-HLA antibodies that activate segs and monos initiating an inflammatory response causing gradual thickening of the vessel walls, lumen narrowing, and eventually ischemia and a very slow and painful death of the organ

Front 150

What is the most important action of Corticosteroids in preventing transplant rejection?

Back 150

it interferes with NF-kB which activates the transcription of cytokines

Front 151

How do rapamycin, tacrolimus and Cyclosporin A help in preventing transplant rejection? How long do patients need to be on them after transplant.

Back 151

They inhibit T cell activation.

For ev ver...for ev ver...for ev ver

Front 152

FTC, 3TC, and Tenovir are active against HIV and what else? What class of drug are they?

Back 152

Hep B

They are Nukes (Nucleoside Reverse transcriptase inhibitors)

Front 153

Abacavir is an anti-hiv drug, but before giving it you should test for HLA B57-01, why?

Back 153

If they have that marker they are at risk for hypersensitivity syndrome

Front 154

Efavirenz the non-nuke HIV drug has CNS side effects in 50% of people, based on this who could it really Eff up?

Back 154

fetuses, so don't give it to pregos

Front 155

The drugs Efavirenz, Rilpivirine, etravirine, Atripla, and complera are all part of what class?

Back 155

Non-nukes

Front 156

If an HIV drug ends in -navir what class does it belong to?

Back 156

The protease inhibitors

they will navir have protease in their town (french accent)

Front 157

If you prescribe a protease inhibitor what are some side effects you might see?

Back 157

huge number of drug interactions and fat accumulation giving the patient a buffalo hump of fat, also elevated LDL, triglycerides, and glucose intolerance

Front 158

What is special about the protease inhibitor drug Darunavir?

Back 158

It is the most difficult HIV drug to become resistant to

Hint: Darrun is irresistable, he's so hot right now

Front 159

If a drug ends in -tegravir what class is it?

Back 159

Integrase inhibitor

Hint: teg-ravir obviously inhibits in-teg-rase

Front 160

What is the one drug that inhibits entry of HIV by blocking CCR5?

Back 160

Mariviroc

Hint: Mari is a Huge credence fan, at the concerts she goes by Mari V. Iroc. In other words she's pretty white trash

Front 161

When treating HIV what drug combination do you use?

Back 161

Use 3 or more drugs with at least 1 very potent drug like a protease inhibitor, an non-nuke, or an integrase inhibitor

Front 162

What are some side effects of the antiviral drugs ganciclovir and valganciclovir?

Back 162

They are toxic to the bone marrow and can cause anemia and neutropenia, you also need to monitor CMV serum PCR with ganciclovir

Front 163

The antiviral pyrophosphate analog Foscarnet is given to a patient to block polymerase, what is this patient at risk of?

Back 163

Major renal toxicity

Front 164

You have a patient with Hep C and you give them simeprevir which is a protease inhibitor, what allergies do you need to worry about, and how is the drug metabolized?

Back 164

Sulfa allergies, and the drug is metabolized by CYP 3A4

Front 165

Another patient With Hep C is given the drug Sofosbuvir which is a NS5B inhibitor, How is this drug metabolized?

Back 165

via p-glycoprotein

Front 166

If you had a Hep B patient who was resistant to 3TC/FTC what drug could you give them?

Back 166

Entecavir, adefovir, or tenofovir

Hint: 3TC and FTC not cutting it, just grab your ten entech ades and VIR in another direction

Front 167

Zanamivir is a inhaled neuraminidase inhibitor that is effective against flu A and B, but what can happen if you give it to someone with asthma or bronchitis?

Back 167

Since it's an inhaled powder it can cause bronchospasm

Front 168

What is oseltamivir used for?

Back 168

The flu, it's also called Tamiflu

Front 169

What percent of infections with Polio have symptoms and what percent develop paralytic poliomyelitis?

Back 169

5% develop symptoms and 1% develop the flaccid paralysis of the lower limbs and respiratory paralysis

Front 170

What causes Autoimmune Polyendocrinopathy Candidiasis-Ectodermal Dystrophy (APECED)?

Back 170

The absence of the transcription factor AIRE which is important for negative selection. Without this the self reactive T-cells don't apoptose

-This is one way T cell tolerance fails: incomplete deletion

Remember the japanese dude in AIRE jordans, if he leaves the body goes APE shi (APECED)

Front 171

What happens when CTLA4 is not working properly?

