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Immuno Flashcards

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USMLE® Step 1 flashcards
1
Q

Dongenital neutropenia

A

Recurrent bacterial infections, e.g., gingivitis, otitis media, respiratory infections, and cellulitis due to Streptococcus and Staphylococcus

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2
Q

Lambert eaton vs myasthenia gravis

A

However, patients with LEMS typically have diminished deep tendon reflexes and weakness that is worse in the morning, with symptoms usually improving by the end of the day and muscle strength increasing with repea

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3
Q

will digeorge preent with oral candiadisis

A

yes and t cells dysfunction presents with oral candiasis, list the tc ell dysfunctions

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4
Q

how does disseminated mycobacterial infection present with

A

HSM/LAD and constitutional symotoms

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5
Q

discharging neck sinus congenital cause

A

brachial cleft cyst

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6
Q

wherd do you see cleft palate

A

chromosomal trisomies (e.g., Patau syndrome), 22q11.2 deletion syndrome, sonic hedgehog signaling defects, Pierre Robin sequence, or drug teratogenicity (e.g., isotretinoin, antiepileptics).

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7
Q

what is a complication of CVID

A

gastric adenocarcinoma

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8
Q

disseminated tb

A

il12 recetpro deficiency

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9
Q

is the nodules in strep pyogenes painful or painless

A

painless

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10
Q

which factor of GAS is responsible for necrotizing fascitis

A

hyaluronidase, another GAS virulence factor that facilitates tissue invas

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11
Q

which interleukin secreted by dendriti cells in viral infection

A

il28

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12
Q

a person with psoartic arthirits comes to you he takes adalilumab later there is decreased effectivety of treatment why

A

because neutralising antibodies form against tnf apha

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13
Q

patients with il12 deficieny are at risk of what infections

A

mycobacterium and salmonella disseminated

no cytotoxicity in cells infected with intracellular pathogens (

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14
Q

a women comes with tampon what complication can she have how would she present? TSST symtoms

A

tsss, associated with erythroderma This leads to the typical symptoms of high fever, rash, altered mental status, and shock. A

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15
Q

EXPlain maturation of B Cells and t cells

A

B cells get matured

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16
Q

what is affinity maturation

A

A process in which B cells interact with Th cells within the germinal center of secondary lymphoid tissue in order to secrete immunoglobulins with higher affinity for specific antigens.

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17
Q

2 mechanisms of affinity maturation

A

somatic hypermutation/clonal selection

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18
Q

what stimulates IGM secretion by plasma cells

A

IgM is also secreted by plasma cells (stimulated by IL-6)

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19
Q

where does t cell activation occur

A

paracortex

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20
Q

which protein required for HIV genome transcription

A

TAT gene

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21
Q

what codes for p24 and p17 gene on hiv

A

gag

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22
Q

what is rev for

A

he rev gene encodes a regulatory protein that acts to induce the transition from the early to the late phase of HIV gene expression

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23
Q

pathophys of giant cell arteritis

A

Giant cell arteritis (GCA) is thought to be caused by a cell-mediated immune response to endothelial injury that results in the activation of dendritic cells in the adventitia of blood vessel walls and the recruitment of T lymphocytes (Th1 and CD8+ cells) and monocytes. Monocytes differentiate into macrophages and giant cells that produce cytokines such as interleukin-6 (IL-6). IL-6 is an acute phase reactant that is highly expressed in GCA lesions and functions to sustain the inflammatory activity. IL-6 also mediates the systemic symptoms seen in GCA (e.g., fever, weight loss) and is responsible for this patient’s elevated ESR. Tocilizumab is an IL-6 receptor inhibitor shown to reduce relapses and lower the dose of glucocorticoids required to maintain disease remission.

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24
Q

pathophys of delayed hypersensitivity reaction

A

w

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25
Q

what is the hallmark of type 1 hypersensitivity reaction

A

eosnophilic infiltration

PAF promotoes that

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26
Q

type 3 hypersensitivity reaction damage caused by

A

neutrophils

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27
Q

a patient recieves a amoxicilin, differentiate between

serum sickness, delayed hypersensitivy, anaphylactic,dress syndrome,erythema multiforme

A

anaphylactic is sudden, SSLR is after 2 weeks low grade fever more common,DRESS,common in sulfonamides, minocycline, and vancomycin; occurs after 2-8 weeks

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28
Q

differentiate between serum sickness and sslr

A

Symptoms of true serum sickness are typically more severe (e.g., high-grade fever), with an acute or subacute onset, while symptoms of SSLR are usually less severe (e.g., low-grade fever), with a more insidious onset.

