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Pathology 2-Systemic > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

Nitric oxide

A
  • Macrophage produce NO through 2 NO synthase enzymes
  • Causes vasodilation & NO free radicals are toxic to microbal & mammalian cels
  • Reduces leukocyte adhesion
  • Reduces platelet adhesion
  • Endothialial stimulation = Ca+2 influx & endothelial NOS activation
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2
Q

Congestion of Liver

A
  • Cardiac failure (right heart = venous congestion)
  • Damming of blood in the IVC
  • Central veins & sinusoids are DISTENDED with blood
  • Hepatocytes around the central vein (necrosis & degeneration)
  • Hepatocytes on the periphery of portal area better O2 (hepatic arteriloles)
  • Periportal hepatocytes (periphery) show FATTY change
  • Histology: central areas are red & depressed COMPARED w/surrounding tan parenchyma = NUTMEG liver pattern
  • Cetrilobular necrosis w/degenerating hepatocytes = enlarged liver
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3
Q

Hemorrhage

A
  • LOW platelet count
  • Purpura: small on dots on surface of skin
  • Due to = Trauma or vascular inflammation (vasculitis)
  • Ecchymoses: Subcutaneous hematomas (bruises) larger Surface area
  • LARGE hemmorrhages w/in body cavities-
  • Hemopericardium = Blood in the pericardial sac
  • Can cause cardiac temponade
  • Hemoperitoneum = Blood in between inner lining of abdominal wall & outer of abdominal organs
  • Causes: trauma, abdominal aortic aneurysm, HIGH does of anti-coags
  • Hemothorax= Blood in pleural cavity
  • Causes: narrowing pulse pressure, hypotension
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4
Q

Thrombosis

A
  • Intravascular mass formed from Blood components adhered to Vessel wall
  • Vrichow triad
  1. Endothelial injury
  2. Statis or turbulence flow
  3. Blood hypercoag
  • Endothelial injury:
  • ulcerated plaques in atherosclerosis
  • Vascular injury = Vasculitis
  • Causes: Hypertension, turbulent flow, scarred valves, bacterial endotoxins
  • Stasis or turbulent flow - Prolonged bed rest, aneuysms (abdominal)
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5
Q

Hemostatic Process (Primary)

A
  1. Reflex vasoconstriction
  2. ECM collagen exposed from basement membrane
  3. Endothelin release causes secondary vasoconstriction
  4. Platelet adhesion DUE to vWF = shape change & granule release
  5. Granule = ADP & TxA2 = FURTHER platelet aggregation = hemostatic plug (END of primary hemostatis)
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6
Q

Hemostatic process (secondary)

A
  1. Tissue factor & platelet phospholipids = THROMBIN activation
  2. Results in Fibrin polymerization-cementing platelets into secondary hemostatic plug
  3. Fibronogen to Fibrin = Crosslinked - STABLE
  • Antithrombic events:
  • Release of t-PA (fibronolytic)
  • Thrombomodulin (blocks coag cascade)-binds with thrombin->protein C proteolysis F 5 & 8
  • antithrombin 3 inactivates thrombin along w/heparin like mols & F10,9,12,11
  • NO, PGl2, ADP from endothelium=INHIBIT platelet aggregation
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7
Q

Def in Platelet adhesion & aggregation

A
  • Glanzmann thrombasthenia:
  • Def in Gp2b-3a complex - originally Gp1b ADP induces confromational change
  • Gp2b-3a allows for Fibronogen to bridge platelet (adhesion)
  • Bernard-soulier syndrome:
  • Def. in Gp1b binds w/vWF which allows platelet adhesion to damaged endothelium
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8
Q

Hypercoagulability

A
  • NOT common cause of thrombosis
  • Causes: Hereditary
  • Mutations in factor 5 gene (Leiden)
  • Prothrombin gene-correlates w/elevated lvls of homocysteine (hardening of major arteries)
  • Def oF antithrombin 3, Protein C & S
  • Causes: Aquired
  • Oral contraceptive
  • Cardiac failure
  • Heparin induced thrombocytopenia syndrome (HIT) = LOW platelet, PF4 antibodies to heparin form CHECK PTT/Intrisic pathway
  • Antiphosolipid syndrome = can cause miscarriage and can form clots in arterial and venous system
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9
Q

Intrinsic & extrinsic

A
  • Intrinsic = PTT (heparin decreases)
  1. Hageman factor - HMWK collagen - 12A
  2. 11, 9, 8 Associated w/Thrombin
  • Extrinsic = PT (Coumadin decreases)
    1. Tissue injury - Thromboplastin - F7
  • Common pathway- Factor 10
  • activated by Ca+2 influx from BOTH intrisic & extrinsic
  • F 5, 2, 1-(fibronogen)
  • Fibrinogen to Fibrin to CROSS-linked fibrin - active Factor 13 = Stabilizer
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10
Q