Back 171

It is associated with the second signal needed to activate T-cells and helps keep them from binding to self. Without this the T-cells can become

Front 172

What are some examples of type II autoimmunity?

Back 172

diabetes Type II , AIHA, Myasthenia Gravis, Grave's

Hint: DAM G!, type II autoimmunity is 2 legit

Front 173

What are some examples of type III autoimmunity?

Back 173

mainly Lupus

Front 174

What are some examples of type IV autoimmunity?

Back 174

MS, Rheumatoid arthritis, Type I diabetes, Hashimoto's thyroiditis

Front 175

How could you test to see if an autoimmunity is caused by antibodies? What if you wanted to see if it was T-cell mediated?

Back 175

you can transfer serum into an animal or mom can transfer to baby and they cause the disease.

For T-cell you have to transfer the T-cells between inbred rodents to see a similar response

Front 176

If the body produces less soluble CTLA-4, which competes for CD28 on T-cells, what happens in the body?

Back 176

More T-cells can react to self increasing the susceptibility to Graves, Hashimoto's and type I diabetes and autoimmunity due to Treg cells which are activated by CTLA-4

Front 177

The disease Immune dysregulation, polyendocrinopathy, enteropathy, x-linked syndrome (IPEX) is caused by what?

Back 177

caused by a deficiency of FoxP3 transcription factor which is needed for Treg cells to be produced

Front 178

Which diseases are associated with an increase in Th-17 cells?

Back 178

Rheumatoid arthritis and Crohn's Disease

Front 179

Although deficiencies in AIRE, FoxP3, and CLTA-4 contribute to autoimmunity, what is the main genetic factor that affects a persons susceptibility to autoimmunity?

Back 179

HLA, it affects susceptibility by presenting specific subsets of peptides

Front 180

What are some non-genetic causes of auto-immunity?

Back 180

smoking, trauma (like to the eye), inflammation, and infections that result in molecular mimicry in which the Ig reacts with the bacteria and also host cell component

Front 181

What is epitope spreading that can occur in auto-immunity?

Back 181

As auto-immune disease progress more epitopes are exposed as cells are destroyed T-cells may recognize an epitope and escape apoptosis and then present the antigen, activating multiple B-cell clones

Front 182

What is the mechanism for metronidazole

Back 182

Rocacea, Anaerobic bacteria, Gardnerella

Trichomonas, Amebiasis, Giardia

It produces ROS to induce DNA damage, and also brown urine

The RAG TAG group that rides the Metro, where ROS is gonna do some serious DNA damage. Also theres a no drinking sign on the metro b/c riding it has an antabuse-like effect

Front 183

What is the mechanism of action of pyrimethamine? What should you combine with it?

Back 183

It disrupts folic acid. Combine with atovaquone which interferes with electron transfer

Front 184

What type of drugs inhibit fungal ergosterol synthesis? What is the mechanism and who should probably avoid them?

Back 184

the ones that end in -azole

Works by inhibiting cytochrome P450 enzyme

-potential for drug interactions. you should be careful with pregos

Front 185

Fluconazole is a good drug to use if you need access to what?

Back 185

Unlike itraconazole this one has access to the CNS, although there is some resistance because of excessive use of the drug

Front 186

What is the broadest spectrum drug in the azoles?

Back 186

Posaconazole

Front 187

If you treat someone with clotramizole what should you tell them, especially if they're a girl?

Back 187

it may interfere with contraceptive devices, and also that the lozenges are not for pregos

Front 188

How do the echinocandins drug that end in fungin work?

Back 188

They inhibit fungal cell wall synthesis

Front 189

How do the polyene drugs like amphotericin B and AmBisome work?

Back 189

it binds to ergosterol altering permeability and causing irreversible damage so it is actually fungicidal.

Combine w/ flucytosine to enhance effects

Front 190

What are some side effects of using amphotericin B?

Back 190

You get the Shake and Bakes (chills and fever) and also renal toxicity

Front 191

How does chloroquine work?

Back 191

It accumulates in RBCs and stops malarias shenanigans

Front 192

How does mefloquine work?

Back 192

it prevents the flow of malarial heme detoxification, and it makes you dizzy while doing it (high incidence of nervous system toxicity)