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Foundations Exam 2 > missed questions, review > Flashcards

missed questions, review Flashcards

1
Q

eosinophils contribute to parasite defense via…..

A

immediate hypersensitivity

via IgE/mast cell system: stimulated mast cells chemoattract eosinophils

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2
Q

neutrophilia is characteristic of _______ infections
eosinophilia is characteristic of _______ infections

A

neutrophilia = bacterial infections
eosinophilia = parasitic infections

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3
Q

burn blister is an example of _____ inflammation

A

serous inflammation - produces serum-like exudate due to increased vascular permeability

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4
Q

fat necrosis occurs when….

A

pancreatic acinar cells release lipase

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5
Q

antigenic vs immunogenic

A

antigenic: stimulates production of and binds antibodies

immunogenic: induces immune response

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6
Q

if a person received a tetanus booster 10 years ago and comes to your office today with a deep cut, what should they be given?

A

only tetanus toxoid (booster) to stimulate immune cells

they do not need immunoglobins because they still have memory cells that will quickly jump into action

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7
Q

_____ rejection can occur weeks/months/years after transplant, and is characterized by CD8+ T cell infiltration

bonus: how do you treat it?

A

acute cellular rejection - treat with corticosteroids

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8
Q

what are characteristic features of chronic rejection

A

interstitial fibrosis and blood vessel thickening

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9
Q

what is characteristic of hyperacute rejection (within minutes)

A

fibrinoid necrosis and thrombosis

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10
Q

T/F: passive transfer (adoptive immunity) of sensitized T cells does not produce protection

A

passive transfer (adoptive immunity) of sensitized T cells does NOT produce protection ALONE (need to be activated by MHC)

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11
Q

which of these is NOT a mechanism of Tregs?
a. central tolerance
b. cytolysis
c. inhibitory cytokines
d. metabolic disruption
e. targeting of DC

A

central tolerance is mediated by medullary thymic epithelial cells

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12
Q

stratum germinativum renews
a. epidermis
b. dermis
c. both

A

a. epidermis

amplification pools are key

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13
Q

which renews faster, thick or thin skin?

A

thick

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14
Q

liquefactive necrosis

A

dead tissue transforms into liquid, viscous mass (cells are dying and releasing digestive enzymes)

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15
Q

why can burns be life-threatening?

A

loss of fluids and subsequent dehydration

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16
Q

classically activated macrophages (M1) vs alternatively activated macrophages (M2)

A

M1 (via IFN-y) —> microbicidal actions (ROS, NO, lysosomal enzymes), inflammation (IL-1, IL-12, IL-23)

M2 (via IL-13, IL-14) —> anti-inflammatory (IL-10, TGFb), wound repair/fibrosis (TGFb)

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17
Q

where do the antibodies come from in the classical complement pathway (given that innate immunity occurs before active immunity stimulation)?

A

antibodies can be poly reactive IgM from marginal zone B cells, or memory Ig, or low affinity IgG made early in adaptive response (goes back to activate more complement)

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18
Q

explain (basically) cross-presentation

A

any time virus/endogenous antigen does not infect/trigger DC: MHC II converted to MHC I (exogenous antigens are taken up, now they are intercellular, and can be presented on MHC I) —> T cells activated via MHC I

can happen on any cell type

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19
Q

T/F: all antibodies start out as membrane bound BCR

A

TRUE

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20
Q

which are more diverse BCR or TCR

A

TCR !

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21
Q

which require processed antigens, TCR or BCR?

A

TCR - recognize processed antigen via MHC I or MHC II

BCR - recognize unprocessed/whole antigen

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22
Q

which of these is NOT a common adverse side effect of glucocorticoids?
a. osteoporosis
b. hypotension
c. muscle wasting
d. redistribution of fat
e. bacterial and opportunistic infections

A

b. hypotension

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23
Q

aspirin (acetylsalicylic acid) is cardio protective because:
a. aspirin binds irreversibly to COX-1 in platelets
b. aspirin binds selectively to COX-1 compared to COX-2
c. aspirin on promotes the formation of TXA2
d. aspirin inhibits production of PGI2

A

a. aspirin binds irreversibly to COX-1 in platelets

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24
Q

Pt is a 52yo M presenting with blisters on the back of his hands, which erupted shortly after tennis season began. Pt denies exposure to poison ivy or use of new soaps. SHx includes moderate alcohol intake. Urine sample was red-orange, and 24-hour urine showed elevated uroporphyrin. What does this indicate?

