Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FPP > week 1 > Flashcards

week 1 Flashcards

1
Q

•Barrett’s esophagus

A

•In chronic gastric reflux the normal stratified squamos of the the lower esophagus change to intestinal type columnar epithelia that secretes protective mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cells swell Why?

A

–Cells swell bc no ATP available to power NA/K pumpà

Increased Na inside cell à

increases water in cellà

swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

necrosis vs apoptosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

coagulative necosis.

A

ischemia

maintian archtectire but no nucleas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Liquefactive necrosis

A

infection

brain ischemia

  • abscess, pancreatitis
  • Seen in bacterial or fungal infections when microbes stimulate accumulation of inflammatory cells and the enzymes of leukocytes digest (Liquefy) the tissue •For unknown reasons hypoxic death of brain tissue results in liquefactive necrosis. Brain tissue gets completely digested and liquid is left behind eventually cleared by macrophages •abscess, pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Caseous necrosis

A

TB

•Found in foci of tuberculosis infections •Caseous = cheesy •Looks friable, yellow-white •Tissue architecture completely gone unlike coagulative •Area of caseous necrosis is encircled by an inflammatory border •The necrosis and inflamm border = granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

fat necrosis

A

•Occurs in areas where there is a lot of fat •Classic examples are acute pancreatitis- pancreas releases lipases due to cell injury and these lipases digest triglycerides of fat cells into free fatty acids • Free Fatty acids and calcium combine to produce white chalky substance = saponifaction •Other area fat necrosis occurs is after trauma to the breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

antibody classes

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MS?

A

T cells and macrophages attack CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Thrombocytopenia?

A

autoantibodies agaisnt platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

guillain barre

A

autoantibodies against the schwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hasimotos thyroiditis

A

autoantibodies against thyroglobulin

hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

celiac disease

A

glutenenteropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

systemic lupus erythematous

A

autoantibodies against dna histones proteins

nephritis arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

rheumatoid arthritis

A

autoantibodies against the joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

rheumatic fever

A

mimicry

autoantibodies to myosin following group a strep infection M protien is close to the myosin. licks joints and bites heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

primary immune is diff from secondary how?

A

primary is inherited

secondary is aquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

chronic granulatomas disease?

A

NADPH deficiency

it is needed for the respitory burst in neutrophils

without it the neutrophils wont kill the infection and are succeptible to more infections.

nadph is needed for superoxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what kind of organisms are a problem in people with CGD?

A

infections with catalase positive organisms.

Cause catalase will degrade the H2O2. it is the only toxic material they have around to kill the organism.

20
Q

CGD

test?

Tx?

onset ?

in whom?

A

•Onset by age 2 •X linked and AR •Pneumonia •Osteomyelitis •Abscesses •Test: DHR •Treatment—Trimethoprim+sulfamethoxazole prophylaxis •Definitive tx= bone marrow transplant

21
Q

Leukocyte Adhesion Defects

signs?

where is defect?

A

umbilial cord wont fall off

dont form pus

gingivitis

  • Defect is in LFA-1/MAC-1 integrin on phagocytes
  • Autosomal recessive •Neutrophils cant attach to endothelium and get to site of bacterial invasion •Since neutrophils cant get to endothelium there are increased neutrophil levels =neutrophilia

you keep sending out signal and even though you are sending alot none are getting in and you keep sending out that signal.

22
Q

c2 deficiency

screeening test?

what does it usually associate with?

A

test: –Screening test is CH50 —tests classical complement pathway

–Most common complement deficiency –Autosomal recessive –Associated with Lupus —1/3 of pts with C2 defect have lupus –Assoc with other vascular problems- vasculitis, dermatomyositis –Screening test is CH50 —tests classical complement pathway –Repeat infections from H. Influenzae, enteric bacteria

23
Q

Late complement deficiencies

A

•C5-C9 of the complement pathway make the membrane attack complex that makes a whole in the bacteria and kills it. •Main infection if the pt has a C5-C9 deficiency is recurrent infections with Neisseria only. •Neisseria gonorrhea and neisseria meningitis •CH50 is screeing test

24
Q

SCID

A
  • Severe combined immunodefeciency –Severe defects in T and B cells –Onset in infancyà live in a bubble –Infant will have recurrent diarrhea, recurrent otitis media, thrush(candida infection), failure to thrive –Repeat infections with viruses, bacteria, fungi especially Candida, pneumocystis, psuedomonas –100% die without bone marrow transplant –Screening test—CBC will show WBC below 1,500 –Confirmatory test-CBC with differential which will show breakdown of T cell, b cell #s
  • Multiple defects at cellular level can cause variety of immune deficiencies that all are referred to as SCID
25
Q

X-linked SCIDs

A

•Due to mutation in the gene encoding the Gamma chain shared by cytokines IL-2, IL-4, IL-7 plus other •IL-2 receptor gamma chain mutation-normally stimulates growth of helper of helper T cells and Cytotoxic T cells •Without helper T cells, B cells don’t develop normally or if they do they stay immature •Labs will always show very low or absent T cell numbers….Mature B cells will be low as well but immature B cells can be normal or high.