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29
Q

a baby is born with these vitals 172/min, respirations are 58/min, and blood pressure is 74/45 mm and IL6 what does she have

A

neonatal sepsis

30
Q

function of macrophage csf

A

Also has a role in bone remodeling by activating precursor osteoclasts to undergo further differentiation.

31
Q

a person has Hiv infection and developes acute meningoencephalitis

A

which cells are infected

32
Q

why patients with CGD only get infected by catalase +ve organism

A

failure of superoxide free radicals due to NADPH oxidase deficiency, leads to bacteria to produce h2o2 as metabolic waste this h2o2 kills the bacteria however catalase bacteria digest h2o2

33
Q

tuberculousus skin test is in hiv is limited by

A

anergy

34
Q

give a review of all HIV associated conditions

A

w

35
Q

what is the mcc of cerebral abscee in Hiv

A

toxoplasmosis

36
Q

isoproisas

A

Watery diarrhea, abdominal pains, fever, weight loss

37
Q

hiv associated encephalopathy

A 
Subcortical dementia (memory loss, depression, movement disorders) 
Progression to severe neurologic deficits (impaired vigilance, aphasia, gait disturbances)
38
Q

HIV associated using ring enhancing lesions

A

if rapid progressive=pml
if multiple rings=toxo
if single ring-lymphoma

39
Q

explain pathophysiological changes in LAD1 deficiency

A

Leukocyte adhesion deficiency type 1 (LAD1) is caused by an autosomal recessive defect in CD18 (beta-2 integrin), which prevents leukocytes from migrating to the site of infection. As a result, patients have recurrent mucocutaneous infections that can progress to sepsis and a characteristic absence of pus or neutrophils at the site of infection. Other features of the condition include poor wound healing with large skin ulcers, delayed separation of the umbilical cord due to omphalitis, and severe periodontitis/gingivitis. A very high neutrophil count (as high as 100,000/mm3 during active infection) is seen because neutrophil activation and recruitment of neutrophils from the non-circulating pool occurs. However, neutrophils are unable to extravasate into tissues, causing pooling within the circulation.

ADDITIONAL INFORMATION

40
Q

which immunodeficiency can cause gi obstruction/urinary retention

A

e GI obstruction and urinary retention caused by granulomas.
NADPH oxidase

41
Q

which disease can lead to systemic candiadisis

A

anything causing neutropenia( precepitates with candida, asperigollus mucor and rhizophus
chediak hegashi

42
Q

cheidak hegashi what cancer can it cause

A

Hemophagocytic lymphohistiocytosis (can occur in the accelerated phase and is potentially fatal)

43
Q

explain formation of granulomas in tb

A

After replication, the following sequence in mycobacterial infection is transportation of bacterial peptides to the regional lymph nodes, migration of T-helper cells to the lungs, production of interferon-gamma by T-helper cells, and formation of a nodular tubercle in the lung.

TUBERCULOSIS

44
Q

cutaneus b cell lymphoma vs sezary

A

cutaneous B-cell lymphoma.confiend to skin non puritic and localised

45
Q

immune changes due to aging

A

Impaired immune response and regulation of inflammation predispose individuals to recurrent infection, impaired wound healing, malignancy, and autoimmune disease.
Decreased antibody and cell-mediated immune responses to a new antigen
A decline in the counts of most subsets of B cells and T cells (exception: memory T-cell and memory B-cell counts increase)
Decreased affinity of antibodies for new antigens
Decrease in the variety of B-cell receptors for antigens
Increase in the proportion of monoclonal cell lines
Impaired affinity maturation and impaired V(D)J recombination
Total immunoglobulin level remains the same.
Macrophage and neutrophil co

46
Q

why do b cells decrease in aging

A

microenvironment of the bone marrow and impaired responsiveness to growth-stimulating cytokines.

47
Q

why autoimmune disease common in elderly

A

synthesis of Treg cells decreases and the synthesis of autoantibodies increases.