Prolonged Bleeding Time

A
  • Tests Platelet function UP to the formation of temp plug (primary hemo)
  • PROlonged BT=
  • Aspirin/NSAID - Plt count normal
  • Bernard-soulier- Thrombocytopenia (low), GIANT platelets (Big Suckers)
  • Glanzman’s disease - No fibronogen bridging - Low platelet, renal failure, scurvy
  • vWB disease- combined platelet and coag defect
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11
Q

Prothrombin Time

A
  • Used to measure effectiveness of extrinsic pathway - formation of fibrin clot - meshwork (secondary hemo)
  • Factors 7, 10, 5, 2, 1
  • Normal - 11-15 seconds
  • Helpful for checking on patients warfarin response - anticoag time
  • PROLONGED PT - liver disease
  • Detect Factor 7 def
  • Normal Thrombin time - 9-13 seconds Measures fibrinolytic pathway (fibronogen-fibrin)
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12
Q

Partial Thromboplastin Time

A
  • Measures intrinsic pathway (til formation of fibrin-meshwork)
  • Factors 12, 11, 9, 8, 10, 5, 2, 1
  • Norm = 25-40 seconds
  • Measure pts on heparin therapy
  • Detect factors def in intrisic pathway
  • Normal Thrombin time - 9-13 seconds Measures fibrinolytic pathway (fibronogen-fibrin)
  • Test:
  • Kaolin-Activation of contact-depen Factor12
  • Cephalin-Sub platelet phospholipid
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13
Q

Reasons for Bleeding Disorders

A
  • Increased fragility of BV:
  • Patachiae, purpuras (appear in bacterial infection that activate hagmans factor or DEF of Vit C)
  • Platelet, bleeding time, coag (PT, PTT) are normal
  • Platelet def & dysfunction
  • Derangement of coag-PT, PTT prolonged, BT normal, Hemm in joints, LL (trauma)
  • Combo of all these factors
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14
Q

Henoch-Schonlein purpura

A
  • Seen in childhood
  • Following upper resp infection
  • Infective endocarditis
  • Pathogenesis:
  • systemic hypersensitivity disease
  • widespread inflammatory rxn of capillaries & small vessels
  • Symptoms:
  • Purpuric rash
  • Abdominal colic (intense cramping)
  • Polyarthralgia (pain in multiple joints)
  • Acute glomerulonephrtis (RBC urine)
  • Skin Signs: Deposition of IgA (found in mucus membranes tears, saliva, Resp, GI)-Fibrin deposits
  • Platelet, bleeding, coag = NORMAL
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15
Q

Disseminated Intravas Coag (DIC)

A
  • Complex systemic thrombohemorrhagic disorder (small blood clots throughout)
  • Causes a hemostatic defect
  • Results from utilization of coag factors & platelets (Consumption Coag)
  • Pathogenesis:
  • NOT a primary disorder - secondary to other causes:
  • Obstetric complication, infections, neoplasms, MASSIVE tissue injury
  • Release or entry of tissue factors (coagulants) OR extensive endothelial injury
  • Results in formation of coag sequence-FORMATION of micro thrombi (microcirculation)
  • CAUSES ischemia
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16
Q

DIC pathogenesis

A
  • 2 enzymes involved: Thrombin & plasmin
  • Balance between the 2 determines bleeding or thrombotic tendencies
  • Thrombin promotes fibrin clot formation
  • Plasmin clot inhibiting factor
  • INITIAL phase = widespread deposition of FIBIRIN clots
  • Hemmorraghe=Consumption of platelets & clotting factors
  • Plasmin breakdown fibrin (D-dimers) - proteolysis of various clotting factors = HEMOSTATIC failure
  • Symptoms: Thrombi seen in various organs (brain, heart, kidney, lungs)
  • Ex. WFS (waterhouse), sheehan postpartum pit necrosis
17
Q

DIC Lab Findings & Treatment

A
  • Platelet count: decreased (consumption)
  • PTT & PT = prolonged (intrisic & extrinsic)
  • Thrombin time = prolonged
  • Fibronogen levels = reduced
  • Fibronogen degradation increased - (D-dimers)
  • Peripheral blood smear (fragmented RBCs)
  • Treatment:
  • Volume replacement (Fresh frozen plasma)
  • Correction of hypotension & oxygenation
  • Heparin (PTT or Intrisic)
  • Acute DIC (obst complication) dominated by bleeding diathesis (EXCESS bleeing w/NO clotting)
  • Chronic DIC (aortic anuerysms) thrombic complications
18
Q

Disorders associated w/DIC

A
  • Obstetric:
  • Retained dead fetus
  • Septic abortion
  • Aminolic fluid embolism
  • Infections:
  • Sepsis (gram + & -)
  • Meningococcemia (meningetis)
  • Histoplasmosis (fungal spore/caves)
  • Malaria
  • Neoplasms (tumor):
  • Carcinomas of pancreas, prostate, lung, stomach
  • Acute promyelucytic leukemia
  • Massive tissue injury (trauma, burns, surgery)
  • Misc: Snake bite, heat stroke, liver disease
19
Q

