Dr. A's Pathophysiology Final
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
|---|---|---|---|---|---|
| What are the 2 types of edema? | Inflammatory and noninflammatory
🗑
|
||||
| What are the 4 causes of edema? | 1. Increased hydrostatic pressure
2. Decreased plasma colloid osmotic pressure
3. Impaired lymph flow
4. Renal retention of salt and water (JG apparatus)
🗑
|
||||
| What are 2 causes of increased hydrostatic pressure? | 1. Local increases: impaired venous outflow (lower extremities) due to thrombosis/stasis
2. Generalized increases: Heart failure, renal failure and dysfunction.
🗑
|
||||
| What causes reduced plasma oncotic pressure and what are the 3 reasons for it? | Loss of serum albumin:
1. Nephrotic syndrome
2. Cirrhosis
3. Malnutrition
🗑
|
||||
| What are 3 causes of lymphatic obstruction? | 1. Inflammation
2. Neoplasia
3. Parasitic infection (picture)
🗑
|
||||
| What are 2 causes of salt and water retention? | 1. Renal dysfunction
2. Heart disease;
Remember renin overproduction raises aldosterone which raises BP which can increase the chance of edema. Atherosclerosis in renal aa. secrete renin giving same result
🗑
|
||||
| What is a dependent edema most often due to and what can be involved? | Right sided heart failure; lower extremities involved, influenced by gravity
🗑
|
||||
| What type of edema does ascites present with? | Peritoneal edema (Kwashiorkor)
🗑
|
||||
| What is a generalized edema/anasarca most often due to and what can be involved? | Renal failure (can't maintain fluid volumes); More severe than dependent edema, periorbital and pitting edema.
🗑
|
||||
| What can cause a pulmonary edema and what are some presentations? | Left sided heart failure or microvascular (microbial) damage; edematous, proteinaceous (frothy) fluid w/in alveoli; symptoms are dyspnea and chest pain
🗑
|
||||
| A brain edema is usually a consequence of what and what can be involved? | Traumatic Brain Injury; localized or diffuse, a cause of ICP
🗑
|
||||
| What is hyperemia? | Increased blood flow to a tissue, sympathetic or chemically mediated.
🗑
|
||||
| What is congestion and what is the usual result? | Decreased blood flow away from a tissue can be localized or systemic, hypoxia/ischemia of affected tissue; Usually results in edema!
🗑
|
||||
| Give 2 organs effected and the reasons for chronic passive congestion. | Lungs: left sided heart failure
Liver: right sided heart failure (nutmeg liver)
🗑
|
||||
| What are 5 causes of a hemorrhage? | 1. Trauma
2. Aneurysms
3. Erosion; microbes, neoplasia
4. Vitamin deficiency
5. Thrombocytopenia (decrease in circulating platelets)
🗑
|
||||
| What is clinical significance of a hemorrhage dependent on? | Volume of blood loss, rate of blood loss, location of hemorrhage.
🗑
|
||||
| What is hemothorax? | Blood in thoracic cavity
🗑
|
||||
| What is hemopericardium? | Blood around heart
🗑
|
||||
| What is hemoperitoneum? | Blood in peritoneal cavity
🗑
|
||||
| What is hemarthrosis? | Blood in joint capsule
🗑
|
||||
| What is hematoma? | nonspecific: bruise-small localized hemorrhage
🗑
|
||||
| What is purpura? | Widespread bruising d/t metabolic imbalance
🗑
|
||||
| What is ecchymosis? | Common skin bruise
🗑
|
||||
| What is petechia? | Pinpoint hemorrhages tend to be in mucous membranes.
🗑
|
||||
| What is hemostasis? | Maintenance of clot-free blood w/in the vascular system while allowing for the formation of a solid plug of blood under conditions of vessel wall injury.
