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Maturing Granulation Tissue Vessels decreasing Fibrocytes
decreasing Type III replaced by Type I collagen Inflammation
resolved Epithelium restored
Wound StrengthPrimary intention: 10% when sutures removed (4-10
days) Rapid increase 4 weeks
Granulation tissue remodeling 70-80% strength plateau 3
months
Synthesis > degradation first 2 months Collagen III replaced
by collagen I Cross- binding and increase in fiber size
strengthen
Secondary intention: Wound contraction up to 95% at 6 weeks
Myofibroblasts and Elastin remodeling participate
Scars never have the same tensile strength, even when healed
back by primary intention.
Remodeling Scar By the end of 3 months: Vessels absent
Fibrocytes few Type III replaced by Type Icollagen Contraction
complete Inflammation resolved Epithelium restored
Above: FIGURE 326 Repair, regeneration, and fibrosis after
injury and inflammation.
FIGURE 320A Healing of skin ulcers. A, Pressure ulcerof the
skin, commonly found in diabetic patients. Thehistologic slides
show: B, a skin ulcer with a large gapbetween the edges of the
lesion; C, a thin layer ofepidermal re-epithelialization and
extensive granulation
tissue formation in the dermis; and D, continuing
re-epithelialization of the epidermis and wound contraction.FIGURE
321B A, Granulation tissue showing numerousblood vessels, edema,
and a loose ECM containingoccasional inflammatory cells. Collagen
is stained blue bythe trichrome stain; minimal mature collagen can
be seenat this point. B, Trichrome stain of mature scar,
showingdense collagen, with only scattered vascular channels.
Test q:A 22y/o female succumbsto peer pressure and has her
ears
pierced. Two months later, thesites of piercing develop
firmnodules that are the same color as
the surrounding skin. There is noevidence of infection. You
wouldexpect the histopathology to show:
Broad bands of collagen.Test q: A well-healed scar that is6mo
old contains primarilycollagen type: I
Test q: The principal cells ofgranulation tissue are:
fibroblasts
and endothelial cells,
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Hemodynamics Fri. 08/27/10
Topics: Homeostasis - Water/Compartments
Edema Congestive Heart Failure Congestion/Hyperemia
Hemostasis: Hemostasis - Normal Hemostasis - Thrombosis
Atherosclerosis Thrombosis/Embolism Infarct Shock
Vascular Fluid Hemodynamics Body Compartments: Body Water (60%
of body weight) Intravascular Space: 5% Cellular Space: 40%
Interstitial (Extracellular) Space: ~ 15% Lymphatic Space: small %
Blood Flow: Blood Pressure Maintenance
Cardiac Output
Vascular Perfusion Pressure - Vascular Tone Vascular Resistance
- Organs
Increased Hydrostatic Pressure Impaired Venous Return
Congestive Heart Failure Constrictive Pericarditis Ascites
(liver cirrhosis) Venous Obstruction
Thrombosis External pressure mass Lower extremity inactivity
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Congestive Heart Failure: Below: Congestive Heart Failure -
Vascular Pressures Left Sided CHF: Decreased Cardiac Output
Etiology: Myocardial dysfunction -Atherosclerosis, Infarcts,
Hypertension,Aortic/Mitral valve diseases, Myocarditis,Constrictive
Pericarditis
Findings: Decreased Cardiac Output - Decreased
tissue perfusion Reactive vasoconstriction (increased
vascular tone) Peripheral and Pulmonary Edema Organ Congestion:
Liver, Spleen,
Kidneys, GI, etc. Effusions: Pleural, Peritoneal (ascites)
Symptoms/Findings: Dyspnea, decreased activity level
PND (paroxysmal nocturnal dyspnea) Orthopnea Jugular-venous
distention Increased BNP (B type nutriuretic peptide
produced by distended ventricle) Peripheral edema
Pulmonary rales
Right Sided CHF: Etiology: Left sided failure most common
cause, pulmonary hypertension,pulmonary/tricuspid valve disease,
myocarditis
Findings: Similar to Left Sided except nopulmonary edema
Congestive Heart Failure Mechanisms: Myocardial
Infarction:Decreased Cardiac Output
Constrictive Pericarditis:Decreased Cardiac Output
Test q:A 74y/o woman w/left heart failure develops pulmonary
edema. This
accumulation of fluid is best explained by which of the
following mechanisms?Increased hydrostatic pressure.
