Fluid & Hemodynamics Flashcards
Anasarca
generalized, sever edema
Effusion
liquid in body cavities
pericardial, pleural, peritoneal or joint cavities
Ascites
effusion of the peritoneal cavity
Hydrothorax
watery fluid in pleural space
Empyema
pus/purulent effusion in pleural cavity
Hydropericardium
watery fluid in pericardial cavity
Hydrocephalus
too much CSF
Hydrocele
extra fluid in membrane around testes
Hydrosalpinx
too much fluid in fallopian tube
Ileus
too much fluid in small bowel
Seroma
non-infected fluid in surgical incision
Loculated effusion
more than one compartment filled with fluid
- due to scarring
Blister
fluid between epidermis and dermis or within epidermis
Bulla
big blisters
Vesicles
little blisters
Transudate mechanisms
- Excess total body fluid (iatrogenic, kidney failure)
- Increased pressure in small veins of body
- Decreased total plasma protein/albumin
- Lymphatic vessel obstruction
Lymphedema
often due to cancer, surgery/radiation therapy
Filarial disease
causes epidemic elephantiasis
Podoconiosis
“dust-foot”, sand plugging lymphatics
- seen in desert-dwellers
Milroy’s disease
lymphatics are malformed producing lifelong lymphedema
- worse in legs
Orangepeel skin
seen in breast signifying cancer plugging dermal lymphatics
Chylous Effusions
damaged lyphatics (thoracic duct) - turbid, lipid-rich fluid
Exudate mechanisms
- Leaky vessels (inflammation)
Where can you get non-inflammatory exudates?
neovascularization, deep wound healing (granulation tissue), cancer growth
Cardiac edema
edema appears first in feet after standing
- heart failure
Renal edema
edema appears around eyes
- total- body water overload
- low blood albumin
Liver disease
edema appears as excess fluid in abdomen
- low blood albumin plus increase resistance from portal venous system
Pulmonary edema is a warning sign for
heart failure and pneumonia
Angioedema
blood vessels become extra-permeable
- hereditary C1-esterase deficiency (larynx)
Hyperemia
increased BF to organ (arterial)
- red and throbs
Congestion
decreased BF from organ (venous)
- purple and doesn’t throb
- from transudate mechanisms
Where does blood pool after death?
around hepatic central vein
- appearance is “nutmeg”
Causes of viscous blood
too much IgM, cyroglobulin, high Hgb
Hemorrhage
blood cells escape blood vessel
- severity dependent on location
Hematoma
enough blood in tissue to palpate
Cauliflower ear
organization of a hematoma (formation of scar tissue)
Hemothorax
blood in pleural cavity
Hemopericardium
blood in pericardial sack
Hemoperitoneum
blood in peritoneal cavity
Hemoarthrosis
bleeds into a join space
Petechiae
little bruises
Purpura
big bruises (> 3 mm)
Ecchymoses
large bruises over 10 mm
What does petechiae in lower eyelid warn us of?
Endocarditis
- piece of valve –> ECA –> lower eyelid
Dengue
complex viral infection
- damages microvasculature
Hemoptysis
coughing up blood
Hematemesis
throwing up blood
Hematochezia
bright red blood from rectum
Melena
blood digested through gut
Thrombus
blood solidified within vascular lumen/cardiac chambers
Clot
blood solidified anywhere in body (not vascular lumen/cardiac chambers)
Initiation of hemostatsis
arterioles constrict once injury
Primary Hemostasis
platelets plug injury within seconds
- aggregation and release of granule contents
Secondary Hemostasis
clotting cascade turning liquid blood solid (minutes)
How do you inactivate thrombin
Thrombomodulin binds on intact endothelium
- activates protein C –> stopping clot formation
What factor cross-links fibrin?
Factor XIII
Virchow’s Triad
thrombus formation
- injured epithelium
- altered blood flow
- hypercoaguable blood
What is a hallmark sign of a thrombus?
Lines of Zahn
Recanalization
thrombi turn into granulation tissue –> contraction opens little channels
Describe a post-mortem thrombus
plasma (chicken fat) & sedimented RBC’s (currant jelly)
Mural thombus
thrombus on the wall of a vessel/chamber
Vegetations
thrombi on valves
White Clot Syndrome
“Heparin induced thrombocytopenia”
- antibodies against complex of heparin and PF-4
- platelets become white clots –> thrombocytopenia
Disseminated Intravascular Coagulation (DIC)
blood clotting is activated throughout circulating bloodstream
- platelets are consumed and plasmin is activated
Schistocytes and thrombocytopenia
DIC
fragmented red cells, too few platelets
Causes of DIC
- Thromboplastin gets into blood
- Damaged endothelium
- Both mechanisms (bad trauma, infarcts)
Paradoxical embolus
systemic v –> systemic a
Fat embolism
commonly fracture of long bone
- can get petechiae in white matter
What embolus is formed during cardiopulmonary resuscitation?
Bone marrow embolus from broken ribs
Cholesterol emboli
form from atherosclerotic plaque
What causes talc granulomas in lung?
IV heroin use
White Infarct
Arterial insufficiency, not reperfused
- single blood supply
Red Infarcts
Venous insufficiency or reperfused
- dual blood supply (liver, lungs)
Infarcts
area of ischemic necrosis from loss of blood supply
Shock
systemic hypoperfusion
Watershed infarcts
necrosis at places farthest from arterial supply
Cardiac Shock
MI, PE, rupture, diphtheria, poisons, tamponade
Hypovolemic shock
Hemorrhage, sweat/vomiting/diarrhea
Lost vascular tone shock
septic/total body inflammation, anaphylactic, meds, neurogenic
Compensated Shock
shunting blood to brain and heart
- underperfusion of gut/kidneys/skin
- patient feels cold
Calculation for shock
heart rate/systolic BP > 0.7
Progressive/Decompensated Shock
patient is going anaerobic
- kidney and liver cells mostly dead
- anaerobic metabolism increases lactic acid –> brings pH down –> dilates arteries and blood pools, interferes with heart function
Irreversible Shock
death is coming
- lysozymes digesting cells
Sepsis
bacteria flourishing in bloodstream
- need Rx or fatal
- patient feels warm
Most common cause of Sepsis
gram-positive cocci
Cyanosis
> 5 gm of unO2 Hb in glood
- poor oxygenation, poor perfusion, cold body part