🗑
|
||||
| What are the 3 key players in hemostasis? | Vascular endothelium, platelets, coagulation system
🗑
|
||||
| What does intact endothelium do to prevent plug formation? (4) | 1. Insulates platelets from subendothelial collagen
2. Prostacyclin (PGI2) synthesis inhibits platelet aggregation
3. ADPase synth. inhibits platelet aggregation
4. Nitric oxide synthesis vasodilation and inhibits platelet aggregation
🗑
|
||||
| What does heparin like molecule synthesis do? | Activates anti-thrombin III (degrades thrombin) It removes thrombin from the equation stopping end-product (clot)
🗑
|
||||
| What is a fibronolytic property of intact endothelium? | Tissue plasminogen activator (t-PA) converts plasminogen to plasmin (plasmin degrades fibrin)
🗑
|
||||
| What are 4 pro-thrombotic properties of damaged endothelium? | 1. von Willebrand's factor synthesis
2. tissue factor synthesis
3. Platelet activating factor
4. t-PA inhibitor synthesis
🗑
|
||||
| What is von Willebrand's factor synthesis for, what is the disease and what can it cause/symptom? | Essential for platelet adhesion; There are mild, moderate and severe von Willebrand's disease which are bleeding diseases where can't fuse clots where needed. Can cause infertility sign is heavier than normal menstrual flow
🗑
|
||||
| What is tissue factor synthesis? | A glycoprotein which activates coagulation system.
🗑
|
||||
| What does platelet activating factor do? | Makes platelets sticky
🗑
|
||||
| What happens with t-PA inhibitor synthesis? | Clot not degraded b/c t-PA inhibited
🗑
|
||||
| What are the "bricks" of a thrombus? | platelets
🗑
|
||||
| Platelet actions oppose those of __________. | endothelium
🗑
|
||||
| What is secreted by platelets to activate them? | Thromboxane (TXA2), ADP, factors V and VIII, calcium
🗑
|
||||
| An activated platelet does what to exposed collagen and what factor does that mean? | binds to exposed collagen; von Willebrand's factor
🗑
|
||||
| Activated platelets are involved in initiation of what? | Coagulation cascade, role of Ca and phospholipid complex
🗑
|
||||
| How does a temporary plug become definitive? | Formation of fibrin from thrombin = fused mass of platelets
🗑
|
||||
| What are the 3 roles of the coagulation system w/ damaged endothelium? | 1. Activated by factor XII or tissue factor (initiation)
2. end product is formation of fibrin monomers (polymerize and trap)
3. Fibrin is the "cement" of a thrombus (fibrin, platelets, RBCs and WBCs)
🗑
|
||||
| What is thrombosis? (3) | 1. An aggregate of platelets, fibrin and blood cells w/in the non-interrupted vascular system
2. Adherent to the vascular endothelium (vs a post-mortem clot)
3. May arise in arterial or venous circulation
🗑
|
||||
| What are 3 predisposing factors to arterial thrombi? | 1. Damage to endothelium
2. Alterations in normal blood flow
3. Increased coagulability of blood
🗑
|
||||
| What are 5 causes of endothelium injury? | 1. Atherosclerotic lesion progression
2. Hemodynamic stress
3. Radiation, trauma, chemicals, microbes
4. Ischemic damage to endocardium
5. Valvular damage
🗑
|
||||
| What are the roles of stasis and turbulence in regards to alterations in normal blood flow? (4) | 1. Physical damage to endothelium
2. Disrupts laminar flow
3. Prevent renal clearance of coagulation proteins
4. Retards flow of anticoagulants to site of injury
🗑
|
||||
| What are 5 causes of increased coagulability of blood? | 1. Genetic defect in anticoagulant proteins or coagulant proteins
2. ?homocysteine
3. Neoplasia - release of procoagulants
4. Polycythemia vera (RBC neoplsia)
5. Smoking, obesity
🗑
|
||||
| What are the 3 most common sites of arterial thrombi and what is the result? | 1. Coronary
2. Cerebral (stroke)
3. Femoral arteries;
ischemic infarction = loss of blood supply
🗑
|
||||
| What are deaths from arterial thrombi d/t? | MC: myocardial infarction
cerebral infarction
renal infarction
🗑
|
||||
| What are 4 types of venous thrombosis? | 1. MC site: superficial leg veins (varicose veins)
2. MC clinical manifestation: Deep leg vein thrombosis
3. "red" thrombi (looks red, cyanotic)
4. Phlebothrombosis
🗑
|
||||
| What are Lines of Zahn? | Start/stop growth pattern w/in a thrombus, shows that thrombus is growing and chronicity of thrombus in a vessel
🗑
|
||||
| What are Mural Thrombi? | Thrombus w/in wall of an organ typically w/in ventricles of the heart. Weakening of ventricular wall, dislodge
🗑
|
||||
| What is a postmortem clot? | Blood stasis following death, not adherent to vascular wall.