Test q: The most common cause of right-sided congestive heart
failure is:left-sided heart failure.
Test q: Which of the following is seen predominantly in acute
left heartfailure? Pulmonary edema.
Test q:A 50y/o male w/a history of previous MI develops
shortness of breathand dies after 2wk in the hospital. At autopsy
the patient exhibits necrosis ofhepatocytes surrounding the central
veins. The most likely cause is:
congestive heart failure.
Above: fibrous bands constrictthe pericardium to
heartsurface.
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Sodium Retention: Increased Plasma Volume
Pulmonary Congestion and Edema: Congestive Heart Failure:
Pulmonary Edema:
Pulmonary edema: fluid/transudate Frothy/blood-tinged edema
fluidw/few RBCs
Test q: On day 3 after an acute MI, the patient developed
congestive heart failure and died. The lungs would show: congested
capillaries andtransudate in alveoli.
Peripheral Edema: Reduced Osmotic/Oncotic Pressure:
Test q: Choose the best answer concerningcongestive heart
failure (CHF): May result in
increased sodium retention from increasedaldosterone action.
(Other choices-Peripheral edema seen w/CHF is the result of
decreased osmotic/oncotic vascular pressure;Pulmonary edema seen
w/CHF is the result ofincreased right ventricular pressure;
Left
ventricular failure is commonly the result of
pulmonary embolisms; Is most often acomplication of portal
hypertension.)
Exaggeration of pulmonary
vasculature. Filling of air spaces
w/fluid.
Above: pitting edema.Discoloration = chronicvenous stasis.
Test q:A 48y/o man w/alcoholic cirrhosis has ascites
and dependent pitting edema in the lower legs. Fluidaccumulation
in the peritoneal cavity and legs occur bywhich of the following
mechanisms? Decreasedplasma oncotic pressure.
Reduced Osmotic/Oncotic Pressure: Reduced Plasma Colloid
Osmotic/OncoticPressure
Protein losing states: nephroticsyndrome
(glomerulonephritis),protein losing enteropathies
Cirrhosis/Malnutrition: decreasealbumin production (protein
has
strong effect of pulling H2O back intovascular system)
Effect: Peripheral edema Non-dependent edema,
periorbital/facial Effusions: Ascites (Peritoneal),
Pleural Sodium and H2O Retention: IncreasedPlasma Volume
Acute/Chronic Renal Failure Abnormal Renin-Aldosterone
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Test q: The mechanism for the production of anasarca is:
extensive loss of albumin in the urine. (Anasarca = extreme
generalized edema)REPEATED TWICE
Lymphatic Obstruction Reduced Lymphatic Flow: Lymphatic
Obstruction
Neoplasms, Infections, Post-surgery, Post-Rad Tx Lymphomas -
neoplasms Filarisis - infection Mastectomy - post surgery Abdominal
lymph node obstruction - Rad Tx
Localized Edema Inflammation, vessicle/bullae, injury, etc
Lymphatic Obstruction: Filarial Infection Local Edema:
Inflammation
Cerebral Edema Cerebral Edema: Localized from Trauma: Localized
or Diffuse:
Localized - Trauma, Infections/abscess Diffuse - Hypertensive
Crisis, Venous obstruction, CSF
Obstruction, Trauma Effects:
Decreased Mental Status Tissue destruction, infarct, paralysis
Brain stem herniation - death
Cerebral Edema: Diffuse Swelling Herniation:
Hyperemia/Congestion: Active vs Passive:
Inflammation ActiveExercise ActiveHeat Active
Congestive HeartFailure Passive
Venous Obstruction Passive
Above: herniation of cerebellum.Compresses midbrain/spinal
cord.