A

Porphyria cutanea tarda: deficiency in UROD (uroporphyrinogen decarboxylase), essentially acquired

hints: blisters, ethanol intake, exposure to sunlight (tennis), red-orange urine, uroporphyrin in urine

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25
Q

what is the committed step of heme synthesis?

A

the first step: ALAS condenses glycine + succinyl CoA into delta-aminolevulinic acid (ALA)

*remember that ALAS requires pyridoxal phosphate (vitamin B6) as a coenzyme

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26
Q

aminolevulinic acid synthase activity:
a. catalyzes rate-limiting reaction in porphyrin biosynthesis
b. is strongly inhibited by lead
c. is decreased in the liver in individuals treated with barbiturates
d. occurs in the cytosol

A

aminolevulinic acid synthase activity:
a. catalyzes rate-limiting reaction in porphyrin biosynthesis

*remember that first step of heme synthesis is the committed step, catalyzed by ALAS

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27
Q

which porphyria is often acquired?

A

PCT: deficiency in hepatic enzyme UROD (uroporphyrinogen decarboxylase), presents with skin fragility and bullae on sun-exposed sun

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28
Q

Pt. is 29yo F admitted to the ICU 3w after bariatric surgery with decreased level of consciousness, psychomotor agitation, confusion, abnormal pain, and proximal tetraparesis. Urine same appeared dark red and showed high levels of delta-aminolevulinic acid and porphobilinogen. What is likely diagnosis?

A

AIP (acute intermittent porphyria): deficiency in hepatic PBGD

hints: dark red urine, neuropathy (proximal tetraparesis), delta-aminolevulinic acid and porphobilinogen in urine, altered mental state - likely that surgery triggered the attack

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29
Q

which two enzymes of heme synthesis pathway does lead inhibit?

A

ALAD (ALA Dehydratase) and ferrochelatase

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30
Q

Pt is 35yo F admitted with fatigue, weight loss, and fever. PE was remarkable for pallor of nail beds and conjuntiva. CBC indicated microcytic and hypochromic anemia, bone marrow imaging revealed ring sideroblasts. PMHx includes tuberculosis, being treated with isoniazid. The reduction of what enzyme explains this anemia?

A

ALAS (ALA synthase)

remember that isoniazid causes vitamin B6 deficiency, which is required as a cofactor for ALAS

31
Q

a blood donor is Type O - to what recipient blood types can they give plasma? Explain.

A

only to other Type O, because donor plasma contains anti-A and anti-B Ab

32
Q

A mother with B/B, Rh-/- has a greater risk of having an immune response to their B/B, Rh+/- child than if she were O/O, Rh-/-. Explain this discrepancy

A

if mother was O/O and child was B/B, anti-B antibodies would cause cell lysis of any fetal cells that reach maternal blood before anti-Rh+ antibodies could form

if mother and child were the same major blood type (such as B/B, B/B), fetal RBC will be able to reach maternal blood and anti-Rh antibodies will form

33
Q

what is the goal of indirect vs direct anti-globulin test?

A

indirect: look for antibodies in serum

direct: look at RBC for antibodies attached

34
Q

Which 2 immunosuppressants, esprcially when in combination with glucocorticoids, can cause diabetes?

A

Cyclosporine and tacrolimus

35
Q

For each of the follpwing therapies, name what blood disorder they are used for:
a. Phlebotomy
b. Sunscreen
c. Hemin
d. chelators
e. Vitamin B6

A

A. Phlebotomy - PCT
B. Sunscreen - cuteaneous symptoms of porphryia seen in EPP/PCT
C. hemin - AIP
D. Chelators - lead
E. Vitamin B6 - X-linked sideroblastic anemia due to ALAS2 deficiency

36
Q

After a blood transfusion, a patient soon begins complaining of difficulty breathing, chills, and pain, and dark-colored urine is seen. This is most likely due to:
A. Mediator release from mast cells
B. Complement-mediated cell lysis

A

B. Complement-mediated cell lysis

ABO INCOMPATIBILITY - TYPE II HYPERSENSITIVITY, DUE TO NATURAL ANTIBODIES

37
Q

immunity provided by complement is:
a. innate and humoral
b. innate and cell-mediated
c. acquired and humoral
d. acquired and cell-mediated

A

a. innate and humoral

humoral - via soluble proteins

38
Q

a Cluster of Differentiation (CD) was originally defined as a set of…

A

antibodies that will bind to epitopes on the same antigen

39
Q

what process is most responsible for feelings of muscle/joint pain, fever, fatigue, loss of appetite, and malaise that accompanies viral infections?