🗑
|
||||
| What are Vegetations (infective endocarditis? | Fingerlike, wartlike or hairlike growth typically on heart valves associated w/ bacterial infection of heart consequence of rheumatic fever (cardiac sequelae) upon 2nd exposure untreated sequelae reaches 50% -> murmur, defect, arhythmias.
🗑
|
||||
| What are Verrucous (Libman Sacks) Endocarditis? | Produce vegetations not d/t bacteria
🗑
|
||||
| What are the manifestations of DVTs? | Edema of foot and ankle, pain of foot and ankle (Homan's sign = broad hand on gastroc.), local ischemia - bacterial skin infections, PULMONARY EMBOLIZATION
🗑
|
||||
| What are the 4 potential fates of a thrombus? | 1. Dissolution
2. Propagation
3. Organization
4. Recanalization
🗑
|
||||
| What is organization and recanalization with a thrombus? | Phenomenon of permanence of a clot; increase in blood flow is variable, attempt to increase amount of blood flow.
Recanalization forms thru channels by migration of endothelial cells w/in body of clot, added flow thru clot
🗑
|
||||
| What is embolization? | Worst possible fate, detach from vascular wall and travels downstream, )MC: thromboembolus) until hits smaller diameter vessel -> infarction with partial or complete occlusion of vessel lumina.
Pulmonary is venous
Systemic circulation is arterial
🗑
|
||||
| What is an embolism? | A detached intravascular mass that is carried by the blood to a site distant from its point of origin.
🗑
|
||||
| What is thromboembolism and what is the result? | MC = thromboembolus
results in partial or complete occlusion of vessel lumina, may lodge in pulmonary or systemic circulation.
🗑
|
||||
| What are 3 subtypes of thromboembolisms and what are common manifestations? | 1. Fat: MC during long bone fxs primarily the femur
2. Air: rare, air in wound, injected into blood stream >100 ccs, bends more common
3. Amniotic: @ birth associated w/ tearing of placenta perinatally; systemic circ. sucks up amniotic fluid -> toxic
🗑
|
||||
| Discuss pulmonary emboli as a case scenario. | MC preventable death in hospitalized pts (role of ambulation and anticoaculants), arise from DVT, small vs. large emboli.
🗑
|
||||
| What is a saddle embolus? | An embolus that cradles at the bifurcation of pulmonary trunk and propagates -> occlusion of blood to lungs -> shock
🗑
|
||||
| What are systemic emboli? | Arterial in origin includes left ventricle and ruptured atherosclerotic plaques.
🗑
|
||||
| What are 3 sites of lodgment with systemic emboli? | 1. Lower extremities (75%) -> acute infarction -> sudden gangrenous necrosis
2. Brain (10%)
3. Viscera (10%)
🗑
|
||||
| What is an infarction? | An area of ischemic necrosis w/in a tissue or organ most often caused by thrombotic or embolic occlusion = acute loss of blood supply or hemorrhage.
🗑
|
||||
| What are 2 types of infarction and what shape do they tend to be? | 1. White infarct: d/t thromboembolus - area becomes pale
2. Red infarct: d/t hemorrhage - bleed into tissue b/c breach in vascular wall
Both tend to be wedge shaped
🗑
|
||||
| What are determining factors of an infarction? | Nature of vascular supply, rate of development of occlusion, vulnerability of tissue to hypoxia i.e. heart very, skin not so vulnerable
🗑
|
||||
| What is the morphology of an infarct? | Wedge shaped, margins lined by rim of hyperemia/inflammation, surface covered by fibrinous exudate (release clotting factors), coagulative necrosis (esp. in myocardial tissue)
🗑
|
||||
| What is hemodynamic shock? | Hypoperfusion of tissues: all tissues decrease blood flow to everything -> series of changes, 1st reversible, 2nd irreversible.