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Congestion: Increased amount of blood in capillaries, venules
Pulmonary Congestion:
Active Hyperemia: Increased blood flow toarea due to
inflammation or vascular control Inflammation: Vasodilatation,
increasedvascular permeability Exercise: Increase muscle tissue
blood flow Heat: Increase skin blood flow
Passive Congestion: Reduced venousreturn/obstruction, Edema,
Common withCHF Lung Congestion: Edema, extravasatedRBCs,
interstitial thickening (chronic), heartfailure cells = hemosiderin
ladenmacrophages Liver Congestion: Centrilobular
congestion,centrilobular necrosis/fibrosis (chronic, i.e.cardiac
cirrhosis) Spleen Congestion: Splenomegaly, fibrosis(chronic)
Localized, venous thrombosis
Test q:A 62y/o male is found dead at home. At autopsy, the
alveolar wall capillaries are congested w/RBCs and alveoli contain
macrophages thatexhibit brown, granular material. This patient most
likely has a history of: Left heart failure.
Hepatic Congestion: Centro-lobular Congestion/Atrophy
Test q: Nutmeg liver is a descriptive term for liver changes due
to: chronic passive congestion.
Hemostasis: Coagulation/Fibrinolytic Pathways
Bleeding/Hemorrhage vs Hemostasis/Clotting Hemostasis Vascular
Injury:
Dynamic Equilibrium: bleeding vs clotting Vascular
Endothelium/Platelets/Coagulation
Factors/Fibrinolytic Factors
Primary Hemostasis - Vascular Seal = Platelets Vasoconstriction
Platelet Adhesion Platelet Aggregation
Secondary Hemostasis - Coagulation Pathway Endothelial/Platelet
Activation Coagulation Cascade
Thrombolytic/Fibrinolytic Elements Regulatory Factors for
Clotting vs Clot Lysis
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Primary Hemostasis Hemostasis - Platelet Adhesion/Aggregation:
Clotting: Platelets
Platelet adhesion (Von Willebrand Factor (vWF),collagen)
Platelet shape change (discoid) Platelet release of aggregation
factors: ADP, Thromboxane A2
Aspirin inhibits production of Thromoboxane A2 Platelet
recruitment/aggregation
New anti-platelet drugs inhibit aggregation Platelet hemostatic
plug
Anti-platelet aggregation/adhesion Prostaglandin I2, nitric
oxide, ADPase (derived from
endothelium) Platelet Adhesion Mechanism: (Gp1b receptor)
Inadequate Platelet Function or #: Platelet - Inadequate Primary
Hemostasis:
Petechiae - pinpoint loss of blood into tissues, ex. Skin
Purpura - larger loss of blood into tissues, ex. Skin Hemorrhage -
severe bleed (Brain, GI, etc)
Inadequate Platelet #/Function: Petechiae Congestion/Hemorrhage:
Bowel, Brain:less than 2 mm hemorrhage:
Purpura: Platelets and Coag Factors Ecchymosis: Subcutaneous
Secondary Hemostasis -> 3 mm hemorrhage: Hemorrhage
Platelets/Coag Coagulation System
Factors > 1-2 cm hemorrhages
Above: Tissue factor is primary drivingfactor.
Test q:A 35y/o woman takes acetylsalicylic acid (aspirin) for ar
thritis.Although her joint pain is reduced w/this therapy, the
inflammatory processcontinues. The aspirin therapy alleviates her
pain mainly through reductionin the synthesis of which of the
following mediators? Prostaglandins.REPEATED TWICE.
Test q:A 59y/o obese woman w/a history of diabetes mellitus had
an MI3mo ago. She is now taking a low dose of aspirin to reduce the
risk of
arterial thrombosis. On which of the following steps in
hemostasis doesaspirin have its greatest effect? Aggregation of
platelets. REPEATED
TWICE.
