Hemodynamics and Autoimmune Diseases Flashcards Preview

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Flashcards in Hemodynamics and Autoimmune Diseases Deck (268)
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What is decreased plasma osmotic pressure? Describe a clinical example.

- Pressure exerted by proteins, notably albumin, in blood vessel’s plasma that tends to pull water into circulatory system

- Albumin: accounts for nearly 50% of total plasma protein and is major protein maintaining plasma osmotic pressure

- Nephrotic syndrome –> edema from decreased plasma oncotic pressure due to protein loss through kidneys



What is hemorrhage? Describe 5 subcategories.

- Hemorrhage: extravasation of blood due to blood vessel rupture; common, commonly serious, and described with large number of precise terms (continuum of trivial to fatal)

- Hematoma: hemorrhage enclosed in tissue

- Hemothorax: hemorrhage into pleural cavity

- Hemopericardium: hemorrhage into pericardial space

- Hemoperitoneum: hemorrhage into abdominal cavity

- Hemarthrosis: hemorrhage into a joint (commonly associated with hemophilia) 


What is Glanzmann thrombasthenia? Describe 2 drugs that use a similar mechanism in a beneficial way.

- Rare deficiency of platelet Gp2b3a receptors causes bleeding tendency due to deficient platelet aggregation

- Some snake venom contains substances that bind to platelet Gp2b3a receptors, mimicking this disease

- Eptifibatide (Integrilin): similar mechanism to the snake venom; given IV to pts who are clotting off coronary arteries

- Clopidogrel (Plavix): blocks platelet ADP receptors (preventing conformational change that mediates binding of Gp2b3a to fibrinogen, and aggregation) –> taken orally by pts who have suffered clotting of critical coronary or cerebral arteries 


How might shock cause pulmonary alveolar edema? What is the most common cause of this type of edema?

- Shock (total body ischemia) causes acute lung injury (ALI)

- ALI causes increased vascular permeability, in turn causing alveolar edema

- However, this is NOT the most common cause of pulmonary alveolar edema -> increased hydrostatic pressure from left heart failure is

1. Blood gets backed up due to increased pressure, which, when it gets too high, loosens the junctions b/t pulmonary alveolar capillary endothelial cells, and leaks into the airspaces


What is this? Why are there dimples in the skin?

- Peau d'orange: lymphedema due to breast cancer causing the skin over the tumor to resemble the skin of an orange 

- Cooper's suspensory ligaments are pulling back on the skin


How does stasis promote thrombosis?

- Allows platelets to spend more time sitting on endothelial cells (vs. normal blood flow, where platelets concentrated in center of vessel, with plasma toward outside)

- Any factor slowing blood flow makes intravascular clot formation more likely



How does cancer cause HS?

- Inflammatory response to malignant tumors and necrotic debris they release into general circulation when they outgrow their blood supply

- Also compress or invade veins, obstructing blood flow, and creating turbulent flow or stasis

- Mucin: high molecular weight, heavily glycosylated thrombogenic proteins produced by malignant glandular tumors

- Migratory thrombophlebitis: simultaneous VT and inflammation at multiple sites due to malignant tumors, aka Trousseau syndrome



What is antiphospholipid antibody syndrome?

- Rare, life-threatening acquired HS that causes arterial thrombosis

- Common in young females

- Autoantibodies against phospholipids (plasma protein antigens unveiled by binding phospholipids) –> may be in association with lupus erythematosus

- Present with recurrent miscarriages, DVT in legs, cerebral infarctions, migraine headaches, cardiac vegetations, ischemic hands/feet, thrombocytopenia, and others

- Abs present in 1-5% of asymptomatic individuals, suggesting syndrome requires more than just their presence 


What is the difference between medium-sized and large-sized PE?

- Medium sized -> can cause hemorrhagic infarction (if bronchial arterial blood supply impaired), leading to hemoptysis (uncommon)

- Large size –> acute cor pulmonale (leading to right heart failure) and sudden death (must block >60% or more of pulmonary circulation to have this effect 


What is PTPN22?

- PTPN22 is a tyrosine phosphatase gene

- Polymorphisms in this gene are associated with rheumatoid arthritis and type 1 diabetes mellitus, among other autoimmune diseases


What are the gross and microscopic pathology, symptoms, and signs of Sjogren syndrome?

- Gross: dry ocular and oral mucosa, enlarged salivary and lacrimal glands

- Microscopic: 1) intense infiltration of CD4 T cells, 2) destruction of gland architecture, +/- plasma cells, +/- germinal centers. Renal involvement: interstitial nephritis rather than glomerulonephritis.

- Symptoms: dry eyes, dry mouth

- Signs: dry mucous membranes of eyes and mouth, conjunctival ulcers, oral ulcers, enlarged salivary and lacrimal glands


IMPORTANT CONCEPT: Symptoms of dry eyes and dry mouth suggest the possibility of Sjogren syndrome


How are kidney transplant biopsies evaluated for evidence of BK virus infection?

- Aka, polyomavirus nephropathy

- Can be manifested by intranuclear inclusion bodies and epi cell injury and lysis. Immunostains used to confirm sighting of BK virus inclusions. Urine also checked for BK virus by “BK virus activation assays,” including quantitative PCR assays, urine cytology and/or urine electron microscopy, but positive urine assays must be correlated with plasma assays b/c clinically significant urine assays associated with simultaneously positive plasma assays


What is the consensus definition of sepsis?

