Labs, clinical signs + symptoms Flashcards
Anterior uveitis (iris inflammation)
2 categories + ex
infections (herpes, syphilis, Lyme)
inflammation (HLA-B27-related disease such as AnkSpon; sarcoidosis)
Erythema nodosum (red/violet subcutaneous leg nodules)
3 categories of causes + examples
Bacterial infection (S. pyogenes pharyngitis, S. aureus, Chlamydia)
fungal infections (blasto, coccidio, histo)
inflammations (Crohn’s, sarcoidosis, etc.)
Skin sign in Celiac
dermatitis herpetiformis
red, pruritic papules, vesicles and bullae that are bilateral and symmetric on extensors, elbows, knees, upper back + butt
acanthocytes
assoc. disease
RBCs with projections of diff. lengths; spur cells are most severe form
assoc. with abetalipoproteinemia
bite cells
G6PD defic. after monocytes eat Heinz body (Hb aggregates) out of RBCs
target cells
4 causes
bullseye look with central Hb aggregation surrounded by halo
seen in obstructive liver disease, thalassemia, IDA and asplenia (increased surface area to volume ratio)
teardrop cells
seen in myelofibrosis
when BM is replaced with fibrosis or metastatic cancer, RBCs have to squeeze thru fibrous strands and get deformed
schistocytes
fragmented RBCs
seen in DIC and thrombotic microangiopathies (HUS etc.) as fibrin clots exert shear forces on RBCs and cause fragmentation
flame/dot hemorrhage in retina
hypertensive retinopathy
cotton-wool spots on retina
hypertensive retinopathy; small foci of retinal ischemia
cherry red macular spot
central retinal artery occlusion with diffuse retinal ischemia
via atheroscler, cardioembolism, vasculitis (GCA)
also assoc. with Tay-Sachs and Niemann-Pick sphingolipidoses (think hyphens… cherry-red, T-S, N-P)
optic disc cupping
glaucoma
hypersegmented neutrophils (>5 lobed nuclei)
megaloblastic anemia
folate deficiency (happens faster) or B12 defic. (takes years due to body stores)
anti-mitochondrial antibodies
primary biliary cirrhosis
sx include pruritus, jaundice + malabsorption
Kussmaul sign
normal = inspiration decreases JVP as venous return increases
Kussmaul = increased JVP on inspiration
cause = impaired R-side diastolic filling via constrictive pericarditis (chronic), restrictive CMP, or tricuspid stenosis
pericardial knock
brief, high-frequency precordial sound in early diastole (just after S2; earlier than S3)
seen in constrictive pericarditis
(can be confused with opening snap of mitral stenosis)
Pulsus paradoxus
what is it?
4 causes?
drop in SBP > 10 mmHg on inspiration
seen in cardiac tamponade, constrictive pericarditis, severe asthma or COPD
(normally inspiration > increased venous return > right chambers bulge into left + decrease L-sided filling > slight SBP decrease; in PP this effect is more pronounced due to restriction of the movement of R chambers into pericardium)
(the “paradoxus” part is because when SBP decreases significantly, you can detect heartbeats that don’t have corresponding pulses peripherally)
S3
where heard? what is it?
rapid cessation of passive diastolic filling into an enlarged ventricle (“ventricular gallop”)
heard with bell at apex, best with pt in left lateral decubitus
HLA associations for T1DM
HLA-DQ and DR
specifically HLA-DR3 and DR4 (seen in 90% of T1DM pts)
signs of portal hypertension with no liver abnormalities
cause? how is it different from usual portal htn signs?
portal vein thrombosis
a “presinusoidal” cause of portal htn; can have esophageal varices + other portocaval anastamoses with splenic enlargement but NO ASCITES
membranous nephropathy antibody
anti-PLA2R
highly specific + correlates to disease activity
hemosiderin
appearance, stain
brown or yellow-brown pigments in granules or crystals in cytoplasm of macrophages
prussian blue stain
amyloid protein
stain + appearance; sequelae
Congo red stain > pale rose color
can cause CMP, nephrotic syndrome etc.
lipofuscin
appearance + cause of accumulation
insoluble yellow-brown pigment (lipids + P-lipids complexed with proteins)
accumulates with age in multiple organs
loud, blowing holosystolic murmur heard at mid or lower LSB
no other symptoms
difference in newborn vs. later infancy?
small VSD - non-cyanotic so no other sx at first
larger VSD or later Eisenmenger > HF, failure to thrive, and diaphoresis with feeding
NOT HEARD JUST AFTER BIRTH > pulmonary vascular resistance declines in first week and significant L-to-R shunt can begin > heard by age 4-10 days
most small VSDs close spontaneously
Peripheral Pulmonary Stenosis
murmur? cause?
