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82 Cards in this Set

  • Front
  • Back
2 components of extracellular fluid volume
Plasma volume

Interstitial Fluid Volume
Pressure that tends to drive fluid out of capillary
Hydrostatic pressure
Pressure that tends to drive fluid into capillary
Colloid oncotic pressure
Causes of extracellular edema
- Increased capillary pressure (excessive kidney retention, high venous pressure, decreased resistance)

- Decreased plasma proteins (proteinuria, burns, failure to produce proteins)

- Increased capillary permeability (immune reactions, toxins, bacterial infections, vit defficiency,prolonged ischemia, burns)

- Blockage of lymphatic return (cancer, infections, surgery, congenital abnormalities)
3 stages of shock
- Compensated hypotension

- Signs of cerebral, renal, and myocardial insufficiency and increased sympathetic activity

- Severe ischemia with capillary and endothelial damage + acidosis
Management of shock (general)
- Ensure adequate oxygenation

- Bladder catheter to measure urine output

- Vasopressors
Cardiogenic treatment of shock
Inotropic agents, Intra aortic balloon pump, diuretics, correction of underlying lesion (if possible)
Hypovolemic treatment of shock
Fluids/blood products

Correction of underlying pathology
Anaphylactic shock treatment
Epinephrine

Antihistamines
Systemic illness caused by spread of microbes (or toxins) via bloodstream
Septicemia
Sepsis is a syndrome - T/F
True
Describe progression of sepsis
SIRS --> Sepsis --> Severe sepsis --> Septic shock --> Multiorgan dysfunction syndrome
General syndrome that may have causes other than microbial - pancreatitis, trauma, burns, ischemia, tissue injury etc
Systemic Inflammatory Response Syndrome SIRS
Criteria for SIRS
Oral temperature more than 38 or less than 36 C

Respiration rate over 20 breaths a minute

Heart rate over 90 beats per minute

Leukocyte count over 12000 or less than 4000 or more than 10% of bands
SIRS + confirmed (suspected) infection
Sepsis
Patient presents with fever or hypothermia, tachycardia, subnormal BP, subnormal urinary output, increased CO, or decreased peripheral vascular resistance - ?
Clinical sepsis
Sepsis + hypotension that can be corrected by administration of fluids
Severe sepsis
Sepsis + persistant hypotension that cannot be corrected by administration of fluids
Septic shock
Patient presents with sepsis with hypotension that is unresponsive to fluid resuscitation, organ dysfunction and perfusion abnormalities - diagnosis
Septic shock
Sepsis + altered organ function
MODS - multiorgan dysfunction syndrome
#1 cause of bacteremia
Gram positive organisms
#1 cause of septic shock
Gram negative rods
Important cause of invasive fungal infections in sepsis
Aspergillus
Things necessary for sepsis to occur
Large inoculum

Immune defect

Microbes escape host defence

Stimulation of cytokine cascade

Toxin production and distribution
Gram negative rods risk factors
Diabetes mellitus

Lymphoproliferative diseases

Cirrhosis of liver

Burns, invasive procedures, treatment with drugs that cause neutropenia
Bacterial mediator of sepsis in gram negative bacteria
LPS
Bacterial mediators of sepsis in gram positive bacteria
Peptidoglycan

Lipoteichoic acid

Superantigens
Extremely potent toxin - elicits production of cytokinesm activates complement cascade and activates coagulation cascade
LPS
Pyrogenic cytokines
TNF alpha

IL 1

IL 6
Cytokine that activates T cells
IL 12
Cytokine chemotactic for leukocytes
IL8
Pro inflammatory response leads to early or late mortality
Early mortality
Anti inflammatory response leads to early or late mortality
Late mortality
This cytokine contributes to fever, wasting, increased breathing and HR, hypotension and hemorrhages in organs
TNF alpha
This cytokine stimulates prostaglandin release in hypothalamus - fever, contributes to hypotension, anorexia and increase in PMN's
IL1
_ promotes neutrophil reactions - chemotaxis and aggregation, degranulation and radical production
C5a
Gram positive cocci risk factors
Vascular catheterizations