Thrombocytopenia

A
  • Quanitative:
  • Decreased production of platelets (aplastic anemia, leukemia) Bone marrow does not make enough RBCs
  • _Decreased platelet survival _(immunological or non) - qualitative
  • Sequestration <u><strong>(hypersplenism)</strong></u> in red pulp
  • Dilutional <strong>(massive transfusions)</strong>
  • Skin/Mucusosal bleeding
20
Q

Essential Thrombocytopenia

A
  • Uncontrolled proliferation of megakaryocytes
  • Recurrent episodes of thrombosis/Hemorr
  • Platelet count above 600,000
  • Increased megakaryocytes ALSO a feature of CML
21
Q

Quantitative Thrombocytopenia (ITP)

A
  1. ITP (immune thrombocytopenia purpura)-Coag time normal
  2. Pts w/SLE or auto-immune or w/corticosteroid treatment
  • Acute: seen in children after viral infection, Formation of anti-platelet antibodies,_ EPISTAXIS (nose bleeds)_
  • Chronic: seen in woman 20-40 increase in megakaryocytes
  • Antibodies against platelet membrane glycoproteins 2b/3a or 1b/9 complexes detected in BW
  • Megakaryocytes found in bone marrow
  • Treatment: splenectomy normalizes platelet count due to less destruction
  • Melena (tarry feces), Bleeds from mucus membranes
  • Sub arachonoid & intracerebral hems
22
Q

Quantitative Thrombocytopenia (TTP)

A
  1. Thrombotic thrombocytopenic purpura (autoimmune or inherited)
  • Def. in ADAMTS 13 metalloproteinases (zinc co-factor) degrades VHMW multimers of vWF
  • presents w/Large vWF multimers that accumulate in plasma.
  • This accumulation promotes formation of platelets microaggregates throughout circulation (DIC) w/endothelial injury
  • Platelets involved in thrombus formation=Thrombocytopenia
  • Symptoms: (pentad/5)
  • Fever, Thrombocytopenia, Renal failure, Microangiopathic anemia (schistocytes pointed RBCs due to destruction), NEURO issues (hallucinations or stroke)
23
Q

Quantitative Thrombocytopenia (HUS)

A
  1. Hemolytic uremic syndrome (children)
  • triggered by infectous gastroenteritis by E.coli 0157:H7 (found in undercooked meat)
  • ANEMIA only no Thrombocytopenia
  • E-coli Shiga like toxin(stop protein production) damages endothelial lining = platelet activation/aggregation
  • Presents: bloody diarrhea, acute renal failure, anemia & **NO neuro **
  • RENAL FAILURE
24
Q

Qualitative Thrombocytopenia

A
  • Due to Defective adhesion or aggregation or secretion
  • Adhesion: Benard-soulier syndrome: Def of platelet membrane glycoprotein (Gp1b receptor for vWF)
  • Aggregation: *Glanzmann’s thromboasthenia*: Platelers LACK glycoprotein 1b/3a = NO fibronogen bridging can occur = INCREASED BT
  • Secretion: Storage pool defects in granule non metabolic ADP
25
Q

Bleeding disorders (vWF)

A
  • Resembles hemophilia
  • Pathogenesis: Defect in platelet function=Prolonged BT, Coag defect due to def of Factor 8 (activated by vWF)
  • vWF functions:
  • Platelet adhesion mol, binds platelets to exposed collagen, Platelets have receptor Gp1B - binds to vWF
  • Complexes w/ factor 8->C protein w/help from vWF prevents degradation of complex
  • DECREASE in vWF decreases 8:C activity (prone to coag)
  • TEST: Ristocin helps determine vWF functtion
  • Lab: Platelet normal, BT increase, PT normal, PTT increased (Factor 8 & vWF)
26
Q

Hemophilia A-8

A
  • X-linked
  • Females are carriers
  • Lab: Platelet normal, BT normal, Prothromnin time normal (Extrinsic)
  • PTT: Prolonged *due factor 8* levels reduced (intrinsic)
  • Symptoms:
  • Easy bruising
  • Hemorrhage following trauma
  • Spontaneous bleeding (knee joints) Hemarthroses
  • Petechiae are ABSENT
  • Hemo B is same as A BUT decrease in factor 9 NOT 8
27
Q

Vit C Role

A
  • Hydroxylation of lysine and proline-collagen synthesis
  • Antioxidants (stops production of free radicals cause cell injury)
  • Prevents nitrosylation: Inhibits amides from binding with nitrites (food perserv)
28
Q

Vit C Def

A
  • Scurvy:
  • Collagen synthesis affected
  • POOR wound healing
  • Bone diseases in growing children (osteoid matrix) - insuff production by osteoblasts - FAILURE to reabsorb catilaginous matrix = cartilaginous overgrowth (Lack strength = BOWING)
  • Hemorrahge & healing defects
  • Occurs in ederly or alcholics
  • Impaired collagen = Poor vessel support(bruising) petechia, impaired osteoid matrix, bleeding periosteum in joints.

Pathology 2-Systemic (15 decks)

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