stenosis in a more distal branch of the pulmonary artery
murmur heard AFTER FIRST DAY of life when ductus arteriosus closes
low-grade, mid-systolic, high pitch/blowing ejection murmur
heard in pulmonary area (2nd ICS LSB) with radiation to AXILLA and BACK
Labs in sarcoidosis
what’s altered and why?
hypercalcemia / calciuria - 1-alpha-hydroxylase form activated macrophages produces PTH-independent vitamin D
elevated serum ACE - due to lung inflammation
S3
causes
generally, abnormal ventricular enlargement (eg volume overload > eccentric hypertrophy)
normal in healthy adult <40 or pregnancy; age >40 suggestive of…
severe mitral regurg
chronic aortic regurg
Dilated CMP
HIGH OUTPUT - in pregnancy or hyperthyroid
S4
what is it? how does it sound? causes?
sudden rise in END-DIASTOLIC pressure as blood strikes a stiff ventricle after atrial contraction (“atrial gallop”)
low-frequency, late diastolic sound
causes of CONCENTRIC LV hypertrophy such as chronic hypertension or severe aortic stenosis
Light Criteria
what for + what are they?
to determine if a pleural effusion is an exudate (infection, malignancy or AI disease) vs. transudate (HF, cirrhosis, nephrosis)
pleural/serum protein ratio > 0.5 -or- pleural/serum LDH ratio > 0.6 -or- pleural LDH >2/3 of normal upper limit serum LDH (normal upper limit = 90 U/L, so >60 U/L
Courvoisier sign
painless palpable gallbladder in jaundiced patient
sign of pancreatic head adenocarcinoma causing obstruction of gallbladder evacuation
Labs in dermatomyositis
name of Ab and what it targets
anti-Jo1 (most specific) - targets histidyl-tRNA synthetase
ANA
creatine kinase and aldolase (may be high via muscle damage)
anti-hemidesmosome Ab
bullous pemphigoid
anti-desmosome Ab
pemphigus vulgaris
hypotension, jugular distension, clear lungs
signs/sx of MI
what is it? other hemodynamic parameters
isolated right ventricular infarct (RCA occlusion)
DECREASED pulmonary capillary wedge pressure
S4
how + when is it best heard?
bell over apex, pt in left lateral decubitus
on EXPIRATION (increased flow from lungs back to left atrium)
ALP vs. GGT
ALP - group of enzymes with metabolic activity in many tissues (but mainly BONE + LIVER)
GGT - mostly in liver + biliary epithelium; in other tissues as well, but not in bone! can help differentiate btwn liver and bone causes of ALP increase
urinary eosinophils
MCC, less common causes, trigger, other sx
MCC is ACUTE INTERSTITIAL NEPHRITIS from drugs (nsaids, penicillins)
may be due to kidney transplant rejection or pyelonephritis
rash, fever + eosinophilia
Arteriovenous nicking
funduscopic finding in chronic htn
early sign of retinopathy due to exudative vascular changes via endothelial necrosis
“Xanthochromia”
blood in CSF
non-specific, but if SAH suspicion is high and CT is negative, is highly sensitive for SAH
Hypokalemia
s/s?
muscle weakness
cramps
possible rhabdomyolysis
Hyponatremia
s/s?
nausea
malaise
headache
CNS - mental status, seizures
cramps usually only in chronic hyponatremia
Leser-Trelat sign
many seborrheic keratoses suddenly
sign of GASTRIC ADC or other internal malig. (maybe via IGF-1 production)
Internuclear Ophthalmoplegia
what is it? what causes it?
impaired adduction during lateral gaze
“convergence testing” (cross-eyed) is normal > not a medial rectus issue, rather a nerve conduction issue
seen in MS
(demyelinating lesions in the MEDIAL LONGITUDINAL FASCICULUS impair saltatory conduction from the ABDUCENS NUCLEUS (pons, controls lateral rectus of unaffected eye + transmits lateral gaze signal to CN III nucleus)
CSF tap:
normal glucose, high protein, RBCs
“Traumatic tap”
CSF tap:
low glucose, very high protein, very high neutrophils
bacterial meningitis
CSF tap:
normal glucose, high protein, RBCs and lymphos
Herpes encephalitis
also see acute-onset fever, HA, mental status and FOCAL DEFICITS / SEIZURE
predominantly TEMPORAL LOBE; see temporal edema on img (virus goes via olfactory tract to olfactory cortex in medial temporal lobe)
RBCs are via hemorrhagic inflammation of temporal lobe
CSF tap:
low glucose, high protein, lymphos
Fungal or TBC meningitis
CSF tap:
normal glucose, high protein, normal cellularity
Guillain Barre Syndrome
called “albuminocytologic dissociation”; prob via incr. permeability of “blood-nerve barrier” at nerve roots
progressive, symmetric ascending weakness
CSF tap:
normal glucose, normal -or- high protein, lymphos
viral encephalitis
OTHER than herpes (herpes has RBCs via temporal hemorrhagic inflammation)
HbA2
when is it seen? what does it cause? what testing does it interfere with?