Indwelling mechanical deves

Burns

IV drug use

Malignancy and chemotherapy

Toxin mediated (TSS)
Bacteria that produce superantigens
S aureus + S pyogenes
Activate T cells, induces huge cytokine response and septic shock - do not interact with MHC or TCR like conventional antigens
Staph Aureus

Step pyogenes
Which cytokine leads to stimulation of TNF alpha and shock
IL2
Treatment of sepsis
Treat with broad spectrum antibiotics until organism is identified
This infection:

- Comes from infected foci
- Associated with influx of host neutrophils
- Set off inflammatory cascade
- Doesnt trigger as intense TNF alpha response
Gram positive
This infection

- arise from within host - GI tract, billiary tract and urinary tract

- may be controlled by antibody and complement

- Have fewer virulence factors but do have endotoxin
Gram negative infections
_ sources are associated with intermittent bacteremia
Extravascular
_ sources associated with continuous bacteremia
Intravascular (IE, catheter, mycotic aneurysm)
Sickle cell patients tend to have what type of sepsis
Salmonella
How many blood cultures should be taken in patient with sepsis
3 - 99% sensitivity
p ANCA is found in what diseases
Churg Strauss

Microscopic polyangitis

PAN
Most common form of systemic vasculitis in adults
Temporal arteritis
What type of inflammation in Giant cell arteritis
Granulomatous
What size vessels affected in temporal arteriits
Large and medium size
Ophthalmic blindness - medical emergency - which vasculitis
Temporal arteritis
Screen test for temporal arteritis
ESR
Treatment for temporal arteritis
Steroids
What type of inflammation in Takayasu arteritis
Granulomatous
What size vessels in Takayasu
Large vessels to medium sized
In this type of vasculitis there is thickening of vascular wall and narrowing of the lumen with subsequent thrombosis
Temporal arteritis
40 year old Asian female with complain of coldness/numbness of fingers, visual disturbances and hypertension
Takayasu disease
Fibrous thickening of aorta (arch and branches) and narrowing or total occlusion occur in which type of vasculitis
Takayasu
PAN - what type of inflammation
Segmental necrotizing
What size arteries involved in PAN
Medium size arteries
Pulmonary involvement in PAN?
NO
This problem is usually dominant and cause of death in PAN
Renal involvement
PAN associated with what other disease
Hep B
Patient presents with tender erythematous nodules with central "punched out" ulcerations - diagnosis
PAN
Microscopic polyangitis - type of inflammation
Necrotizing
Size of vessels involved in microscopic polyangitis
Small - arterioles, capillaries, venules
Lung involvement in microscopic polyangitis?
YES
Patient presents with hemoptysis, hematuria, proteinuria, abdominal pain, arthralgia and muscle pain/weakness
Microscopic polyangitis
UA shows RBC casts -which vasculitis
Microscopic polyangitis
Splinter hemorrhages - which diseases
Microscopic polyangitis

Infective endocarditis
Person with asthma + eosinophilia - which vasculitis
Churg Strauss syndrome
Childhood vasculitis
Kawasaki disease
Which arteries involved in Kawasaki
Coronary arteries
4 year old child presents with high fever, conjunctival and oral lesions, rash and lymphadenitis - diagnosis
Kawasaki
Necrotizing vasculitis of respiratory tract and kidneys
Wegener granulomatosis
Patient presents with pneumonitis and sinusitis, nodules seen on chest x ray - diagnosis
Wegener granulomatosis
cANCA present in _
Wegener granulomatosis
Peripheral vascular disease in smokers
Buergers
34 year old male presents with intermittant claudication and ulcers on lower leg, heavy smoker
Buergers
Intermittant bilateral attacks of ischemic vasospasm in skin
Raynaud phenomenon
Murmur in acute RF
Mitral regurgitation