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Coagulation Cascade:
Coagulation Pathway - Platelet Surface: Fibrin Generation:
Hemostasis Equilibrium: Coagulation Control Clotting Stimulating
Factors (Pro-coagulants):
Exposed collagen, vWF = Platelet activation Platelet aggregation
factors = ADP, ThromboxaneA2
Tissue Factor (Thromboplastin) = tissue injury Activated Factors
= XIIa, XIa, IXa, Xa, VIIa, IIa
Plasminogen Activator Inhibitor (PAI) = anti-fibrinolytic
Alpha-2-antiplasmin = anti-fibrinolytic
Anti-coagulation Factors: Antithrombin III (ATIII) : Inactivates
Xa, IXa, IIa Protein C (+Protein S): Inactivates Va, VIIIa
Thrombomodulin: activates Protein C Tissue Factor Pathway Inhibitor
(inactivates VIIa+Xa)
Clot Lysis Factors: Tissue Plasminogen Activator (tPA)
Plasminogen = Plasmin: Degrades Fibrin
ATIII is a key anti-coagulant.
The function of the extrinsic pathwayis measured by PT.
Vascular injury activates Factor VIIa +TF, which activate the
conversion ofFactor X to Factor Xa. Factor Xa is thecentral area
within the clotting cascade.
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Anti-coagulants: Anti-coagulants use in blood tubes to yield
whole blood or plasma:
EDTA (lavender top) binds Ca++, used for hematology tests
Citrate (blue top) binds Ca++, used for coagulation testing Oxalate
(grey top) binds Ca++, used for some whole blood
testing Heparin (green top) inhibits AT III
Therapeutic Anticoagulants: Heparin, Unfractionated: Binds to
Anti-thrombin III and inhibits Thrombin (II) and Factor Xa; Monitor
with Partial
Thromboplastin time aPTT or activated clotting time Heparin, Low
molecular weight: Binds to Anti-thrombin III and inhibits Factor Xa
mostly; Monitor with Anti-Xa
assay Warfarin (coumadin): Decreases factors II, VII, IX, X,
production (Vitamin K factors); Monitor with Prothrombin
Time (PT, INR) Direct Factor Xa Inhibitors; effects PT, aPTT,
and Anti-Xa
assay Direct Thrombin Inhibitors
Thrombin Equilibrium Thrombosis vs Anti-thrombosis: Thrombin
effect on thrombosis:
Fibrinogen to Fibrin reaction Activates XIII to cross-link
fibrin
Activates VIII, V Stimulates Platelet
Aggregation and Secretion Endothelial leukocyte
adhesion molecules Thrombin effect on anti-thrombosis =
Fibrinolytic Process Stimulation: Tissue Plasminogen
Activator
(tPA) Vasoactive - NO, PGI2
(inhibits Platelet aggregation) Cytokines
Heparin + Antithrombin III inhibits Thrombin
Thrombolysis/Fibrinolysis Tissue Plasminogen Activator (tPA)
released from adjacent normal endothelium:
Activates Plasminogen to Plasmin Plasmin lyses fibrinogen with
release of d-dimers (d-dimer assay used to rule-
out DVT or Pulmonary Embolus) Fibrinogen breakdown products
inhibits coagulation
Thrombomodulin released from endothelial cells inhibits
coagulation by inaction withthrombin in activating Protein C
Anti-fibrinolysis actions
Alpha2-Anti-plasmins Plasminogen Activator Inhibitors
Fibrinolytic System: Activation and Regulation
Test q: Lysis of a thrombus isenhanced by which of the
following
mechanisms? Thrombinstimulation of tPA release.
Test q:A 66y/o woman comes tothe ER 30 min after the onset
of
chest pain that radiates to her neckand left arm. She is
diaphoretic andhypotensive; the serum troponin I
level is elevated. Thrombolytictherapy is begun. Which of
thefollowing drugs is most likely to be
administered? Tissue plasminogenactivator.