SIRS due to infection, proven or highly suspected, meeting at least 2 of these 4 criteria:

1. Fever >38 or hypothermia

2. P >90/min

3. Tachypnea >20/min or hyperventilation (arterial pCO2

4. Leukocytosis (WBC > 12,000/cu mm), leukopenia (WBC 10%)

NOTE: sepsis and SIRS are on a continuum, and the criteria for the subsets are arbitrary -> the consensus definitions of sepsis and SIRS have always been problematic, and do not work for small children (high resting HR and WBC), for example -> IN DISEASE DX, THERE IS NO SUBSTITUTE FOR EXPERIENCE


What is primary hemostasis, and what are its mediators?

- Platelet adhesion to thrombogenic ECM

- Platelet adhesion to ECM mediated by von Willebrand factor, which binds to Gp1b receptors on platelets –> change in shape from smooth-surfaced discs to spheres with long, spiky projections

- Change in shape associated with conformational change in Gp2b3a receptors, making them bind fibrinogen, which then binds to altered receptors on adjacent platelets, linking them in aggregate

- All of this is associated with release of ADP and thromboxane A2 (a COX derivative) from platelet granules, causing additional platelet recruitment and aggregation, resulting in primary hemostatic plug 


What are the two "stages" of acute kidney injury (AKI)?

1. Earliest finding: tubular epithelial edema 

2. Later, worse injury: acute tubular necrosis, but tubular epithelial cells can regenerate and be replaced (glomeruli cannot, but are not typically affected in shock)


What is the nature of the fluid on the cut surface of this lung in a patient who died of shock?

- This is alveolar edema fluid, which is typically white and bubbly 

- Pulmonary alveolar edema is the typical manifestation of acute lung injury (ALI) in the early phase (first day)

1. Note: ALI has many causes, not just shock


What 5 things must you describe of any infarct, hemorrhage, tumor, or lesion?

1. Size
2. Shape
3. Color
4. Consistency, including texture (this is the only one that requires more than seeing, i.e., palpation)
5. Relationships (including location and proximity to other things) 


Describe the relationship between heart failure and kidney function.

Heart failure reduces renal blood flow, activating renin-angiotensin-aldosterone system, and causing retention of Na and H2O –> 2 simultaneous types of edema (Na retention and increased hydrostatic pressure


What is Bernard-Soulier syndrome?

Rare deficiency of platelet Gp1b receptors for von Willebrand factor causes bleeding tendency 


A 45-year-old obese black female mother of three comes to the emergency department with constant severe epigastric abdominal pain radiating to her back, associated with nausea and vomiting.  Her temperature is 39 degrees C (102.2 degrees F), pulse 130/minute, blood pressure 100/60 mm Hg and respirations 25/minute.  She sits on the gurney with her knees to her chest.  Her abdomen is tender in the right upper quadrant.  Her skin is warm.

Shock due to SIRS due to acute pancreatitis due to gallstone obstruction of pancreatic duct


Why is treatment of DIC so complex?



What are the four fates of a thrombus?

1. Dissolution: dissolving by fibrinolysis (endogenous or exogenous)

2. Propagation 

3. Embolization 

4. Organization (and recanalization): can occur in pneumonias, exudates, injuries, etc., and not just thrombus




What are anergic lymphocytes?

Functionally unresponsive


What are the definition, epidemiology, and pathogenesis of systemic lupus erythematosus?

- Definition: prototype multisystem autoimmune disease

- Epi: “fairly common" -> up to 13X more common in women, more common in blacks, affects 1 in 245 black women, most common in child-bearing age (15-45), more severe in blacks and Asians

- Pathogenesis: failure of self-tolerance, antinuclear antibodies, genetic factors, environmental factors (meds, UV light, sex hormones), immunologic factors (activation of helper T cells and B cells, IgG autoAb production, immune complexes)


What is Prothrombin G20210A mutation?

- Leads to elevated prothrombin levels and an almost 3-fold increased risk of VT 

- Single mutation in 3' untranslated region of prothrombin gene (1-2% of population) associated with hypercoagulability


What is this?

- Passive congestion: caused by right heart failure due to backup of blood inadequately pumped out of heart; associated with gross pathological finding of nutmeg liver

- Hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas (can be acute or chronic) 


What is going on here? What is the most likely pathophysological mechanism of this condition?

- Lung tissue: abnormal, lots of RBCs, congested capillaries, no air exchange possible b/c airspaces filled w/pink proteinaceous fluid -> pulmonary alveolar edema 

- Most common cause is: left heart failure (congestive heart failure) 

- Increased hydrostatic pressure is the most likely mechanism



What is this and what is the most common cause?

- Nutmeg liver: passive congestion of the liver 

- Right heart failure is the most common cause (the most common cause of right heart failure is... left heart failure)


What are the 4 fates of a thrombus?

1. Dissolution: complete or partial removal of the clot by fibrinolysis 

2. Propagation: growth of the clot 

3. Embolization: travel of a detached, intravascular solid, liquid, or gaseous mass from its point of origin in the vascular system to a distant site (this is not likely to be the way a large thrombus would evolve)

4. Organization (and re-canalization -> may lead to partial, or no, reopening of the channel; you could call this a scar)

NOTE: these are NOT mutually exclusive


Why is it important to monitor how long you leave in venous catheters (that you put in, and others put in pts you are responsible for)?

- Thrombi being propagated every day you leave a catheter in place, and these can become infected -> infection, embolization, and o/complications of peri-catheter thrombi kill pts every day 


- EXTRA: used to be guideline to change every 5 days, but intensivists pushed back because there are only so many sites to put these in –> there is an active discussion about whether these should stay in every day (typically on a blood thinner too if not contraindicated and need this for a long time; also long-term catheters designed specifically for this)