in BETA THALASSEMIA
high in trait; very high in major
compensation for beta globin chain underproduction
resulting MICROCYTIC rbcs are prone to HEMOLYSIS
increased cell turnover > FALSE LOW HbA1c in diabetics
anti-smooth muscle Abs
autoimmune hepatitis
Murphy sign
what is it?
positive in what? negative in what?
doc puts hand under ribs @ R midclav
pt breathes out, then on inhalation doc watches for wincing + stopping of inhalation due to pain
positive - cholecystitis
negative - choledocholithiasis, pyelonephritis, ascending cholangitis
Systemic Sclerosis (Diffuse Scleroderma) antibody
Anti-Scl70 (aka anti-DNA topoisomerase I)
CREST syndrome antibody
anti-centromere
CREST acronym
CALCINOSIS - subcut Ca deposits +/- pain
RAYNAUD’S - via cold/emotional stress
ESOPH DYSMOTILITY - distal fibrosis
SCLERODACTYLY - starts as a NON-PITTING EDEMA
TELANGIECTASIA - face, hands, upper trunk, mucosa
most specific Ab for SLE
anti-dsDNA
Ab for DRUG-INDUCED Lupus
anti-histone
no renal/CNS involvement in drug-induced
Abs for Sjogrens
Anti-Ro (SSA) and Anti-La (SSB)
How is the extent pulsus paradoxus measured?
BP cuff on arm > inflate to above BPsys > listen for when intermittent sounds are first heard on EXPIRATION ONLY, then for when sounds are heard through WHOLE RESP. CYCLE
the difference between these is the drop in BP during inspiration …. normally 10 mmHg or less…. >10 mmHg is pulsus paradoxus
Labs in hypovolemia
4 things (think renal / urinary parameters + 1 related to how many lab values will change in general)
- High BUN/creatinine ratio - >20:1
- low urine sodium / FENa - <20 mEq/L or <1%
- high urine spec. gravity / osmolality - >1.015 or >450 mOsm/kg
1-3 are signs of “prerenal azotemia”
- Hemoconcentration - albumin, Hb, urate etc. concentrations will all rise due to low volume
Main, most specific urinalysis sign of pyelonephritis
how does it form?
what other disease can it be seen in?
WBC casts
WBCs precipitate with Tamm-Horsfall proteins secreted by tubular epithelium
also seen in ACUTE INTERSTITIAL NEPHRITIS, but this will have signs of AKI (BUN, creat, etc.) as opposed to urinary symptoms
ERYTHROCYTE GLUTATHIONE REDUCTASE activity can be reduced in deficiency of what?
why?
(s/s of this?)
vitamin B2 (riboFLAVIN)
because glutathione reductase uses FAD (made from B2) and NADPH as cofactors to reduce S-S bonds on glutathione
(normocytic anemia with lip, mouth, tongue inflamm (cheilosis, stomatitis, glossitis))
increased serum protoporphyrin levels
occur in what? (3 conditions)
iron deficiency anemia
lead poisoning
erythropoietic protoporphyria
C-ANCA
what is the actual protein targeted?
1 example of disease with C-ANCA?
usually PROTEINASE-3
Wegener’s granulomatosis (aka granulomatosis with polyangiitis)
P-ANCA
what is the actual protein targeted?
examples of diseases with P-ANCA
(5 total: 2 vasculitides, 2 GI disorders, 1 autoimmune)
usually MYELOPEROXIDASE
CHURG-STRAUSS (eosinophilic granulomatosis with polyangiitis)
MICROSCOPIC POLYANGIITIS
ULCERATIVE COLITIS and PRIMARY SCLEROSIS CHOLANGITIS
RA
main serum marker correlating with disease severity in GIANT CELL ARTERITIS (temporal arteritis)
IL-6
basophilic stippling
in what (2)? is what?
- sideroblastic anemias - Pb poison, MDS, x-linked
- thalassemias
seen in PERIPH not marrow (sideroblasts in marrow)
is AGGREGATED RIBOSOMES
sideroblasts
seen where? stain? what makes the rings?
in MARROW of sideroblastic anemias
PRUSSIAN BLUE stain
excess IRON in MITOCHONDRIA