Test q: The clotting factors that are produced in the liver
andare vitamin K dependent are: II, VII, IX, X.
Test q:A 33y/o female presents to the ER w/a deep veinthrombosis
in her left leg. She is treated w/heparin untilstable. On
discharge, you wish to change her anticoagulant
to Coumadin (Warfarin). What lab test should you order tomonitor
drug effectiveness after discharge? PT.
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Hemodynamics/Hemostasis Lecture # 2 Thrombosis/Embolism
Atherosclerosis Thrombosis Formation: Infarcts Shock
Pathologic Causes of Thrombosis: Genetic Disorders:
Hyper-coagulable States
Mutations in Factor V (Leiden Mutation): 2-15% of whites;
reduced degradation of Factor V by Protein C
(decreased aPC) Antithrombin III Deficiency: Autosomal dominant
(1:2-5000); or
acquired (i.e. nephrotic syndrome or DIC) Protein C or S
Deficiency: Anti-coagulant Allelic Variations in Prothrombin:
1-2% Population; Increased Levels (3 xs risk) but notstructural
change.
D5, 10 Methylenetetrahydrofolate reductase mutation (C677T
homozygous) increased homocysteine
Fibrinolysis defects Homocysteinemia - genetic disorder or
folate deficiency
Acquired: Hyper-coagulable States
Tissue damage (release of activating factors) Cancer
(pro-coagulant factor release)
Trousseaus Syndrome: Pancreatic Ca, Thrombi Disseminated
Intravascular Coagulation (DIC):
Diffuse endothelial injury (sepsis, toxins) Anti-Phospholipid
Syndrome (Lupus Anticoagulant)
Systemic Lupus Erthyematous, Pregnancy (causesmiscarriages and
stillbirths), Viral Infections Antibodies to cardiolipin, beta-2
glycoprotein I,phosphotidylserine
Heparin induced thrombocytopenia (HIT) 10 % of patients;
Antibodies to heparin bound to plateletfactor 4 results in platelet
activation and initiation of
thrombus formation
Endothelial Cell Injury Necrotic Tissue - Infarct Valve Disease
- Rheumatic
Fever Atherosclerosis - Plaques Traumatic Injury Vasculitis -
Autoimmune
Disorders Infections - Endotoxins Other
Disseminated Intravascular Coagulopathy DIC - Small Vessel
Thrombi: Etiology: Diffuse activation of Thrombin/Coagulation
System, example:Diffuse endotoxin injury of endothelium
Findings:
Diffuse clotting in small vessels Ischemic injury to organs,
especially brain, lung, heart, kidneys Consumption of clotting
factors (Platelets, Factor VIII, V, etc)
bleeding can result (increased aPTT and decreased
plateletcount)
Activation of Fibrinolytic System = dissolution of clots
andsubsequent bleeding (fibrinolytic products inhibit
clotting);increased d-dimers
Test q:An elderly man presents w/multiple deepvein thromboses
over the past several months withone episode of pulmonary embolism.
Which of thefollowing is the most likely underlying
condition?Adenocarcinoma of the pancreas. (Not cirrhosis,
Von Willebrands disease, FH, or renal cellcarcinoma w/lung
metastases)
Test q:A 55y/o former baseball player presents tohis doctor w/a
small thrombus in his lower leg and
1mo later is hospitalized for a pulmonary embolus.Further workup
reveals a malignancy. Which ismost likely? Adenocarcinoma,
pancreas.
Test q: A 45y/o present w/multiple venousthromboses in his legs
and also in the mesentery ofhis intestinal tract. He most likely
has a history of:
Pancreatic cancer.
Test q:A 45y/o white male is mildly overweight, butotherwise
healthy. During the past year he has
developed thromboemboli in his lower extremities.The most likely
cause is Leiden mutation.REPEATED TWICE.
Test q: The Leiden mutation of the gene for FactorV is commonly
seen in persons who: have history
of thombosis of the deep veins. REPEATEDTWICE.