🗑
|
||||
| What are 5 major subtypes of hemodynamic shock? | 1. Cardiogenic shock
2. Hypovolemic shock
3. Septic shock
4. Anaphylactic
5. Neurogenic (result from SC injuries, vasomotor responses altered, ANS - HR, vascular tone affected.
🗑
|
||||
| What is cardiogenic shock? | Heart fails as pump to everywhere.
🗑
|
||||
| What is an MI as a cause of cardiogenic shock? | Acute loss to ventricular wall -> death.
🗑
|
||||
| What is cardiac tamponade as a cause of cardiogenic shock? | Wall of heart dev. breach -> bleeds into endocardial sac and CO exceeds ventricular limit, tears up heart. Can be d/t cocaine abuse or klenbuterol.
🗑
|
||||
| What is Cor pulmonale as a cause of cardiogenic shock? | Saddle embolus most often deoxygenated blood not getting to lungs so oxygenated blood not getting to body -> heart pumps faster, HR goes up, heart exhasts itself and quits.
🗑
|
||||
| What is hypovolemic shock? | Loss of blood volume, bleed, decrease BP.
🗑
|
||||
| What are causes of hypovolemic shock? | Hemorrhage, severe trauma, extensive burns (weep blood plasma -> infection and hypovolemic shock; BP hard to maintain.
🗑
|
||||
| What is septic shock? | Shock d/t presence of bacterium or toxin. Usually LPS of gram-neg. bacteria -> activation and secretion of inflam. mediators, vasodilate all, BP goes down, vasoconstrict all BP can get dangerously low.
🗑
|
||||
| What is the pathophysiology of septic shock? (3) | Endotoxin release from gram-neg. bacteria, endotoxins stimulate release of cytokines (IL-1, 6 & 8, TNF), cytokines trigger release of PAF, NO, bradykinin, complement, protaglandins, leukotrienes
🗑
|
||||
| What are the stages of shock? | Non-progressive stage -> progressive stage -> irreversible stage
🗑
|
||||
| What is the non-progressive stage of shock? | compensatory mechanisms to maintain BP = ANS, SNS, Renin-angiotensin-aldosterone axis, autoregulation.
🗑
|
||||
| What is the progressive stage of shock? | Tissue hypoxia and metabolic acidosis.
🗑
|
||||
| What is the irreversible stage of shock? | Enzyme leakage, organ shutdown:
Tissues die massively, multiple organ shut down, all enzymes in blood that shouldn't be, regardless of attempts to normalize BP.
🗑
|
||||
| What does the tunica intima of blood vessels provide and what is it composed of? | Provides interface b/w blood and tissues; composed of vascular endothelium which possesses important multifunctional and metabolic properties.
🗑
|
||||
| What are the functions of the tunica intima? | Semi-permeable membrane, maintenance of non-thrombogenic blood-tissue interface, modulation of blood flow and vascular resistance, regulation of immune and inflam. reactions, growth regulation of other cells, esp smooth muscle cells.
🗑
|
||||
| What can endothelial cells do based on stimuli? | Can change their behavior based on pathophysiological stimuli - this process is called endothelial activation.
🗑
|
||||
| What are inducers of endothelial activation? (7) | Cytokines, bacterial products, hemodynamic stress, lipid products, viruses, complement proteins, hypoxia; essentially anything that can damage endothelium or act upon it.
🗑
|
||||
| What can endothelial cells do once they are activated (4)? | Express adhesion molecules, produce cytokines, chemokines, produce growth factors, produce vasoactive molecules.
🗑
|
||||
| What can actions of activated endothelial cells lead to? | vasoconstriction/dilation, pro/anticoagulant moieties, and influence the subendothelial environment (smooth muscle cells) through production of relaxing and contracting factors
🗑
|
||||
| What causes arterioclerosis? | Endothelial activation and subsequent pathological changes.
🗑
|
||||
| What are the 3 distinct patterns of arteriosclerosis? | Atherosclerosis (most clinically significant)
Monkeberg medial sclerosis (calcific deposits in muscular aa.)
Arterioclerosis (affects small arteries and arterioles: related to metabolic and autoimmune diseases, diabetes mellitis)
🗑
|
||||
| Where do atherosclerotic lesions most often occur? | Elastic and large and medium muscular arteries.