A

secretion of cytokines by monocytes and T cells - esp interferon !

40
Q

what class of antibodies binds to ABO antigens?

A

IgM

41
Q

the open circulation in the spleen occurs where blood cells pass from:
a. trabecular arteries into central arteries
b. capillaries into cords
c. sinuses into cords
d. sinuses into veins

A

capillaries —> cords —> endothelial slits —> sinuses

42
Q

chronic inflammation is characterized by tissue infiltration by…

A

mononuclear cells - macrophages and lymphocytes

[acute inflammation - neutrophil infiltration]

43
Q

a poison ivy rash is a type IV (cell-mediated) hypersensitivity due to:
a. granuloma formation in tissue
b. activation of CD4+ T cells

A

activation of CD4+ T cells - remember Type IV hypersensitivity mediated by TH1

44
Q

a patient who receives equine antiserum for the second time develops serum sickness, in which complement is activation - what products of activated complement bind to receptors on Mast cells and stimulate release of inflammatory mediators?
a. C3a and C5a
b. C3b and C5b
c. C1qrs

A

a. C3a and C5a

bind receptors on Mast cells, stimulate release of inflammatory mediators

45
Q

Six months after transplantation, a transplanted kidney shows signs of acute rejection. What immune mechanism is primarily responsible?
a. deposition of immune complexes in blood vessels of the new kidney
b. production of IgG antibodies to minor histocompatibility antigens of the transplant
c. synthesis of anti-ABO antibodies to antigens present in the transplant but not donor tissue
d. a cell-mediated immune response to donor MHC antigens not present in the recipient

A

d. a cell-mediated immune response to donor MHC antigens not present in the recipient

acute rejection is CELL MEDIATED (T cells !!)

46
Q

3 days after a TB test, there is induration and erythema at the site of infection, giving a positive test result - which interpretation is most accurate?
a. the patient made a humoral immune response to antigens in tuberculin
b. the patient has made a cell-mediated immune response to antigens in tuberculin

A

delayed hypersensitivity = T CELL mediated

the patients has made a CELL-MEDIATED response to antigens in tuberculin

47
Q

a patient with Goodpasture’s syndrome has deposits of C3b of basement membranes of lung and kidney epithelia - which process stimulated this C3b deposition?
a. activation of macrophages by interferon-gamma
b. activation of neutrophils by C3a and C5a
c. binding of IgG to antigen
d. binding of IgG to macrophage Fc receptors

A

c. binding of IgG to antigen

Type II hypersensitivity —> classical complement pathway activated by antigen/antibody complex

48
Q

will a patient with A- blood who has never been pregnant or received a transfusion have antibodies against Rh?

A

NO - you need to be exposed to Rh to have antibodies against it

49
Q

respiratory allergies related to a persons occupation (near daily exposure, but symptoms go away on the weekends) are most likely what kind of hypersensitivity

A

Type III hypersensitivity

50
Q

how does positive selection ensure that the right T cells survive?

A

positive selection generates survival/proliferation signals

51
Q

if a patient lacked the receptor for interferon-gamma, which of these processes would be most severely defective?
a. phagocytosis of bacteria by neutrophils
b. mast-cell degranulation in response to allergens
c. killing of intracelular pathogens which require cell-mediated immunity for effective control

A

c. killing of intracelular pathogens which require cell-mediated immunity for effective control

TH1 produce IFN-gamma

52
Q

which of these processes would be most directly affected by absence of beta2-microglobulin?
a. positive selection of CD3+CD8+ cells in the thymus
b. phagocytosis of antigen by DC
c. antigen presentation to helper T
d. antibody response to bacterial polysaccharides

A

a. positive selection of CD3+CD8+ cells in the thymus

beta2-microglobulin is part of MHC I

no MHC I = no positive selection for CTL in the thymus

53
Q

a 55yo women shows signs of transplant rejection 2 hours following surgery - which mechanism is the cause?
a. antibodies in donor tissue recognizing recipient antigens
b. T cells in recipient recognize donor antigens
c. antibodies in recipient circulation recognizing donor antigens

A

c. antibodies in recipient circulation recognizing donor antigens

2 hours later = hyperacute rejection (<48 hours) —> antibody mediated

[acute rejection is T cell mediated]