26
Q

autosomal recessive SCID

A

•AR is 40% •Mutation in adenosine deaminase (ADA) •ADA is needed for purine metabolism and without it adenosine and deoxyadenosine triphosphate metabolites accumulate •This is directly toxic to T and B cells

27
Q

trecs are a marker for?

in SCID what is TREC level like?

A

•TREC’s are nonreplication pieces of circular DNA of naïve T cells generated when a T cell receptor is being made •TREC’s are a marker for normal naïve T cells •The more TREC’s there are, the more recombination of T cell receptors is occuring •In SCID, TREC’s will always be low

28
Q

DiGeorge Syndrome

A
  • Microdeletion in chromosome 22q11.2 •Disorder results from malformation of the 3rd and 4th pharyngeal pouch during embryology •3-4 pharyngeal pouch is where the Thymus Parathyroid, aortic arch and parts of face develop from
  • Malformed parathyroid à low PTH à low calcium à tetany •Thymic hypoplasia –T cells originate from here –Low numbers of T cells –Recurrent VIRAL and FUNGAL infections
29
Q

Digeorge

A

•Catch 22 •Cardiac defects •Abnormal facies •Thymic hypoplasia •Cleft palate •Hypocalcemia (LOW PTH) •22nd chromosome deletion

30
Q

tetany?

A

involuntary muscle contractions from a problem with the parathyroid gland.

31
Q

how do you test?

digeogre

A

•Preferred Dx test is chromosome microarray/DNA duplication deletion test •RT-PCR •FISH • •Live vaccines can cause disease in these pts •Absent thymic shadow on CXR

32
Q

XLA

A

•X-linked recessive •Defect in Btk- a tyrosine kinase gene needed for B cell maturation •B cells make antibodies •Labs will show decreased number of B cells •Decreased number of antibodies of all classes •IgG, IgA, IgM, IgE •Onset in infancy, early childhood

B cells dont mature right.

•Recurrent bacterial infections starting at about 6 months of age after maternal antibodies fade away •H. influenze, S. pneumonia, mycoplasma pneumoniae

33
Q

CVID

A

•B cell maturation defect with many causes •Low IgG •AND •Low IgM or IgA or both •Onset in 20’s •Pulmonary disease is common initial presentation •Increase risk of Non hodgkins lymphoma, gastric cancer, autoimmune disease

34
Q

acute vs chronic inflamation?

A
35
Q

leukocyte migration through blood vessels?

A
36
Q

granulatomous inflamation?

what casues multinucleated giatn cells?

seen in what diseases?

A
37
Q

type 1 hypersensativity?

what do you need?

how is it mediated

what are some causes of it?

A

1st exposure-

Free antigen enters body gets recognized by B-cell

B cell produces IgM

7-10 days later there is class switching IgMà IgE

IgE binds to mast cells via Fc portion on IgE and Fc receptor on mast cell

2nd exposure

Free antigen enters body

Antigen binds IgE on mast cells

Release of vasoactive amines-histamine, recruitment of Eosinophils, BASOPHILS

Itchy, vasodilation, bronchoconstrictionàdeath

Examples of type I reaction

1-bee stings

2-peanuts, pine nuts, other nuts

3-seasonal allergies- pollen

2 exposures must occur before anything happens !!!

ANAPHYLAXIS/ ASTHMA

IMMEDIATE!!!!

38
Q

type 2 hypersensativity.

what is it mediated by?

what are some examples of it.

