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187 Cards in this Set

  • Front
  • Back
what is autoregulation?
If systolic stays between 60-160 ⇨ perfusion is constant
If a patient has a BP <60, what could be the outcome?
Ischemic infarct:
Most common cause of bleeding into any cavity:
HTN
If a patient has a BP >160 , what could be the outcome?
Hemorrhagic infarct:
describe the aorta: smooth muscle, compliance, type of cell, Plinear
thickest layer of smooth muscle
• highest compliance= Δvolumel Δpressure (due to elastin)
• stratified squamous cell epithelium=> made for abrasion due to speedy RBCs
• higher Plinear => blood rarely touches sides of aorta
why does the elderly have a wide pulse pressure
⇧ Pressure, little ⇧ volume ⇨ thick aorta in elderly = wide pulse pressure
treatment for wide pulse pressure in the elderly
Tx: ⇩Cholesterol intake, Ca2+ channel blockers to control calcification
Arteries how are they controlled?
sympathetic control, α1 receptors
Monkenberg arteriosclerosis
old people
Arteriosclerotic occlusive disease: sx and symptoms (3)
intermitted claudication
mm. pain w/ exercise
impotence
Hyaline arteriosclerosis
chronic intermittent HTN
Hyperplastic arteriosclerosis
malignant HTN, capillaries ready to burst
Arteriole receptors
β2 receptors; this is why they widen when the nerve is cut
function of the arteriole
>>do the most to protect BP
>>most smooth muscle by cross section=> "stopcock" to control BP
>>to protect the capillaries
what is "reactive hyperemia" of arterioles
cut nerve=> arteriole dilation=> sympathetic control
malignant HTN complication
end organ damage
how would a clot look like in the arteriole if
>>low BP and 1 blood supply or low BP with 2 blood supplies?
low BP/clot => pale infarct (1 blood supply), red infarct (2 blood supplies)
Thickest layer of SM:
Aorta
Most SM:
Arteriole
Largest cross-sxn area:
Capillaries
Highest compliance
Aorta
Capillaries describe (4)
cross sectional area
wall of the capillaries
filtration
effect if there is a decrease in # of capillaries
• largest cross-sectional area
• thinnest walls => diffusion
• max filtration=> push nutrients out
• any loss of capillaries will increase resistance
how are Veins and Venules controlled?
parasympathetic control
describe the veins and venules
capacitance
smooth muscle
valves
how does blood flow
>>most capacitance => 60% of blood is pooled here
>>least smooth muscle, 1-way valves, blood flows superficial to deep
how do veins work when it gets cut?
venoconstrict (α 1 receptors) to mobilize this blood if skin gets cut (from GI, skin first)
how does the vein reabsorb fluid back into the vessel
vein ⇨ venule ⇨ higher osmolarity ⇨ suck stuff into vessel
Pulse pressure
volume rising in aorta, but blood is not flowing (Systolic -Diastolic)
Ex: Stiff aorta
what is Transmural pressure? at what situations is this increased?
pressure on the sides of the vessel (⇧ collagen vascular dz)

Ptotal = PTransmural + Plinear
Linear pressure: what vessel is this the highest?
1/2pv2 =pressure in the middle of the vessel (highest in the aorta)

Ptotal = PTransmural + Plinear
filtration forces: Hydrostatic:
think water (⇧CHF)
filtration forces Oncotic:
think protein; mostly albumin (⇩Cirrhosis)
what is flux
Δhydrostatic-Δoncotic (capillary- interstitial)
(think of this as "transudate- exudate")
transudate vs. excudate: specific gravity
Transudate: Mostly water specific gravity< 1.012
Excudate: Mostly protein (>2g/ dL): specific gravity >1.012
transudate vs. excudate: LDH levels
Transudate: Low LDH ( <200)
Excudate: High LDH (>0.6 of serum or >200)
trasudate causes
Too much water:
• Heart failure
• Renal failure
not enough protein:
• Cirrhosis (can't make protein) or (not eating protein)
• Kwashiork
• Menetrier's (GI losing protein)
• Nephrotic syndrome (pee protein)
excudate causes
Too much protein:
• Purulent (bacteria)
• Hemorrhagic (trauma, cancer, PE)
Fibrinous (collagen vascular dz, uremia, TB)
• Granulomatous (non-bacterial)
• Caseous (TB)
Systole
mechanism
blood flow
O2
krotkoff sound
squish
⇩blood flow to coronary aa
more extraction of 02
(Phase 1 Korotkoff)
Diastole
filling, ⇧blood flow to coronary aa., less extraction of 02 (Phase 5 Korotkoff)
Why does diastole have more blood flow?