Test q:A 25y/o woman has had multiple episodes
of deep venous thrombosis during the past 10 yearsand one
episode of pulmonary thromboembolismduring the past year.
Prothrombin time, partial
thromboplastin time, platelet count, and plateletfunction
studies are all normal. Which of thefollowing risk factors has most
likely contributed to
the patients condition? Factor V mutation.
Test q:An athletic, 51y/o man w/ahistory of diabetes mellitus
goes to theER because he has had left-sided chest
pain that radiates to the arm for the past5 hr. Serial
measurements of serumcreatine kinase-MB levels show an
elevated level 24hr after the onset ofpain. Partial
thromboplastin time andprothrombin time are normal. Coronary
angiography shows occlusion of the leftanterior descending
artery. Which of thefollowing mechanisms is the most likely
cause of thrombosis in this patient?Damage to endothelium.
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Test q: Choose the best answer concerning Disseminated
Intravascular Coagulation (DIC): It is often seen with septicemia
and endotoxin release.(Other choices- It is commonly assocd w/an
increased platelet count, Fibrin split products are increased which
enhance clotting, Thrombi in small
vessels commonly result in pulmonary emboli.)Test q:A 32y/o
female gives birth to a 10lb male infant at 42 weeks gestation
after induction and stressful delivery. She develops multiple clots
as wellas large hematomas and hematuria. Lab studies would show:
Elevated D-dimer.
Test q:A 13mo old male presents to the ER w/a swollen right
knee. The family reports that the child bruises easily. There is no
family history ofbleeding disorders. Lab results: PT: 12s (10-14s).
APTT: 43s (21-35s). Bleeding time: 5min (3-6min). Platelet count:
300,000 (150-450,000). Mixingstudies: APTT corrected to normal.
What is the diagnosis? Factor VIII deficiency. (Did not
specifically discuss this?)
Hemodynamics: Abnormal Blood Flow Turbulence - Arterial/Cardiac
Thrombosis Atherosclerotic Plaque:
Abnormal Valves - Abnormal surface, Stasis with Mitral Stenosis
Atherosclerosis - Plaques/Nodules
Ulcerated Plaques Aneurysms (stasis and abnormal surfaces)
Atrial Fibrillation - irregular atrial contraction Turbulence
can directly injure endothelial cells
Stasis - Venous Thrombosis Reduced circulation: CHF,
Obstructions, Varicose Veins, immobility, etc
Failure to dilute out activated clotting factors Failure to
bring fresh anti-coagulant factors
Promotes endothelial cell activation Sickle Cell Anemia,
Hyperviscosity States, polycythemia rubra vera
Genetic and acquired etiologies:
Above: Top aorta is severeatherosclerosis. There is a largeulcer
overlying the atheroscleroticplaque. The middle aorta
representsmoderate atherosclerosis. The
bottom aorta is smooth and normal.
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Plaque Formation:
Atherosclerotic Plaque:
Fate of Atherosclerotic Plaques: Atherosclerosis:
Coronary Artery
*
* = thrombus overlying plaque
Coronary ArteryThrombosis
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Ulcerated Plaque - Coronary Artery Ulcerated Plaque: Coronary
Artery - Thrombus Aorta Mural Thrombus
Test q:A 50y/o male presents to the ER w/crushing chest pain. A
stress test 2 months ago was suspicious. Cardiac catheterization
one month agoshowed 25% occlusion of the left circumflex artery.
The patient was given a prescription for Atorvastatin (Lipitor) and
told to take 81mg of aspirin daily.
He did neither. What is the likely cause of his MI? Acute
thrombus over an ulcerated plaque.