54
Q

A woman’s serum is tested in a cross-match assay with her husband’s lymphocytes and is found to have antibody specific for his HLA antigens. What is the most likely explanation?
a. the patient and her husband have children
b. the patient and her husband are ABO incompatible
c. the patient has naturally occurring antibodies
d. the patient has had a prior bone marrow transplant

A

a. the patient and her husband have children

during pregnancy, mother can become sensitized to child’s HLA that were paternally inherited

55
Q

which of these are LEAST likely to be involved in termination of immune response?
a. CTLA-4
b. Fas ligand
c. CD28
d. B cell Ig Fc receptors
e. anti-idiotypic antibodies

A

CD28 - activating signal for T cells that binds B7 (on DC cells)

56
Q

At birth, a newborn tests positive for HbF, HbA, and Hb Bart’s and is diagnosed with thalassemia. At the 8 month follow-up visit, Hb Barts is not detected. What does this indicate?
a. incomplete penetrance of gene expression
b. switch from gamma to beta globin production
c. baby has a transient, neonatal form of thalassemia
d. HbF production has increased since birth

A

b. switch from gamma globin to beta globin

HbF = alpha2, gamma2

after birth gene expression changes from gamma to beta

57
Q

for each of these, indicate whether they induce T or R state of hemoglobin:
a. acidosis
b. alkalosis
c. 2,3 BPG
d. O2
e. CO2
f. NO

A

T state (lower affinity) induced by: acidosis (lower pH), 2,3BPG, CO2

R state (higher affinity) induced by: alkalosis (higher pH), O2, NO

58
Q

what is HbA1c caused by

A

hyperglycemia (such as with diabetes) —> increased glycation of hemoglobin —> HbA1c

HbA1c is good measure of blood glucose over time

59
Q

which would be a good target to induce in gene therapy for sickle cell patients?
a. alpha1 subunit gene
b. alpha2 subunit gene
c. gamma subunit gene
d. beta subunit gene

A

c. gamma subunit gene

this would increase HbF (alpha2, gamma2)

60
Q

what is the Hill coefficient of myoglobin binding oxygen?

A

1 —> NO cooperativity

61
Q

Frequent or recurrent types of which of the following infections may strongly indicate the prescence of a primary immunodeficiency diease?
A. Viral upper respiratory tract infections
B. Streptococcal pharyngitis (“strep throat”)
C. Ear and sinus infections

A

Ear and sinus infections

62
Q

Are eosinophils involved in immediate hypersensitivity?

A

YES!!! Eosinophils mediate both allergic and parasitic disease!

63
Q

Amplification pools (of cells) are an important concept everywhere ____ are found

A

Amplification pools (of cells) are an important concept everywhere STEM CELLS are found

64
Q

A burn blister is what kind of inflammation?

A

SEROUS - fluid via increased capillary permeability

65
Q

In Type II hypersensitivity, what is the actual process causing damage?

A

Antigen::antibody complex activates the classical complement pathway —> cell lysis

66
Q

His 146 and Asp 94 interact with each other in which state of hemoglobin?

A

Tense (deoxy) state —> Bohr effect

Form salt bridge that is broken in R state

67
Q

____ and ____ immunosuppressive drugs can cause hyperglycemia/diabetes especially when used with glucocorticoids

A

Cyclosporine and tacrolimus

68
Q

Which enzyme is deficient in porphyria cutanea tarda?

A

Uroporphibilinogen decarboxylase (UROD)

69
Q

What are the Heinz bodies seen in glucose-6-phosphate dehydrogenase deficiency?

A

G6PD deficiency causes ROS damage - oxidant injury occurs to the hemoglobin, which becomes denatured, aggregates, and sticks to internal side of membrane

70
Q

What is the stain required to see iron intracellularly?

A

Prussian blue

if the question doesn’t say prussian blue, you are not looking at iron!!

71
Q

What is a factor viii deficiency

A

Hemophilia A

72
Q

Acute hemolytic transfusion reactions reflect lysis of ____ RBC by ____ antbodies

A

Acute hemolytic transfusion reactions reflect lysis of DONOR RBC by RECIPIENT/HOST antbodies/isoagglutinins

73
Q

What actually causes RBC lysis in acute hemolytic transfusion reaction?

A

MAC (membrane attack complex)

IgM fix/activate complement

74
Q

T/F: if a patient has sickle cells they have no adult hemoglobin

A

TRUE - remember that it is due to genetic mutation, so all hemoglobin will be affected

Foundations Exam 2 (42 decks)

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