🗑
|
||||
| What are the 6 subtypes of atherosclerosis? | 1. Initial
2. Fatty streak
3. Intermediate
4. Atheroma
5. Fibroatheroma
6. Complicated
🗑
|
||||
| What occurs with type 1 of atherosclerotic progression? | First atherosclerotic lesion, isolated macrophage foam cells by age 4-5
🗑
|
||||
| What occurs with type 2 of atherosclerotic progression? | Fatty streak: mainly intracellular lipid accumulation.
🗑
|
||||
| What occurs with type 3 of atherosclerotic progression? | Type 2 changes and small extracellular lipid pools.
🗑
|
||||
| What occurs with type 4 atherosclerotic progression? | Atheroma: Type 2 changes and core of extracellular lipid.
🗑
|
||||
| What occurs with type 5 atherosclerotic progression? | Fibroatheroma: Lipid core and fibrotic layer, or multiple lipid cores and fibrotic layers, or mainly calcific, or mainly fibrotic.
🗑
|
||||
| What occurs with type 6 atherosclerotic progression? | Complicated lesion: Surface defect, hematoma-hemorrhage, thrombus. Produces S/S d/t size and causes complications
🗑
|
||||
| What is the basic progression of atherosclerosis? | Normal -> fatty streak -> atheroma -> larger atheroma -> complicated lesion S/S clinical event horizon.
🗑
|
||||
| What are 7 risk factors associated with atherosclerosis? | 1. hypertension
2. hyperlipidemia
3. smoking
4. sex
5. diabetes
6. "soft risks" sedentary, stress, obesity
7. "new risks" hinge on infective process
🗑
|
||||
| Why can hypertension cause atherosclerosis? | alterations in blood flow
🗑
|
||||
| Which sex is initially at higher risk of developing atherosclerosis? | Males, post menopausal females catch up.
🗑
|
||||
| What sort of risk for atherosclerosis does diabetes cause? | Greatest risk, uncontrolled glucose [] in blood -> endothelial cell harm
🗑
|
||||
| What are 2 lesions of atherosclerosis? | 1. Fatty streaks: early intimal lipid accumulation
2. Atheromatous plaques: raised subintimal plaques of necrotic tissue, lipid, ECM and cells
🗑
|
||||
| What are 4 theories of pathogenesis of atherosclerosis? | 1. Response to injury hypothesis
2. Monoclonal hypothesis
3. Hemodynamic hypothesis
4. Infective hypothesis
🗑
|
||||
| What is the response to injury hypothesis of atherosclerosis? | Endothelial cell dysfunction/activation -> macrophage involvement -> smooth muscle cell involvement -> hyperlipidemia. Or, injury, response and degenerative changes lead to atherosclerotic plaque.
🗑
|
||||
| What do macrophages do when involved with atherosclerosis? | Ingest lipid to produce foam cells, oxidatively damage LDL (form free radicals), recognize damaged LDL (consume damaged LDLs -> form free radicals -> collateral damage), release chemical mediators = chemoattractants and mitogens.
🗑
|
||||
| What occurs with smooth muscle cell involvement of atherosclerosis? | Proliferation of VSM contributes to growth of lesion: role of growth factors PDGF, FGF, deposition of ECM contributes to growth of lesion. Picture pg. 35
🗑
|
||||
| What is the mechanism of lesion progression with atherosclerosis? | Persistent endothelial cell dysfunction -> persistent inflammation -> persistent hyperlipidemia -> ?persistent homocysteinemia, bacterial infection, vitamin deficiencies. picture pg. 36
🗑
|
||||
| What makes up a firbrous cap? | smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization.
🗑
|
||||
| What makes up the necrotic center of an atherosclerotic lesion? | cell debris, cholesterol crystals, foam cells, calcium
🗑
|
||||
| What are 4 possible resulting lesions of atherosclerosis? | 1. Ulceration
2. Thrombosis
3. Hemorrhage
4. Calcification
🗑
|
||||
| What are 4 clinical manifestations of atherosclerosis? | 1. Acute occlusion (MI)
2. Chronic narrowing (-> stenosis; atrophy of downstream organ)
3. Aneurysm formation
4. Embolism
🗑
|
||||
| What is an aneurysm? | A localized dilation of a blood vessel or chamber of the heart.