Atherosclerosis Consequences Thrombi - Organized/New Channel
Deep Vein Thrombosis and Pulmonary EmboliPredisposing Factors:
Venous Stasis/Immobilization especially of lower
extremities Hypercoagulable States Surgery or Trauma, especially
orthopedic and pelvic
surgery Pregnancy Oral Contraceptive Pills 3 fold (higher with
cigarette use) Malignancy Identified in 17% of thrombo-embolism
Emboli Venous Thrombus: Fate 20-25/100,000 hospital patients =
200-600,000 deaths/year(third most common cause of hospital death)
Most from dislodged thrombus (Thrombo-embolism) Pulmonary Embolus
(venous thrombi) - common
Most are small and clinically silent (may lead topulmonary
hypertension over time)
Large emboli infarct or cardiac collapse/death Commonly arise in
large veins in legs or pelvic area
i.e. DVT (60-80% will have emboli) Systemic/Arterial Emboli:
Infarction
Most from mural thrombus in heart: due to MI or MitralStenosis,
atrial fibrillation, endocarditis, Aneurysms,ulcerated plaques,
valve diseases
Result = Organ Injury: Lower Extremities, Brain, GI,Kidneys,
Spleen
Rare forms: Fat, Air/Nitrogen, Atherosclerotic
debris(angioplasty), amniotic fluid, bone marrow
Test q:A 76y/o woman is hospitalized after falling and
fracturingher left femoral trochanter. 2wk later, the left leg is
swollen,
particularly below the knee. She experiences pain on movementof
the leg; on palpation, there is tenderness. Which of thefollowing
complications is most likely to occur after these events?
Pulmonary thromboembolism. Another year- same story,
diffquestion: What is the diagnosis for her current problem?
Deepvein thrombosis.
Test q:A 42y/o obese male suffers a compound fracture of his
tibia playing soccer. He is placed in traction and bed rest. He
is athigh risk for: Pulmonary embolus.
Test q:A 75y/o woman has had discomfort and swelling of the
left
leg for the past week. A venogram shows thrombosis of deep
leftleg veins. Which of the following mechanisms is most likely
tocause this condition? Long-term bedrest.
Bloodclot, a
cause ofMI.
Can break off
embolustissue
infarction.
Blood goingthrough
channel (butnot enough!)
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Pulmonary Emboli Pulmonary Embolus: Saddle Embolus:
Symptoms:
May not have any symptoms if small Dyspnea, pleuritic chest pain
Hemoptysis especially with infarction Cardiac decompensation Sudden
death
Thromboembolus:
Thrombus - Lines of Zahn (alternating bands of fibrin)
Organizing Thrombus:
Organizing Thrombus:
Post-MortemClot Not organized;not adherant(gel-like).
Currant jellyPassivesettling out ofRBCs andplasma. NoLines of
Zahn.
Test q:A pathologist is asked to perform an exam of a diabetic
woman who diedsuddenly w/a history of thrombophlebitis of the left
lower leg. He finds a clot in the
pulmonary artery. Which of the following findings would indicate
that this clot is athromboembolus? Presence of Lines of Zahn.
REPEATED x3!!
Test q: Features consistent w/a post-mortem clot
are:Jelly-like.
Above: Saddleembolus crossingwhere the pulmonaryartery branches
togo to two lungs.
depositionof fibrin
Can see fibroblastsgrowing into thrombus
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Hemodynamics: Infarcts Post-mortem Clot: Infarct
Determinates:
Nature of vascular system (alternative blood supply) Rate of
occlusion Vulnerability to hypoxia (cell type) Oxygen content of
blood/cardiac output Use of thrombolytic therapy (tPA tissue
plasmingen activator
or streptokinase) Red Infarct:
Loose tissues (lung) and/or 2 vascular systems (lung, liver)
Venous infarcts (ovarian torsion) Previously congested organs
(spleen) Re- establishment of blood flow (lysis of thrombus in MI
after
angioplasty or thrombolytic treatment) White Infarct:
Solid Organs with single vascular system (kidney, heart, spleen
(later))Test q:A 60y/o hospitalized woman has sudden onset of
dyspnea, pleural pain, and cough productive of frothy, blood-tinged
sputum. Ventilation-perfusion scintigraphy indicates a perfusion
defect in the left lung. Which of the following would most likely
be present in section of the lung?Hemorrhagic (red) infarct.
