clinical pathology case - lecture notes - julia Flashcards
if your patient has watery loose stool, where in the GI tract does this imply that there might be a problem?
the colon - where water is reabsorbed
what is steatorrhea? how would you test for it? what does it imply if your patient has it?
- 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
what is a normal respiratory rate?
12-14 breaths per minute
what does having distended jugular veins imply?
- right sided heart failure or increased venous pressure (some cause of back up of blood on right side of heart)
what is a crepitant rale? what does it occur?
- 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
where is a normal PMI? what does it mean if it is abnormal?
- 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
how can diarrhea create/be linked to edema?
- with diarrhea, you’re exreting a lot of proteins
- become hypoproteinemic
- oncotic pressure drops
- implies problem with kidney or liver
how would you determine whether blocked lymphatics were responsible for edema?
- 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
what is orthostatic hypertension? how serious is it?
- 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
what does a reduced QRS complex imply?
a problem in the myocardium
what does a poor R-wave progression imply?
something wrong with myocardium - not diagnostic of an MI, but implies
what does troponin level tell you about a patient’s heart?
- 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
what does this ECG imply/show?
- 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
what clinical symtoms would be specific for goodpasture’s (or at least really imply it in a patient with possible kidney problems?)?
- blood in urine
- brownish sputum
what could you look for to identify a type III autoimmune disorder?
vasculitis
how would you detect amalyodosis histolocially (colon)?
- use congo red stain
- will make amaloyd accumulations appear green
- shows up as smooth homogenous pink material without the congo red stain
describe the pathology of multiple myeloma. what causes it and what would you see in patients’ blood and urine?
- 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
what would a bone marrow biopsy of a multiple myeloma patient look like histologically?
- lots of plasma cells (clock-face nucleus and perinuclar hoff)
- will also have a low white cell count, periprotein in serum (not histological, obviously)
what is amyloidosis? what protein types are responsible?
- 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
what is protein A? what diseases has it been found to be involved in?
- 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
what is the difference between primary and secondary amyloidosis, familial amyloidosis, dialysis amyloidosis and senile amyloid?
- 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
what is the pathway/process by which chronic inflammation can lead to amyloidosis?
- get activated macrophages
- these release interleukin 1 and 6
- these tell the liver to make more protein A
describe the structure of amyloid fibrils. how does congo red dye stain these fibril specifically?
- 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)
how does amyloid cause disease?
- replaces and crowds out normal tissue elements so that the tissue/organ can’t function
- it’s not toxic on its own!
what physical appearance would you expect to see in patients with amyloidosis?
- will be very muscular even though they don’t work out
- due to musclular deposition of amyloid
- would also cause enlarged tongue
what might you see on the skin of patients with amyloidosis?
- lichen amyloidosis
- little nodules of amyloid deposits in the skin
- apparently very rare
what would the spleen of a patient with amyloidosis look like upon autopsy (gross level)?
- spleen should be all reddish color
- this has pale areas that look like wax
- these are the depositions of amyloid
what will the kidney of a patient with amyloidosis look like upon autopsy (gross level)?
- 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
what would the liver of a patient with amyloidosis look like upon autopsy? (gross level)
enlarged due to amyloid infiltration
what will the heart of a patient with amyloidosis look like upon autopsy? (gross level)
- thick, rubbery ventricle wall
- deposition of waxy-like material in myocardium
- myocardium get thicker
- heart will be stiff
how is the amyloid in altzheimer’s related to amyloidosis?
- 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
