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44 Cards in this Set
- Front
- Back
RV failure vs. LV failure and congestion
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RV failure- systemic congestion
LV failure- pulmonary congestion |
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heart failure cells
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macrophages in alveoli eat blood cells during congestion- NOT IN LOCATED IN HEART
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brown induration
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lungs become firm and brown due to fibrous thickening of alveolar walls
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cardiac edema
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edema is not in heart but:
subcutaneous in lower extremity, -dependent edema -sacral edema -pitting edema |
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renal edema
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not pitting but not dependent bc it starts in face
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pulmonary edema
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may be lethal
-LV failure |
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transudate vs exudate
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trans- non inflammatory, loww protein, edema fluid
exudate- inflammatory- rich in protein |
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nutmeg liver
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result of chronic congestion of liver in RV failure
-red-blue congested centers rimmed by yellow-tan parenchyma produce mottled appearance of liver |
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repeated chronic external hemmorhange results in
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loss of Fe-iron deficiency anemia
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virchows triad
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three major influences of thrombogenesis (clot formation)
1)endothelial injury 2)changes in blood flow stasis and turbulence disrupt blood flow and contribute to thrombogenesis 3) hypercoagulability of Blood: DONT MISS Deficiency (protein C) Oral contraceptive use Nephrotic syndrome Trauma/Thrombocytes Malignancy Inc platelets Stickiness of Platelets Syndromes |
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plasminogen to plasmin will effect a clot how
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fibrinoloysis, fibrin is degraded to FDPs (Fibrin degradation products)
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mural thrombis vs occlusive thrombis
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mural-non occlusive seen in cardiac chambers and aorta
occlusive- seen in arterial tree and veins |
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fate of thromus (5 steps):
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1) propagation
2) embolization 3) removal (fibrinolytic action, fibrinolysis) 4) organization- organzied by invading fibroblasts and capillaries 5) infection |
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clinical significance of thrombi
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1) obstruction to blood flow (arterial obstruct coronary artery-> MI)
2) embolization (thrombi in deep veins of leg -> pulmonary embolization and infarction) |
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common clinical settings for thrombosis formation:
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1) advanced age
2) bed rest and immobilization 3) heart disease 4) Tissue injury 5) cancer -> Trousseau phenomenon (multiple thrombosis in various places) 6) late pregnancy and delivery |
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disseminated intravascular coagulation
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aka: consumption coagulation
pathologic activation of coagulation-> widespread thrombosis -> consumption of coagulating factors -> blood cant clot -> hemorrhage |
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causes of Disseminated intravascular coagulation
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--obstetric complications
-malignancy -infections -massive tissue injury -endothelial injury (immune complexes, burns, infections) |
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effects of DIC
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-hemorrhage
-FDPs (Fibrin degradation products -microangiopathic hemolytic anemia |
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lab dx: DIC
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dec fibrinoge, dec platelets, inc FDP
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emboli arising in veins vs arteries
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veins- travel to impact lungs
arteries- travel to impact legs, brain viscera |
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systemic embolism
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most arise from thrombi in heart
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pulmonary embolism
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arises from deep veins in legs-> large embolus may cause sudden death or right heart failure (acute cor pulmonale)
chronic cor pulmonare -> pulmonary hypertension |
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fat embolism
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globules of fat circulating in blood stream with subsequent impaction
fat embolism syndrome: consists of thrombocytopoenia, petechiae in skin and conjunctivae, respiratory difficulty, mental deterioration and coma and death |
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infarction factors
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protected by anastomoses (multiple ways for blood to flow) while end arteries are danegerous
slow occlusion- provides time for bypass channels to develop |
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types of infarct
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may be septic, bland (aseptic)
-involve periphery of solid organs and produce a wedge-shaped area with base at external organ and apex at site of obstruction -fate of infarcts- phagocytic removal of dead tissue followed by organization and scar (except in brain, liquefactive necrosis) |
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clinical significance of infarcts
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mycardial, pulmonary and cerebral infarctions responsible for over half of all deaths
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causes of hypovolemic shock
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hemorrhage
trauma surgery burns fluid loss -> vomiting/diarrhea |
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causes of vasogenic shock
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(normal blood volume, but vasodilation inc size of vascular system)
neurogenic shock anaphylaxis septic shock |
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causes of cardiogenic shock
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MI
CHF Arrhythmias |
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causes of obstructive shock
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pulmonary embolism (saddle embolism)
cardiac tamponade cardiac tumor tension pneumothorax (lung collapse leading to mediastinum shift putting pressure and obstructing large BV) |
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hypovolemic shock: symptoms and signs
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hypotension
rapid thready pulse cold clammy skin tachycardia/tachypnia inadequate perfusion of tissues-> inc anaerobic glycolysis-> inc lactic acid -> dec peripheral vascular response to catecholamines |
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compensatory mechanisms for hypovolemic shock
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maintain CO and BP via -
-baroreceptor reflexes -sympathetic stimulation -activation of RAAS -vasoconstriction (except brain and heart) -> cold clammy skin low BP- chemoreceptors -> tachypnia, tachycardia low BP- renal shutdown |
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Vasogenic (distributive) shock results in
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1) hypotension
2) warm skin (initially bc of vasodilation) 3) vasodilation -> hyperdynamic circulatory state -> peripheral pooling - no hemorrhage but due to difference in volume of blood and capicity of vascular system (which is vasodilated because of vasoactice substances released after tissue destruction, allergic rxn) |
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septic shock- stats risks
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most common cause of death in ICU
-major risk: use of catheter -aka Systemic Inflammatory Response Syndrome (SIRS) which leads to Multiple Organ Dysfunction Syndrome (MODS) |
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SIRS results from systemic release of cytokines such as
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TNF, IL-1, IL-6 and PAF
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Sepsis poor prognosis if
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you have hypothermia/leukopenia
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refractory shock
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severe stage of shock showing no response to treatment- leads to multiorgan failure.
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Waterhouse-Friderichsen syndrome
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disease of adrenal gland caused by meningococcal septicemia- severe septic shock- circulatory collapse
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patient presentation of shock
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hypotension- wake rapid pulse, tachypnia, cold and clammy skin (except in vasogenic shock)
3 or more organs fail -> 80-100% chance of death |
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things that worsen shock
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multiorgan failure
ARDS SEPSIS DIC |
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programmed theories
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programmed longevitiy - aging = activation and deactivation of genes
endocrine theory- senescnece results in decrease of hormone production - decrease in bodies ability to repair itself immunologic- programmed decline in the immune system functions leads to increased vulnerability |
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error theories
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wear and tear- years of damage on cells
rate of living- limited number of times a heart beats crosslinking- with age DNA crosslink to each other and interfere with functions free radical theory-damage tissue and normal cell components telomere: telomeres become too short and cell can't do mitosis misfolded protein theory: Hsp fail- misfolded proteins accumulate and interfere with cell function |
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most common fluid and electrolyte disorder the elderly
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dehydration
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most common cause of hair loss in men
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genetics
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