Coronary Artery Occlusion MI Infarct Course:
Biochemical Markers Myoglobin increased at 2-4
hours;non-specific skeletal muscle injury alsoincreases
myoglobin
Cardiac Troponin I or Troponin T increased at 4-6 hours; primary
criteriafor myocardial infarct
elevated for > 3 days Creatine Kinase (MB) increased at
6hours, not as sensitive as troponin I or Tfor MI
Elevated for 1-2 days Lactate Dehydrogenase (LDH),especially
isoenzyme 1 increased at 6hours+; not commonly used today
Elevated for > 3 days
Myocardial Infarct: 6 18 hours MI: Inflammation Can see
contraction bands (arrow) Coag Necrosis 24-48hr
Test q: The main disadvantage of the serum
myoglobin test for acute MI is its: poorspecificity.
Test q:A 57y/o man has just returned from anoverseas trip and
reports having had severesubsternal chest pain 3 days ago. Which of
the
following is the most appropriate lab test to orderfor this
patient? Troponin I.
Complete loss of nuclear andcytoplasmic detail.See some loss of
nuclei.
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Myocardial Infarct: 1-2 days Loss of nuclei and PMNs: Congestion
at edge of infarct: MI: Complete loss of nuclei (48hr)
Myocardial Infarct: Recent (several days old) Below: MI: 2-3
weeksInfarct: softening; pale, hyperemic border MI: Myocardial
Rupture 1-2 wks Macrophages and fibroblasts
Myocardial Infarct: months/years
Lung Infarct: (wedge-shaped) Pulmonary Infarct - Coagulative
Necrosis w/tissuecongestion/hemorrhage; loss of alveolar septae
Test q:An organ from a 70y/o woman at the time of autopsy showed
a focal, wedge-shaped area that was f irm and accompanied by
extensivehemorrhage, giving it a red appearance. Choose the best
answer w/the organ and the situation that resulted in this
lesion:Lung with pulmonary
embolism. (Other choices: heart w/coronary thrombosis, liver
w/hypovolemic shock, kidney w/septic emboli, and brain
w/hypertensive stroke.)
Extravasated blood indamaged area.
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7/30/2019 Pathology Week 2 p19-36
18/18
Kidney Infarct Kidney Infarct Coagulative Necrosis Kidney
Infarct
Renal Infarct: Healed Extremity Infarct: Brain Infarct(organized
w/fibrous scar) Infarct of foot (from embolus or thrombus)
Liquefactive necrosis
Can be from systemic arterial emboli.
Shock: Hypotension/Diffuse Organ Damage Cardiogenic: High
Mortality
MI, Ventricular Rupture, Arrhythmia, Tamponade,Pulmonary
Embolism
Hypovolemic: Hemorrhage, Fluid Loss (burns,vomiting/GI,
trauma)
Septic: 100,000 deaths/year; High Mortality Overwhelming
Infections (septicemia) Endotoxic Shock: Release of bacterial cell
wall
components (LPS) Neurogenic: anesthesia Septic Shock:
Anaphylactic: IgE mediated hypersensitivity
Test q: Platelets are: Created from whole blood donations
orcollected from donors using apheresis machines.
Other choices: Stored for 14 days on a rotator at room temp
Treated w/multiple antibiotics to prevent the growth of bact
and fungi Are the first line therapy for patients the TTP
(what?? typo?) Frozen at -70*C for later use
Test q: Disorders of primary hemostasis include all of the
followingexcept: hypofibrinogenemia. (Other choices: Aspirin or
Plavix
(acquired); Von Willebrands disease; Hereditary platelet
defects)
(Not sure that these qs were covered maybe the testsare outdated
compared to our pptsor maybe I skippedover these while
reading?)
Wedge-shaped.More tan/white incharacter.
Loss of cellulardetail ininfarcted area.
= lipopolysaccharide