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Flashcards in clinical pathology case - lecture notes - julia Deck (31)
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1
Q

if your patient has watery loose stool, where in the GI tract does this imply that there might be a problem?

A

the colon - where water is reabsorbed

2
Q

what is steatorrhea? how would you test for it? what does it imply if your patient has it?

A
  • fat in stools
  • don’t need to test - just ask patient if stool have smelled really really bad
  • implies that pancreatic enzymes are not doing their job => not digesting or absorbing the fats => fat stays in GI tract and goes rancid
3
Q

what is a normal respiratory rate?

A

12-14 breaths per minute

4
Q

what does having distended jugular veins imply?

A
  • right sided heart failure or increased venous pressure (some cause of back up of blood on right side of heart)
5
Q

what is a crepitant rale? what does it occur?

A
  • very fine crackling sound when a person takes a deep breath - similar to crinkling a piece of celophane
  • due to alveoli popping open when you take a deep breath
  • seen with heart failure
  • due to edema in the lungs - implies lungs are damp
6
Q

where is a normal PMI? what does it mean if it is abnormal?

A
  • PMI is the point of maxium impact (of heart)
  • in healthy young person, it’s normally in the midclavicular line
  • if it’s to the left of this line in a patient, this implies that the heart is enlarged
  • implies heart failure of some sort
7
Q

how can diarrhea create/be linked to edema?

A
  • with diarrhea, you’re exreting a lot of proteins
  • become hypoproteinemic
  • oncotic pressure drops
  • implies problem with kidney or liver
8
Q

how would you determine whether blocked lymphatics were responsible for edema?

A
  • if edema symmetrical, blocked lymphatics are unlikely
  • also, if edema goes at least halfway up the belly, blocked lymphatics could only be the cause if the thoracic duct was blocked
9
Q

what is orthostatic hypertension? how serious is it?

A
  • blood pressure drops when you stand up or sit up suddenly
  • lots of people have it - not a health concern
  • but can be if it’s severe
10
Q

what does a reduced QRS complex imply?

A

a problem in the myocardium

11
Q

what does a poor R-wave progression imply?

A

something wrong with myocardium - not diagnostic of an MI, but implies

12
Q

what does troponin level tell you about a patient’s heart?

A
  • whether or not he/she has ischemic heart disease
  • if people have even a little bit of ischemic heart disease, troponin levels will go up
13
Q

what does this ECG imply/show?

A
  • marked left ventricular hypertrophy with a minimal pericardial effusion
  • the white stuff outside of the heart is the pericardial effusion
  • the flakiness that looks like a snow storm isn’t normal - should be more homogenous
14
Q

what clinical symtoms would be specific for goodpasture’s (or at least really imply it in a patient with possible kidney problems?)?

A
  • blood in urine
  • brownish sputum
15
Q

what could you look for to identify a type III autoimmune disorder?

A

vasculitis

16
Q

how would you detect amalyodosis histolocially (colon)?

A
  • use congo red stain
  • will make amaloyd accumulations appear green
  • shows up as smooth homogenous pink material without the congo red stain
17
Q

describe the pathology of multiple myeloma. what causes it and what would you see in patients’ blood and urine?

A
  • patient will be making a lot of IgA lambda chains - these will make up a large amount of the protein in his blood
  • there’s so much of this in the blood that it’s suppressing the normal antibodies that should be there
  • urine analysis will also reveal high levels of excretion of these IgA lambda light chains
18
Q

what would a bone marrow biopsy of a multiple myeloma patient look like histologically?

A
  • lots of plasma cells (clock-face nucleus and perinuclar hoff)
  • will also have a low white cell count, periprotein in serum (not histological, obviously)
19
Q

what is amyloidosis? what protein types are responsible?

A
  • deposition of amyloid fibril in extravascular tissues
  • in primary amyloidosis = monoclonal kappa or gamma light chains
  • rarely, can be monoclonal heavy chains
  • in secondary amyloidosis = protein A
20
Q

what is protein A? what diseases has it been found to be involved in?

A
  • makes up amyloid fibril in secondary amyloidosis
  • derived from serum amyloid A = acute-phase protein
  • also found to be involved in rheumatoid arthritis and Crohn’s disease
  • mutated in familial amyloidosis
21
Q

what is the difference between primary and secondary amyloidosis, familial amyloidosis, dialysis amyloidosis and senile amyloid?

A
  • primary:
  • amyloid deposits in multiple organs
  • deposits made up of kappa or lambda light chains that have been processed by activated macrophages and deposited in tissues as an insoluble protein
  • secondary:
  • deposition of protein A (made by liver) in people who have chronic inflammatory conditions such as TB, leprosy
  • make lots of protein A and then there’s lots of it in the blood - processed by activated macrophages and deposited
  • familial:
  • transthyreitin cna have point mutation in its gene
  • will get processed and deposited
  • dialysis:
  • beta2-microglobulin is normally circulating in the blood
  • normally joins together with another molecule to make MHC class I
  • when on dialysis, this protein can form fibers
  • senile:
  • normal
  • development of amyloids also from transthyreitin but happen cause there’s lots of it and it gets processed and deposted over time
  • will only see in people in their 70s and 80s
  • only happens in heart
22
Q

what is the pathway/process by which chronic inflammation can lead to amyloidosis?

A
  • get activated macrophages
  • these release interleukin 1 and 6
  • these tell the liver to make more protein A
23
Q

describe the structure of amyloid fibrils. how does congo red dye stain these fibril specifically?

A
  • form beta pleated sheets
  • very closely packed together
  • dye aligns itself with longitudinal sheets of amyloid
  • takes on lens-like properties when it does so - when you shine polarized light through it, the “lens” shifts the light from red spectrum to green (see picture)
24
Q

how does amyloid cause disease?

A
  • replaces and crowds out normal tissue elements so that the tissue/organ can’t function
  • it’s not toxic on its own!
25
Q

what physical appearance would you expect to see in patients with amyloidosis?

A
  • will be very muscular even though they don’t work out
  • due to musclular deposition of amyloid
  • would also cause enlarged tongue
26
Q

what might you see on the skin of patients with amyloidosis?

A
  • lichen amyloidosis
  • little nodules of amyloid deposits in the skin
  • apparently very rare
27
Q

what would the spleen of a patient with amyloidosis look like upon autopsy (gross level)?

A
  • spleen should be all reddish color
  • this has pale areas that look like wax
  • these are the depositions of amyloid
28
Q

what will the kidney of a patient with amyloidosis look like upon autopsy (gross level)?

A
  • looks relatively normal but if look closely will see fine little granules of “dirt” spread all of it - tiny little reflections
  • each one is a glomerulus that has filled up with amyloid
29
Q

what would the liver of a patient with amyloidosis look like upon autopsy? (gross level)

A

enlarged due to amyloid infiltration

30
Q

what will the heart of a patient with amyloidosis look like upon autopsy? (gross level)

A
  • thick, rubbery ventricle wall
  • deposition of waxy-like material in myocardium
  • myocardium get thicker
  • heart will be stiff
31
Q

how is the amyloid in altzheimer’s related to amyloidosis?

A
  • it’s not
  • the amyloid in altzheimer’s is alpha-beta amyloid and is only found in the CNS and is encoded on chromsome 21
  • in altzheimer’s the protein gets cleaved in an atypical way that causes it to begin to deposit in the parenchyma and around small blood vessels in the brain