🗑
|
||||
| What are the 5 most common sites of aneurysms? | 1. Aorta
2. Iliac
3. Splenic
4. Renal
5. Vertebral
🗑
|
||||
| How would a patient present with lumbar artery occlusion? | Constant LBP that won't resolve with manipulation.
🗑
|
||||
| What are 2 broad categories of aneurysms? | True: where the aneurysm is bounded by arterial wall components, all 3 layers outpouch.
False: Where a breach in the vasclar wall leads to a vascular hematoma, 1 or more layers -> hemorrhage into other layers creating a false lumen.
🗑
|
||||
| What are 4 causes of a True Aneurysm? | 1. MC: Atherosclerotic
2. Syphilitic
3. Congenital
4. Left ventricular
🗑
|
||||
| What are 3 causes of a False Aneurysm? | 1. MC: Post myocardial infactive
2. Junctional leak at vascular graft
3. Genetic (Marfans)
🗑
|
||||
| What types of aneurysms are there? | 2, true and false
🗑
|
||||
| What are the morphologies of aneurysms? | shape
🗑
|
||||
| What are the etiologies of aneurysms? | what causes particular aneurysm
🗑
|
||||
| What are 4 morphologies of an aneurysm? | 1. Berry
2. Fusiform
3. Saccular
4. Dissecting
🗑
|
||||
| What is a berry aneurysm? | Very small spherical dilations, occur most frequently at brain base, circle of willis, congenital, asymptomatic.
🗑
|
||||
| What is a saccular aneurysm? | 5-10 cm. in diameter spherical dilations whose mechanism is wide and variable.
🗑
|
||||
| What is a fusiform aneurysm? | Gradula and progressive dilation of a blood vessel producing a spindle-shaped expansion. May be eccentric (unilateral) or bilateral. Etiology typically atherosclerotic.
🗑
|
||||
| What is a dissecting aneurysm? | False aneurysm; refers to escape of blood into the tunica media, "double barrel" presentation of lumen, dialtion of blood vessel doesn't need to exist for this type to occur. 2 types.
🗑
|
||||
| What are the 2 types of dissecting aneurysms and what is the etiology? | Type A (arch of aorta) and Type B (descending aorta). Both present with breach in vascular wall and generation of false lumen. Etiology: genetic: Marfans
🗑
|
||||
| What is a pseudoaneurysm? | Not false. Traumatic injury to muscle layer producing focal dilation. Also referred to as traumatic aneurysm or post traumatic aneurysm.
🗑
|
||||
| What are 6 classifications of aneurysm by etiology/location? | 1. Atherosclerosis: MC -> fusiform (true) usually AAA.
2. Infection (sepsis)
3. Post stenotic dilatation
4. Syphillis
5. Arteritis
6. Miscellaneous (congenital)
🗑
|
||||
| Who is most likely to get an atherosclerotic aneurysm, when is it diagnosed and how does it present? | MC is AAA
Men more often than Female (60-80 y/o)
Dx'ed when more that 50% dilation of normal diam. of vessel has occurred.
Associated w/ hypertension and heart disease
Intermittent back/abdominal pain
Claudication
Lower limb ischemia
🗑
|
||||
| What is the difference b/w neurogenic and vascular claudication? | Neurogenic: pain with walking is always present
Vascular: Pain after walking a while, starts to throb b/c muscle needs more blood.
🗑
|
||||
| What does aneurysm size have to do with its chance of rupture? | If <5 cm there is <5% chance of rupture
If >6 cm there is ~15% chance of rupture
If >7 cm there is 75% chance of rupture
🗑
|
||||
| What must treatment of an aneurysm account for and consist of? | Must account for risk/benefit of surgical intervention.
Consists of removal of dilation and replacement w/ graft.
🗑
|
||||
| What are 2 non inflammatory vascular disorders? | 1. Monkeberg medial sclerosis
2. Raynaud phenomenon
🗑
|
||||
| What are 8 inflammatory vascular disorders? | 1. Takayasu arteritis
2. Polarteritis nodosa
3. Allergic granulomatosis and angitis (Churg-Strauss)
4. Temporal arteritis (giant cell arteritis)
5. Kawasaki disease
6. Wegeners granulomatosis
7. Thromoangitis Obliterans (Buerger's)
8. Behcet
🗑
|
||||
| What is Monkeberg medial sclerosis? | A degenerative calcification of the tunica media of large and medium sized muscular arteries, typically older individuals, MC in aa. of extremities (non-elastic), no luminal narrowing, unknown etiology.