48
Q

mjtation in Mutations in the Fas receptor (CD95 receptor)

A

e Fas ligand can cause autoimmune lymphoproliferative syndrome (ALPS). Fas-FasL signaling is essential for proper thymic medullary negative selection, whereby caspases are activated, initiating apoptosis of T lymphocytes. Defects in this pathway lead to proliferation of antigen-specific, autoreactive lymphocyte lineages and result in hepatomegaly, generalized lymphadenopathy, and splenomegaly as well. AUtoimmune cytopenia common manifestation

49
Q

langerhans cell histocytosis

A

Langerhans cells are macrophages of the skin and lymphoid tissue that present antigens to other cells of the immune system. Clonal proliferation of these cells results in Langerhans cell histiocytosis, a condition that causes lytic skull lesions and a skin rash, as seen in this patient. Recurrent otitis media can occur if the mastoid process is involved. Langerhans cells express CD1a, which mediates antigen presentation, and S-100, which is used as a tumor marker for cells derived from the neural crest.

50
Q

which biochemical process impaired in osteogensis imperfecta

A

glycosylation

51
Q

how do you diffeentiate between phenylalanine hydroxlase deficiency and tyrosinase deficiency

A

neurological defects and msuty odoru, high phenylaanine inhibti tyrosinase

52
Q

how do you diffeentiate between phenylalanine hydroxlase deficiency and tyrosinase deficiency

A

neurological defects and msuty odoru, high phenylaanine inhibti tyrosinase

53
Q

common complaint in patient with gullian barre syndrome

A

. Finally, patients with GBS often complain of facial and/or oropharyngeal weakness, which is absent in this patien

54
Q

when does charcot marie tooth disease manifest

A

3rd decade of life

55
Q

hypothyroid neuropathy

A

hypothyroid neuropathy is a symmetric loss of sensation and deep tendon reflexes in the distal extremities, resulting in numbness, tingling, and painful dysesthesias, which is seen in this patient. Patients with hypothyroidism also often complain of constipation. However, weakness is rarely seen a

56
Q

vincristine medication manifests with what cause of syndrome

A

typically mixed sensory and motor Over time, symptoms progress to muscle weakness that is more marked in the hands and feet

57
Q

vincristine neuropathy s due to

A

disturbance in axoplasmic neuronal transport.

58
Q

toxic metabolite of cyclophosphamide

A

acrolein

59
Q

a person has severe oral mucositis what i would give him/her

A

palifmerin

60
Q

ototoxicity of chemotherapetic

A

dose dependant

61
Q

complications of vincristine

A

onstipation, paralytic ileus, and neurotoxicity

62
Q

which phase vincristine acts on

A

g2-m why?

inhibits mitosis or microtiubule formation

63
Q

what is hand food syndrome where do you see it

A

Erythema and swelling of the palms and soles with pain, paresthesias, and desquamation of skin. It typically occurs as an adverse effect of antineoplastic drugs such as 5-fluorouracil, capecitabine, cytarabine, doxorubicin, and docetaxel.

64
Q

how does proteosome inhibtor work

A

When the ubiquitin-proteasome system is inhibited by proteasome inhibitors such as bortezomib, misfolded proteins that have undergone ubiquitination are unable to be degraded in the proteasome. This leads to cell damage and death through a variety of mechanisms, including an accumulation of apoptotic proteins such as p53.

65
Q

which drug cross links purine bases

A

Alkylating agents such as cyclophosphamide and ifosfamide impair DNA replication by crosslinking DNA at the N7 site on guanine.

66
Q

what does methotrexate inhibit

A

also inhibits AICAR transformylase leading to increased intracellular concentrations of adenosine and adenine nucleotides.

67
Q

which phase growth factor inhibitors work on

A

g1 phase because thats where rna. cell organelles are grown

68
Q

side effect of etoposide and irotecan

A

alopecia and diarrhea

69
Q

what is the difference between topoisomerase 1 and 2

A

topoisomerase 1 cuts one strand however 2 cuts 2 strands

70
Q

why if i give folic acid with 5FU will increase its toxicity

A

5-FU can bind to thymidylate synthase only in the presence of methylene-tetrahydrofolate, which a derivative of folic acid and a cofactor of thymidylate synthase. Therefore, the administration of folic acid concurrently with 5-FU or capecitabine augments the effects of these drugs by increasing their binding to thymidylate synthase and simultaneously increases the risk of adverse effects (e.g., myelotoxicity).

usmle (38 decks)

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