1) less resistance (heart relaxed, not compressing coronary vv.)
2) aortic valve closed, coronary vv. ostea are open
3) more transmural pressure in aorta
what is A-vo2 difference:
>>how metabolicly active the tissue is
>>O2 went out-O2 went in came (give and take)
what has highest A V02 difference at rest (very high consumption)
Heart
what will have the highest A V02 after exercise
Muscle
what will have the highest AV02 after a meal
GI
what has the lowest A V02 all the time
Kidney
what will have highest AV02 after test
Brain
how does the blood flow in the body
SVC ⇨ RA ⇨(tricuspid)⇨ RV ⇨ (pulmonic) ⇨ PA ⇨ Lungs ⇨ PVs ⇨ LA ⇨ (mitral) ⇨ LV ⇨
(aortic) ⇨ Aorta ⇨ (Brachial Cephalic, Left Common Carotid, Left Subclavian Carotid) ⇨ rest of body
what factors can Change n (viscosity) Q= ΔPr⁴/nL8π
⇩ via phlebotomy, ⇧via polycythemia or high glucose
Q= ΔPr⁴/nL8π
Change L Length of vv: Q= ΔPr⁴/nL8π
⇧via obesity
how can one change the r (radius) in the poissel's law equation
Q= ΔPr⁴/nL8π
⇩via atherosclerosis
describe resistance in series?
what happens to flow and velocity as resistance increases?
As resistance increases, flow decreases and velocity increases
o Ex: squeezing a garden hose
2 organs that have resistance in series
higher pressure
o Liver - detoxification (portal ⇨ hepatic vein)
Slow stuff down to detoxify, then shoot it out ...
Macrophage "security men" need to find the junk
o Kidney- filtration (afferent ⇨efferent arteriole)
Blood is sitting in "traffic jam"
Resistance in parallel:
what organs have this?
what happens to resistance when organ is removed
what happens during pregnancy? after labor? predict the BP?
most of our organs have this 1/Rtotal= 1/R1+1/R2 ect.
Ex: Remove an organ=> increase resistance (transient ⇧BP)
Ex: Add a baby=> decrease resistance (why BP is low in pregnancy)
Vasodilators:Brain:
⇧pco2, ⇩po2
Ex: High altitude: low p02 => hyperventilation (chronic=> pulm vasoconstrict, secrete bicarb)
Vasodilators: Heart:
Adenosine
Ex: ⇧flow to SA node to prevent ischemia
⇨stop arrhythmia ⇨pause (Na channels reset)
⇨restart heart
Vasodilators: Lungs
⇧po2
Ex: hypoxia vasoconstricts blood vessels to lungs = > polycythemia
Vasodilators: kidneys
Kidney: PG-E, DA, ANP
Ex: DA used in shock to increase blood flow to the kidneys
Ex: NSAIDs will decrease blood flow to kidney => bad for elderly
Vasodilators:GI:
Food
Ex: blood rushes to stomach after meal
what factors would vasodilate the Skin:
Temp, ⇧pC02
Ex: Face flushes in hot summer (builds up w/ walking, need blood flow to wash it
out)
Vasodilators:Muscle:
⇩pH, ⇧pC02
Ex: Exercise
when you stand up what happens normally to heart rate and BP?
when you stand up: BP ⇩5-10mm Hg and ⇧Pulse 10-15 bpm
if after standing up pulse goes up >10 dx.
If pulse goes up >10 =>hypovolemia
Early Shock: what happens to pulse and diagnosis.
CO = HR(pulse) x SV (blood pressure)
PULSE ⇧>10 when stand (orthostatic hypotension = compensated shock)
Late Shock: what happens to BP and diagnosis
CO = HR(pulse) x SV (blood pressure)
BP⇩ >10 when stand (uncompensated=> low CO)
when a person stands up from a sitting
position and the pulse goes up <5
what does it lead to?