🗑
|
||||
| With Monkeberg medial sclerosis what is a presentation that may appear on an x-ray? | "Pipe-stem calcification"
🗑
|
||||
| What is Raynaud Phenomenon? | Typically d/t cold induced vasoconstriction, Fingers change color in sequence white-blue-red, exaggeration of normal central and vasomotor responses to cold or emotion, usually benign, ulceration and gangrene rare, may be primary or secondary
🗑
|
||||
| What is inflammatory vasculitides? | Refers to inflammation of the walls of vessels (any type or size) and its effect. Can be classified based on pathogenesis/etiology, infection, immunologic. (Picture pg. 50)
🗑
|
||||
| What are clinical presentations and treatments of inflammatory vasculitides? | Often a result of affected vessel lumen narrowing/obliteration/dilation/thrombosis. D/T their nature vasculitides are steroid/immunosuppressive therapy responsive.
🗑
|
||||
| What is Takayasu arteritis, who is affected and where is it? | Females <40, involves aortic arch, may involve branches, Charac. principally weakening of peripheral pulses, Exam shows thickening of aorta, esp. aortic arch and branches w/ near obliteration of distal portions of branches.
🗑
|
||||
| What would you expect to find upon examination of a patient with takayasu arteritis? | Higher BP on one side vs. the other
Pulse and BP disparity
🗑
|
||||
| What is polyarteritis nodosa? | Necrotizing vasculititis of small and medium sized visceral arteries with NO LUNG INVOLVEMENT
🗑
|
||||
| How does polyarteritis nodosa present? | Young males, present with necrotizing of vessel wall (fibrinoid necrosis). If affects small aa. may be associated with Perinuclear Anti-neutrophil Cytoplasmic antibody (P-ANCA)
🗑
|
||||
| In what 3 phases can polyarteritis nodosa present? | Acute, healing, scarred (may co-present)
🗑
|
||||
| What are complications of polyarteritis nodosa and what is it usually responsive to? | Aneurysm, thrombosis, infarct; corticosteroid responsive
🗑
|
||||
| What is Allergic granulomatosis and agnitis (Churg-Strauss)? | Systemic vasculatis in young individuals with asthma, 2/3 patients have C-ANCA or P-ANCA, small and medium sized aa. and arterioles of lungs, spleen, kidney, heart, CNS (visceral complaint), shows intense eosinophilic infiltrate.
🗑
|
||||
| What is giant cell arteritis (temporal arteritis)? | >50 y/o, MC systemic form of vasculitis in adults, both acute and chronic, affects lg. and sm. aa., esp. temporal aa. also vertebral and ophthalmic.
🗑
|
||||
| What is the pathogenesis of giant cell arteritis? | Suggests that immune reaction is generated towards components of the vascular wall - still putative; Granulomatous nature suggests t-cell mediated mech. and antigen-driven injury.
🗑
|
||||
| What are clinical features of temporal arteritis? | Facial pain, intense w/ palpation, ocular symptoms, can lead to sudden, permanent blindness, tx w/ anti-inflammatory.
🗑
|
||||
| What is Kawasaki disease? | Disease of the coronary arteries, affecting young children <4 y/o. Unknown etiology. Associated w/ mucocutaneous lymph node syndrome. 20% develop cardiac sequelae...aneurysmal formation.
🗑
|
||||
| What are clincial consequences of kawasaki disease? | Asymptomatic vasculitis, coronary artery ectasia (non-aneurysmal dilation), Thrombosis, MI, sudden death.
🗑
|
||||
| What treatment is given for kawasaki disease? | Aspirin megadoses and intravenous gammaglobulin (gets immune system to fight)
🗑
|
||||
| What is Wegener's granulomatosis? | Necrotizing vasculitis characterized by triad:
1. Acute necrotizing granulomas of upper respiratory tract
2. Necrotizing granulomatosis of small to medium sized vessels
3. Renal disease in form of focal glomerulitis (type 4 like)
🗑
|
||||
| What are some other facts about Wegener's granulomatosis? | Pathogenesis suggests some type of hypersensitivity rxn. 90% present w/ ANCA where 75% is C-ANCA. Rapidly fatal if not treated. Tx w/ cyclophosphamide (chemo agent).
