SEARCH RESULTS FOR: Cryoglobulinemia

Cryoglobulinemia

Cryoglobulinemia: Pathogenesis and clinical findings Inflamed vasculature Seizure is predisposed to Hemorrhagic stroke (blood Lymphoproliferative Hematologic Hepatitis C Autoimmune (self- Deposits in rupture & ↓ seizure vessel leaks into brain) (↑ Lymphocyte (blood) cancers infection (HCV) attacking) conditions cerebral Cerebral threshold production) conditions (brain) vasculitis Ischemic stroke (clot blocks Inflamed vasculature arteries ↓ cerebral blood flow cerebral blood flow) Acute ↑ B cell activity ↑ Chronic B cell activation ↑ Deposits in Retinal Retinal artery hemorrhage (severe bleeding) immunoglobulin (Ig) production immunoglobulin (Ig) production retinal arteries vasculitis Retinal artery infarct (↓ oxygenation à tissue death) of eyes Tingling Type II: Type III: Deposits damage & narrow walls of ↓ Blood flow monoclonal (recognize 1 polyclonal tiny blood vessels supplying to nerve cells Numbness Type I: site on antigen) IgM, IgG or (recognize >1 nutrients to peripheral nerves Weakness monoclonal (recognize 1 IgA & polyclonal (recognize site on antigen) site on antigen) IgM or IgG >1 site on antigen) Igs IgG & IgM Deposits in Alveolar alveolar (lung air capillaries are sacs) capillaries destroyed Exposure to temperatures <37°C Immune complexes deposit & form cryoglobulin (abnormal protein) in small/medium-sized vessels Cryoglobulins activate complement (factors that enhance innate (first-line) immune system responses) Deposits in cardiac (heart) tissue Deposits obstruct mesenteric (abdominal) vasculature Myocardial (heart muscle) inflammation, necrosis & fibrosis (scarring) Mesenteric vasculitis Alveolar Dyspnea (short of breath) hemorrhage (severe bleeding) Hemoptysis (coughing blood) Hypoxia (↓ Tissue oxygenation) Myocarditis (inflamed myocardium)** Inflamed vasculature Gastrointestinal à ↑ rupture risk bleed Mesenteric ischemia (↓ ↓ Mesenteric blood flow oxygen to intestines) à scars & narrows intestines Complement factors are consumed (activated & used) Immune complexes (primarily type I) occlude vessels Immune complexes (primarily types II & III) deposit in vessels à endothelial (vessel wall) damage & vasculitis (inflammation) Abdominal pain Abdominal cramps Bowel obstruction Deposits damage glomeruli (kidney capillary clusters) à triggers inflammation ↑ Permeability (“leakiness”) in damaged capillaries Hematuria (blood in urine) Proteinuria (protein in urine) ↓ Complement factors C3 & C4 Blood in obstructed vessel areas becomes hyper-viscous (thick) Hyperviscosity syndrome Inflammation ↑ proliferation of glomerular basement Blood stasis & vascular congestion ↓ Oxygen delivered to skin Local hypoxia (↓ oxygen delivery) Visual disturbances Confusion Headache Membranoproliferative glomerulonephritis (immune-mediated kidney inflammation) Joint swelling Joint stiffness ↑ Hydrostatic pressure ruptures capillaries Livedo reticularis (reddish-blue patchy skin discolouration) Reactive vasoconstriction (narrowed vessels) Deposits in synovial (joint connective tissue) membrane Deposits damage post- capillary venules in dermis (skin) Red blood cells leak into surrounding tissue Mucosal (moist lining of Raynaud phenomena (extremities exposed tissues) bleeding become white & numb Vasoconstriction obstructs blood vessels Ischemia (restricted blood supply to tissues) Synovial edema (swelling) & thickening Non-blanchable (non-color- fading) purpura (palpable purple skin spots) Necrosis (cell & tissue death)** Authors: Julia Fox, Catherine R Jarvis Reviewers: Navdeep Goraya, Glen Hazlewood* * MD at time of publication **See corresponding Calgary Guide slide(s) Legend: Pathophysiology Mechanism Complications Published Mar 1, 2026 on www.thecalgaryguide.com ↓ Blood flow Sign/Symptom/Lab Finding