pathology week 2 p19-36

7/30/2019 Pathology Week 2 p19-36

1/18

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,


2/18


3/18

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


4/18

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.


5/18

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


6/18

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.


7/18

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


8/18

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.


9/18

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.


10/18

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.


11/18

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.


12/18

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.


13/18

Plaque Formation:

Atherosclerotic Plaque:

Fate of Atherosclerotic Plaques: Atherosclerosis:

Coronary Artery

*

* = thrombus overlying plaque

Coronary ArteryThrombosis


14/18

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!)


15/18

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


16/18

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.


17/18

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.


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

pathology week 2 p19-36

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