=> Autonomic Dysfunction: stand up and pass out w/o warning
most common cause of autonomic dysfunction in Adults:
DM (infarcts carotid sinus)
most common cause of autonomic dysfunction in Elderly: and tx
Sick Sinus syndrome (Tx: Pacemaker)
most common cause of autonomic dysfunction in Parkinson's:
Shy-Dragger syndrome
most common cause of autonomic dysfunction in Babies:
Riley-Day "Familial Dysautonomia" (no reflexes)
Carotid Body:
Chemoreceptor
Carotid Sinus:
Baroreceptor
how does your body respond to Low volume State immediately?
Carotid sinus baroreceptor- ⇧sympathetics => high HR (reflex tachycardia)
how does your body respond to Low volume State Intermediate?
Medulla- releases NE => vasoconstrict = >high HR and TPR
how does your body respond to Low volume State Long-term?
Kidneys - release renin => high TPR, ⇧Na resorption and ⇧K excretion. Excess water
reabsorption leads to dilutional ⇩Na,⇩Cl, ⇩K. ⇧K excretion leads to alkalosis.
Carotid sinus immediate response to low volume state
sv ~>stretch~> carotid sinus~>CN9 (aff) ~>CN10 (eff) ~>sympathetics ~>HR,BP
⇩sv ~>⇩stretch~> carotid sinus~> -⇩-CN9 (aff) ~> -⇩-CN10 (eff) ~> ⇧sympathetics ~> ⇧HR, ⇧BP
how does the carotid sinus regulate BP?
baroreceptor that responds to stretch (volume) => regulate BP
how can we Increase SV?
• Rub carotid sinus
• Vasovagal response (cough, sneeze, urinate) ~> replicate with tilt test
how can we Decrease SV? (3)
• Tonsillectomy (cut CN9) don't do it before 2 years old
• Stand up (blood drained down)
• Nitrates for angina (so ... give β blocker first for MI pts to protect heart)
Medulla's intermediate response: on low volume state
The nucleus tractus solitarius ~> NE release (higher affinity for α receptors) ~> constrict~> increase HR and TPR (reflex tachycardia)
Kidney's long-term (>20 min) response: after the medulla releases NE on low volume state
• NE also vasocontricts blood supply to kidney
• J -G apparatus in afferent arteriole of the kidney responds to flow and volume
How does our body Fix the Pressure:
Mr. J-G releases renin~> Liver (angiotensinogen) ~> ATI ~>Lungs (ACE) ~>
ATII (very potent vasoconstrictor) to efferent arteriole -> ⇧TPR ~> ⇧BP
ATII constricts efferent more than afferent in order to re-establish GFR
how does our body Fix the volume?
ATII ~> Aldo ~> Na + /K pumps in kidney DCT ~> ⇧Na reabsorption ~> ⇧total body water ~> drags in 3
waters with each Na ~> decreases serum Na ~> serum K decreases (secretion) ~> Aldo also secretes H+
~> ⇧pH
Vomiting: alkalosis/acidosis
Alkalosis
Diarrhea: alkalosis/acidosis
Acidosis
Low Volume state normally cause alkalosis, what Low volume state causes acidosis (what are the exceptions)?
Acidosis Exceptions:
• Diarrhea (lose bicarb) => acidosis
• RTA type II (lose bicarb) =>acidosis
• DKA (ketones) = > acidosis
what are the High Na Exceptions:
• Diabetes Insipidus
• Neglected elderly (eating salt, but not drinking pure water)
What is the Physiology of a Man in the Desert? Effect of Low Volume on Heart: Fluid volume~>Preload~> RA filling~>RV filling~>Ventricular contractility~>Softer S1 (pressure)~>Narrow S2 splitting (volume/ pressure)~>CVP~>EKG amplitude~>Vascular pressure ~>Pulmonary resistance~>PCW~>LV filling~>Contractility of heart ~>Stroke volume~>Cardiac output~>Blood flow~>Carotid stretch~>Firing of CN 9/10~> Heart rate
decrease in everything except HR which is increased)
Fluid volume~>Preload~> RA filling~>RV filling~>Ventricular contractility~>Softer S1 (⇩pressure)~>Narrow S2 splitting (⇩volume/ ⇩pressure)~>CVP~>EKG amplitude~>Vascular pressure ~>Pulmonary resistance~>PCW~>LV filling~>Contractility of heart ~>Stroke volume~>Cardiac output~>Blood flow~>Carotid stretch~>Firing of CN 9/10~>⇧ Heart rate
Physiology of a Man in the Desert? Effect of Low Volume on Kidneys:Firing of CN 9/10~>NE release~>TPR~>Blood flow sensed by J-G apparatus~>Renin release~>Angiotensinogen in liver~>Angiotensin I in lung~>Angiotensin II (coverted by ACE in lung)~>Vasoconstriction~>TPR more~>Aldosterone in the CD~>Na/H20 reabsorption~>K/H
⇩Firing of CN 9/10~>⇩NE release~>⇧TPR~>⇩Blood flow sensed by J-G apparatus~>⇧Renin release~>⇧Angiotensinogen in liver~>⇧Angiotensin I in lung~>⇧Angiotensin II (coverted by ACE in lung)~>⇧Vasoconstriction~>⇧TPRmore~>⇧Aldosterone in the CD~>⇧Na/H20 reabsorption~>⇩K/H
Effect of Low Volume on Urine:
?urine Na (?Na/H20 reabsorption)~>?urine K~>?urine pH (?urine H+)~>?FeNa
Effect of Low Volume on Urine:
⇩urine Na (⇧Na/H20 reabsorption)~>⇧urine K~>⇧urine pH (⇩urine H+)~>⇧FeNa
Effect of Low Volume on Serum:
Total body Na (Na reabsorption by Aldo)~>serum Na (H20 reabsorption by Aldo)~>1 serum K ( K excreted by Aldo)~>serum pH (H+ excreted by Aldo)
⇧Total body Na (⇧Na reabsorption by Aldo)~>⇩serum Na (H20 reabsorption by Aldo)~>⇩ serum K ( K excreted by Aldo)~>⇧serum pH (H+ excreted by Aldo)
Effect on Low Volume on Lung:
serum pH~>Harder to breathe in~>Restrictive lung disease~>p02 (hard to breathe in)~>Respiratory rate~>C02~>serum pH~>Respiratory alkalosis
⇧serum pH~>Harder to breathe in~>Restrictive lung disease~>⇩p02 (hard to breathe in)~>⇧Respiratory rate~>⇩C02~>⇧serum pH~>Respiratory alkalosis
Only Veins with No Valves:
• Brain
• Heart
Superficial Vein Thrombosis: describe and tx
• Red cord
• Varicose veins
• Tx: warm compresses
Low Risk DVT: what is the DVT prophylaxis
SCDs
Moderate Risk DVT: what is the DVT prophylaxis
Heparin
DVT Prophylaxis High Risk
(Ortho/Neurosurgeons/Previous DVT): warfarin with INR of 2-3
DVT Tx:
LMW Heparin+ Warfarin (can tx outpatient if no pulmonary sx or co-morbidities)
Thrombus:
artery occlusion
Emboli
moving thrombus
IgA Deficiencies:
• Giardia
• Ataxia Telangiectasia
bugs that have IgA Proteases:
• Strep pneumo
• H. influenza
• N. catarrhalis
diseases with IgA Nephropathies (4)
• Alport's
• HSP
• Berger's
• Ankylosing Spondylitis
Rathke's Pouch =>
• Anterior pituitary
• Hard palate
CVAs:
what is a Stroke:
infarcted cerebral tissue
CVAs:TIA:
neurologic deficits < 1hr w / no infarction
Dx: CVA (2) and medical therapies (3)
US ⇨ carotid stenosis
TEE ⇨ embolus
• Antiplatelets (asa, Clopidogrel)
• Anticoagulate (Heparin, warfarin)
• Thrombolytics (t-PA)
DDX:/Sx Strokes at Carotid: anterior circulation (4)
• TIA
• Amaurosis Fugax
• Aphasia
• Clumsy hands
Strokes at the Vertebrobasilar: posterior circulation
SAND
• N/V
• Syncope
• Ataxia
• Diplopia
Stroke Management:
1) CT: rule out hemorrhagic stroke
2) Treat based on time symptoms began:
• <3hr: t-PA (IV)
• 3-6 hr: t-PA (intra -arterial)
• 7-8 hr: Embolectomy
• 9+hr: Dipyridamole+ asa
Agnosia:
difficulty with comprehension
Agoraphobia:
fear of not being able to escape "can't go"
Anosagnosia:
can't understand that they are sick
Apraxia:
can't follow commands
Aphasia:
can't speak due to brain problem
Dysarthria
can't speak due to muscle problem
Agraphia:
can't write
Anomia
can't remember names
Prosopagnosia
can't remember faces
what would the CBC of every vasculitis would look like?
⇩RBC, ⇩platelets, ⇧WBC, ⇧T cells, ⇧MP, and schistocytes
for collagen vascular disease what would be up as well
eosinophil count will also be elevated.
CBC:⇩RBC, ⇩platelets, ⇧WBC, ⇧T cells, ⇧MP, and schistocytes
tie in the vasculitis into concept into LES
You have a vasculitis, and your RBC count is low. What do you need RBC for?
oxygen. And what do you need oxygen for? Making energy. So what state are we in? The low energy
state.
what would be seen in vasculities
• Low volume state, low energy state, restrictive lung dz profile, cell-med inflammation
• Exposes BM~>shows GP2b3a, which attracts platelets
• ⇩RBC/platelets, ⇧WBC/T cells/ MP, schistocytes
Ankylosing Spondylitis
pt complaint
x-ray
test
HLA association
inheritance
Middle-age male w / back pain, bamboo spine, + Schober test, HLA-B27, AR
Alport's
IgA deposition, deaf or cataract family
Behset's
RA + oral and genital ulcers
Berger's
IgA deposition 2 wk after cold ~> renal failure (hematuria, edema)
Buerger's
Smoking Jews, necrosis of extremities
Churg-Strauss: associated problems, antibody, unique features
Pulmonary eosinophils, asthma, p-ANCA
CREST: syndrome of what kind of scleroderma and its antibody
syndrome Mild scleroderma, anti-centromere Ab
Cryoglobulinemia: what kind of inflammation and Ig
Acute non-bact inflammation ( < 2mo ), IgM
Diabetes mellitus: neuropathy distribution
Glove-and-stocking distribution
Disseminated Intravascular Coagulation "DIC": causes (3) and what would be seen.
Sepsis, amniotic fluid emboli, abruptio placenta, D- dimers = fibrin split products
Felty's
RA + leukopenia + splenomegaly
Goopasture's Lung and kidney
Ab and what would be seen on BM
anti-GBM Ab, linear BM
in imunofluorescence
Hemolytic Uremic Syndrome
"HUS" Child renal failure 2 wk after eating raw hamburgers
Henoch-Schonlein Purpura "HSP"
onset and Ig
associated syndrome
platelet levels
presentation of rash
Tx
down "Hip-South Purpura
"IgA deposition 2 wk after gastroenteritis,
intussusception, normal Plt, purpuric rash from butt
T x: Steroizds/ Immunosuppresants
Immune Thrombocytopenic Purpura:
onset and Ab
Purpura 2wk after URI, anti-platelet Ab
Immune Thrombocytopenic Purpura: tx
Tx:
1) Prednisone
2) IVIg
3) Splenectomy
Kawasaki Disease: presentation
"CRASH"
Strawberry tongue, red eyes/lips, palm/sole rash,
cervical lymph nodes, kid MIs, high platelets, fever,
Kawasaki Disease: tx
Tx: ASA + flu shot, IVIg
Leukocytoclastic Vasculitis
Drug allergy causes vasculitis
Mixed Connective Tissue Disease ab
Anti-RNP Ab
MPGN type l
C3 nephritic factor
MPGN type II
Kidney deposits, tram-tracks, low C3
Polyarteritis Nodosa "PAN"
attacks what organs
antibody
associated disease
apprerance
GI and kidney, P-ANCA Ab, HepB, mottled lace-like
appearance
Polyarteritis Nodosa "PAN" Test:
Biopsy or Visceral Angiography
Post-strep Glomerulonephritis
onset
deposits
strain
2 wk after sore throat, Subepithelial deposit
strain 12
Progressive Systemic Sclerosis
Scleroderma that attacks organs~
Rheumatoid Arthritis
presentation
pathogenesis of pannus and cardia
antibody
joints involved in the head
Worse in morning, attacks synovium => pannus,
amyloid =>restrictive cardia, RF, attacks C1-C2 joint
scleroderma: ab
Anti-Scl70 Ab
Serum sickness
2 wk after vaccination (MMR)
Sjogren's
presentation (3)
antibody
RA + sica (xerostomia/xeropthalmia), anti-SSB Ab,
dental cavities
Still's disease= Juvenile RA
Iridocyclitis + RA
Subacute Bacterial Endocarditis
most common cause
Septic emboli, Strep viridans
Temporal Arteritis
presentation
ESR levels
Unilateral temporal HA, jaw claudication, ESR >60
Syphilis
Aortitis, wriinkled intima, tree-bark appearance, obliterative endarteritis
Systemic Lupus Erythematosis "Lupus"
antibody
MCC of death
deposits (Ig)
complement
rash
Ab: dsDNA/Sm/ Cardiolipin, malar rash, die of renal
failure, subepithelia/ deposit, IgG at derm-epid jxn, granular
complement
Systemic Lupus Erythematosis
"Lupus" TX
Tx: NSAIDs. Cyclophosphamide,
hydroxychloroquine
Takayasu's = "aortic arch syndrome" (4)
Weak pulse, aortitis, Asian women, blind, Raynaud's,
acute pain with cold
Takayasu's = "aortic arch syndrome" tx
Tx: daily high-dose steroids
Thrombotic Thrombocytopenic Purpura "TTP"
presentation
deficiency
and tx
Purpura + neuro symptoms, VWF esterase deficiency
Tx: Plasmapheresis
Trousseau's
Migratory thrombophlebitis, assoc w / cancer
Wegener's "whole lot of crap"
attacks what organs
ab
Lung, kidney, and sinus, c-ANCA Ab
Palm/Sole Rashes:
''TRiCKSSS''
Toxic Shock Syndrome
Rocky mountain spotted fever
Coxsackie A: Hand-Foot-Mouth disease
Kawasaki
Scarlet fever
Staph Scaled Skin
Syphilis
High platelet count
Kawasaki
Normal platelet count:
HSP
ABI:
1.0:
<0.9:
<0.4:
ABI:
1.0: Normal
<0.9: PVD
<0.4: Severe ischemia
what are HLA-B27 Diseases:
• Psoriatic Arthritis
• Ankylosing Spondylitis
• Reiter's
Psoriatic Arthritis:
involves what joints
bones, nails and extensors
stones and associated syndrome
attacks DIP joints, silver oval plaques on extensors, nail pitting, pencil-thin bones, gout, uric acid kidney stones
Ankylosing Spondylitis
Inheritance:
presentation
pathogenesis
x-ray
test
inheritance: AR
pathogenesis: Ligament ossification,
presentation: uveitis, decreased Lumbar curve, stiffer in morning, kyphosis,
x-ray: bamboo spine,
test: (+) Schober test
Reiter's
Uveitis, Urethritis, Arthritis
what are the Pulmonary Eosinophilias:
• Aspergillus (Tx: Steroids)
• Loeffler's (Tx: Antibiotic or Anti-parasitic)
• Churg-Strauss (Tx: Zafirlukast)
Aspergillus tx
Tx: Steroids
Loeffler's tx
Tx: Antibiotic or Anti-parasitic
Churg-Strauss tx
Tx: Zafirlukast
Low C3 diseases
"PMS in Salt Ltke City"*
Post-strep GN
MPGN Type II
Subacute Bacterial Endocarditis
Serum sickness
Lupus
Cryoglobulinemia
CREST:
Calcinosis
Raynaud's
Esophageal dysmotility
Sclerodactyly
Telangiectasia
Bacterial Endocarditis: tx
Bacterial Endocarditis: (Tx: Nafcillin + Gentamycin)
Bacterial Endocarditis: acute vs subacute
Acute: Staph Aureus => attacks healthy valves
Subacute: Strep viridans => attacks damaged valves
bacterial Endocarditis Dx:
TEE
bacterial Endocarditis Septic emboli can lead to what complication?
ischemic stroke
bacterial endocarditis: septic emboli in the Brain
Mycotic aneurysm
bacterial endocarditis: septic emboli in the Retina (describe)
Roth spots (central white hemorrhagic spots)
bacterial endocarditis: septic emboli in the Fingers/Toes:
Osler nodes (painful red nodules) "ouch"
bacterial endocarditis: septic emboli in the Nailbed:
Splinter hemorrhage
bacterial endocarditis: septic emboli in the Palm/Soles
Janeway lesions (painless dark macules)
Cryoglobulinemia: pathogenesis
serum proteins (i.e. globulins) form a gel when exposed to cold
bugs that cause Cryoglobulinemia:
"I AM HE"
Influenza
Adenovirus
Mycoplasma
Hep B/C
EBV