🗑
|
||||
| What is Thromboangitis obliterans (Buerger's disease)? | Distinctive disease leading to vascular insufficiency. Segmental acute and chronic thrombosis of small and medium aa. Microabscesses/granulomatous inflammation.
🗑
|
||||
| What are the principal arteries affected with Buerger's disease and who gets it? | Tibial and Radial aa.
Almost exclusively in heavy smoking men who present with symptoms of claudication, cold intolerance/Raynauds. Lumen obliteration w/ distal necrosis.
🗑
|
||||
| What is Behcet? | Mainly involves mucous membranes, charac. by oral apthous ulcers, genital ulceration, ocular inflammation and lesions in CNS, heart and GI. Unknown cause, immune basis, tends to not be as severe.
🗑
|
||||
| What are varicose veins? | Enlarged tortuous blood vessels from increased intraluminal pressure, affects women>men, familial predisposition, obesity and prego plays a role. Walls may be thinned d/t dilation or thickened d/t hypertrophy. Stasis dermatitis and secondary ulceration
🗑
|
||||
| Where may varicosities present other than the legs? | Rectum and anus: hemorrhoids
Esophagus: esophageal varices, enlarged v in esophagus d/t hepatic diseases MC cirrhosis/liver
Clinically silent until tear occurs and bleeding event depends on how bad liver cirrhosis is.
Scrotum
🗑
|
||||
| What is thrombophlebitis? | Thrombotic condition of veins that implies inflammation present.
🗑
|
||||
| What is Phlebothrombosis? | Thrombus in vein, inflammation not implied.
🗑
|
||||
| What is DVT associated with and what are some symptoms? | Prolonged bed rest, reduced cardiac output, surgery. General swelling in calf, ankle, foot or thigh, increased warmth of leg, redness, pain in leg, night leg cramps, bluish discoloration of skin on legs or toes.
🗑
|
||||
| What is the cause of death w/ DVT and what is a treatment? | Pulmonary embolus resulting in cor pulmonale
Caval filter
🗑
|
||||
| What are benign hemangiomas? | Neoplasia of capillaries.
common congenital vascular lesions, MC on skin but also found on mucosal surfaces and visceral organs, lesions present at birth and grow but limited in size.
🗑
|
||||
| What are capillary hemangiomas? | Vascular channels have the size and strx of normal capillaries, occur on skin (strawberry hemangioma) subcutaneous tissue, mucous membranes of mouth and lips. Strawberry hemangiomas fade at 1-3 y/o.
🗑
|
||||
| What are cavernous hemangiomas? | Lesions consist of large vascular channels, port wine stains, raised spongy masses that do not regress spontaneously, may undergo thrombosis, fibrosis, hemorrhage. Significant in von Hippel Landau disease
🗑
|
||||
| What is angiosarcoma? | rare highly malignant consists of neoplastic endothelial cells, located on skin, soft tissue, breast, bone, spleen, liver. Varying degrees of differentiation. Liver involvement associated w/ carcinogens: vinyl chloride, arsenic, thorotrast
🗑
|
||||
| What is Kaposi's sarcoma? | Derived from neoplastic endothelial and stromal cells, associated with AIDs, painful, purple/brown nodules/plaques on hands, feet, face. Rarely primary cause of death.
🗑
|
||||
| What occurs with a coronary artery bypass? | Vein or artery grafts
long term patency
grafts subjected to thrombosis, intimal thickening, atherosclerosis.
🗑
|
||||
| What is throbolysis? | Tx to lyse thrombi and emboli (leg vein thrombi, pulmonary emboli, prosthetics, catheters) plasminogen activators used. Problems: falure to lyse, reocclusion d/t persistence of orginal disorder.
🗑
|
||||
| What is balloon angioplasty? | Luminal expansion of atherosclerotic arteries, atherosclerotic plaque becomes unstable, complications: plaque rupture, medial dissection, stretching of the media (exposure of collagen), proliferative restenosis
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
kabrown
Popular Chiropractic sets