A
  • Perceived or true antigen is present inside the body and attached to a cell or other structure like basement membrane •Igm or IgG bind to this antigen with the Fab portion of the antibody •The Fc portion of the IgM/IgG is facing away from the cell •Complement factors that are nearby will bind the IgM/IgG Fc portion which triggers complement activationà MAC formation à destruction of cell •AB MEDIATED!!!!!
  • Type II 1.IgM/IgG can also bind regular cellular receptors that the body thinks are foreign 2.This binding can simply interfere with normal cell function by acting as a competitive antagonist-Example-Myasthenia Gravis, pernicious anemia 3.Or once bound complement is activated and the receptor/cell gets destroyed
  • Type II Examples •Noncytotoxic-pernicious anemia, grave’s dz, myasthenia gravis, •Cytotoxic-Transfusion reactions, rheumatic fever, goodpasture’s, bullous pemphigoid, pemphigus vulgarisExample-Goodpasture’s syndrome
39
Q

hypersensativity type 3?

what causes it?

what causes disease in it?

A

•Complex of three things –Antigen+antibody+complement –Once all three are bound together in the blood they get too heavy and precipitate! –Where they settle is where the disease occurs

•Example- “Serum sickness” –occurs when person is given drugs and something in the drug is perceived as foreign. IgMàIgG Antibodies against it are produced and 5-10 days later the Ag+Ab form which activates complement forming the Ag+Ab+complement complexàprecipitates in skin=urticaria, joints=arthralgias

40
Q

what is serum sickness?

what type is it found in?

A

•“Serum sickness” –occurs when person is given drugs and something in the drug is perceived as foreign. IgMàIgG Antibodies against it are produced and 5-10 days later the Ag+Ab form which activates complement forming the Ag+Ab+complement complexàprecipitates in skin=urticaria, joints=arthralgias

41
Q

what diseases are associated with type 3?

A

•Type III •Lupus- ANA, Anti-dsDNA, anti-Smith antibodies are present that bind with their antigen and stimulate complement. •Precipitates in kidneys, joints skin •Other examples-Rheumatoid arthritis, polyarteritis nodosum, post-streptococcal glomerulonephritis

42
Q

type 4 hyper senasativity.

what is the mediator?

what is the a halmark of it?

what are some examples of it?

A
  • Type IV •Delayed response and does not involve antibodies •Mediated by T CELLS •Antigen enters bodyàengulfed by APC and presented to a T CELL •T CELL is now sensitized so that the next time it encounters antigen it will release cytokines •It takes time 12-48hrs for the primed T CELL to get to site of antigen and release cytokines and cause an effect. •Ex-Tuberculosis skin test-redness,swelling 2-3 days after TB test •Others-Poison Ivy, Type I DM, Multiple sclerosis, Guillan Barre, hasimoto’s thyroiditis
  • Ex-Tuberculosis skin test-redness,swelling 2-3 days after TB test •Others-Poison Ivy, Type I DM, Multiple sclerosis, Guillan Barre, hasimoto’s thyroiditis
43
Q

A 45 year old man has a huge appetite. At a meeting he notices there is a pile of cookies that all contain peanuts which everyone brought because they knew this man wouldn’t be able to eat because he normally takes everyones cookies. The man is starving so he decides to eat the cookies with the peanuts. Within minutes he develops blotchy erythematous, pruritic plaques on his skin. Which of the following sensitized cells release a mediator that produces these skin lesions?

A) Mast Cell

B)neutrophil

C)natural killer cell

D) CD4+ lymphocyte

E) Plasma cells

A

Answer is A

This man has hives related to an allergy to an antigen in the nuts. This causes a type I hypersensitivity rxn, in which IgE antibodies that are already bound to a mast cell from a previous exposure get crosslinked by the peanut antigen and cause degranulation

44
Q

• A 32 yo african american women has lupus and has complained of joint aches, muscles aches. Chemistry panel shows an elevated serum urea nitrogen level indicating kidney dysfunction. Kidney biopsy, microscopic exam and staining reveal a granular pattern of antibody-antigen complex bound to complement Cq1.

This pattern is most typically produced by which of the following Hypersensitivity rxns

•I • II • III • IV

A

  • Answer
  • III-this is immune complex deposition and this women has lupus.
45
Q

During the second pregnancy for a 25yr old women an ultra sound at 20 weeks shows hydrops fetalis/increased amniotic fluid. Her first pregnancy was normal. The current pregnancy ends at 31weeks gestation and the baby is shown to have jaundice, scleral icterus and a low hemoglobin.

What are this baby’s symptoms due to?

1) receptor antibodies
2) loss of self tolerance
3) immune complex formation
4) Ab mediated cell destruction

A

Answer

Ab mediated cell destruction

This is Rh incompatibility between the mom and the baby. Maternal antibodies vs a different Rh status in the baby were formed during the birth of the moms first baby and crossed the placenta during the 2nd pregnancy. The antibodies bind the babies rbc’s and destroy them via type II HSN rxn

46
Q
A
47
Q
A

FPP (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions