11. Pathology of Thrombosis and Hemostasis, hemodynamic disorders and shock Flashcards
edema
fluid in ECF
- Increased ECF (transudate = fluid w/out blood products)
○ Exudate (incl proteins) is worse and caused by inflammation or damage
- Collects in interstitium and serosal cavities
○ Effusion = serosal cavity (lined by mesothelium, often leaks)
○ Ascities = effusion of peritoneal cavity
- Localized vs systemic
○ Anasarca = systemic
- Most common
○ Cutaneous, localized
○ Dependent edema (eg due to CHF)
§ Children: nephrotic syndrome
○ Pulmonary edema (fluid in alveolar sacs)
○ Ascites
○ Cerebral edema (tx TBI w/steroids to prevent inflamm)
- Causes
○ Physical/chemical
§ Increased hydrostatic pressure
□ Venous obstruction
□ Lymphatic obstruction (lymphedema)
® “Chylous effusion” due to milky white fluid (pleural cavity thanks to obstruction of thoracic duct)
§ Decreased plasma osmotic pressure
○ Primary damage to capillaries
§ Heat
§ Inflammation
§ Shock (often w/fluid overload)
§ Angiogenesis
§ Often causes congestion as well
pulmonary edema
- Causes
○ Heart failure, acute, and chronic
§ Increased hydrostatic pressure
○ Infections
§ Aspiration, bacterial pneumonia, etc
§ Will also have fibrinous exudate
○ Toxins
§ Kidney disease, cocaine, smoke inhalation
○ Non-inflammation endothelial damage
§ Near-drowning
§ HAPE (high altitude pulmonary edema)
ascites
(hepatic circulation)
- Increased hydrostatic pressure due to scarring (central vein obsrtuction)
○ Intrinsic liver failure vs right heart failure
- May have osmotic component
○ Hypoproteinemia from liver failure
- Splenomegaly
○ Splenic vein-portal vein
generalized edema from decreased osmotic pressures
- Nephrotic syndrome: hypoosmotic
- Cirrhosis
- Protein-losing enteropathy
- Malnutrition: low protein
- Shock
○ Multifactorial:
§ Low albumin
§ Fluid overload
§ Capillary damage
Heart failure
lymphedema
- Radiation
- Surgery
- Parasitic infection (not in USA)
- Neoplasms (lymphoma)
- Cellulitis (obese pts)
- Obstruction of thoractic duct
○ chylothorax
vascular congestion
- Increased fluid (blood) within vascular channels
- Assoc w/edema
- Causes
○ Outflow obstruction
○ Vasodilation - 2 most common types: pulm and liver congestion
hemostasis and thrombosis - progression of vascular thrombi
- Entothelial injury
2. Vasoconstriction
3. Platelet adherence and aggregation
4. Coagulation cascade (tissue factor)
i. Fibrin clot
5. Fibrinolysis/thrombosis equilibrium
virchow’s triad
- Endothelial injury
- Abnormal bloodflow
- hypercoagulability
endothelial injury
- Trauma ○ Primary evolutionary drive for hemostasis ○ Thrombosis is good - Chronic endothelial damage ○ Diabetes ○ HTTN ○ Atherosclerosis ○ Thrombosis is bad
abnormal bloodflow
- Varicosities
- Venous stasis
- Arterial aneurysms
- Dilated heart chambers
○ Atria
§ Afib
§ Mitral valve disease
○ Ventricles
§ Aneurysms from healed infarcts
Dilated cardiomyopathy
hypercoagulability
- Primary
○ Factor V Leiden, prothrombin, homocysteine (MTHFR), protein C, S, others- Acquired
○ Immobilization
○ Carcinomas (esp adenocarcinomas)
○ Antiphospholipid syndrome (APLS)
§ Recall abnormally long PTT even though it’s a hypercoagulable state! (see lecture 10)
○ HIT
○ Low risk: smoking, OCPs, nephrotic syndrome
- Acquired
antithrombotic factors and states
- Iatrogenic ○ Anticoagulation therapy - Genetic ○ Defects in coag factors and platelets - Acquired ○ Liver failure ○ Uremia ○ Infections (esp viral) ○ Leukemia ○ Vit K (also iatrogenic/warfarin therapy - Manifestations ○ Petechiae ○ Purpura ○ Hematochezia ○ Bleeding gums ○ Nosebleeds ○ Hemarthoris ○ Retinal hemorrhages ○ Cerebral hemorrhage
microangiopathic hemolytic syndromes
clotting and hemorrhage - Common features ○ Schistocytes on peripheral smear ○ Diffuse consumption of platelets and fibrin ○ Arteriolar and capillary fibrin-platelet thrombi ○ Usu causes hemorrhage - Causes ○ DIC, TTP, HUS
embolism
movement of physiologic or foreign material w/in artery or vein that lodges somewhere else - What can embolize? ○ Thrombus (most common) § Sterile vs septic ○ Fat (marrow, lipid) § Bone marrow during resuscitation, usu incidental § Lipid vacuoles post surgical or pancreatitis/bone marrow infarct non-surgical § ○ Amniotic fluid § Late pregnancy or delivery § 10% obstetric deaths § Increased risk w/uterine trauma § Coagulopathy and diffuse alveolar damage ○ Tumors ○ Air ○ Foreign materials (iatrogenic) § Therapeutic § Unintentional - Types of embolism ○ Systemic § Sources usu cardiac (valves, ventricles) § Iatrogenic (therapeutic tumor embolization) ○ Pulmonary § Source usu leg veins § Pulmonary thromboembolism □ Predisposing factors: ® Immobilization ® Post Op ® Coag disorder □ Dx: ® VQ scan, CT angio □ Tx: ® Anticoagulation (heparin acute, warfarin chronic, thrombolysis) ○ Paradoxical § Venous source, crosses oval foramen to reach systemic circulation (brain)
infarction
Reversible ischemic injury secondary to hypoxia
- Usu re: occlusion of blood supply (thrombus, embolus)
- Hemorrhagic (red)
○ Bowel, lung, heart (re-perfusion)
- Non-hemorrhagic (white)
○ Heart (non-reperfusion), kidney, liver, spleen
- Factors affecting likelihood of infarct
○ Nature of blood supply
§ Collaterals
§ Dual blood supply
○ Rate of occlusion
○ Vulnerability to hypoxia
○ Oxygen content of blood
