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03 BP1 > 14a Hemodynamics > Flashcards

14a Hemodynamics Flashcards

1
Q

Define: edema, thrombosis, embolism, infarction, hemorrhage

A

Edema: water extravasation into interstitial spaces via contraction, retraction, direct injury, or transcytosis
Thrombosis: clot formation at inappropriate site
Embolism: migration of a clot which ledges in a blood vessel
Infarction: cell death due to obstruction of blood flow, ischemic necrosis
Hemorrhage: inability to clot after injury

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2
Q

Edema vs effusion

A

Edema: fluid in tissues
Effusion: fluid in body cavity

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3
Q

Types of edema

A

Inflammatory: inflammatory mediators causing local increases in vascular permeability; efflux of plasma, proteins, leukocytes, neutrophils, PMN; protein-rich exudate
Non-inflammatory edema: from hydrodynamic derangements; protein-poor transudate; seen in CHF

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4
Q

Pathologic causes of edema

A

Increased hydrostatic pressure: more tendency to push water and salts out of capillaries into the interstitial space; impaired venous return (DVT) or increased venous pressure (CHF)

Reduced plasma osmotic pressure: reduced synthesis or excessive loss of albumin; nephrotic syndrome (hypoalbuminemia), cirrhosis of the liver (dec albumin), protein malnutrition

Lymphatic obstruction: trauma, fibrosis, invasive tumors, infectious agents -> impaired clearance of interstitial fluid -> lymphedema; lymphatic filariasis (genitals and lower limbs), peau d’ orange

*Na and H2O retention: -> increased hydrostatic pressure (intravascular fluid expansion), diminished vascular colloid osmotic pressure (dilution), decreased renal perfusion; 1º kidney disorders, cardio disorders

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5
Q

Subcutaneous edema

A 
Areas with high hydrostatic pressure
Dependent edema (gravity)

Correlates: right-sided CHF, renal dysfunction, nephrotic syndrome, periorbital edema, post-strep glomerulonephritis

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6
Q

Pulmonary edema

A

Blood stays in pulmonary circulation
Heavy lungs
Fluid impairs gas exchange (ventilation and oxygen diffusion), favorable environment for bacterial infection

Correlate: left-ventricular heart failure, pulmonary inflammation/infection, hypersensitivity, ARDS, renal failure

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7
Q

Brain edema

A

Localized: abscess/tumor in brain
Generalized: encephalitis
Narrow sulci, distended gyri

Correlate: hernia through foramen magnum, injury to medullary center

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8
Q

Other effusions

A

Hydrothorax (pleural cavity)
Hydropericardium (pericardial cavity)
Hydroperitoneum/Ascites (peritoneal effusions): portal hypertension

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9
Q

Transudate vs exudate

A

Transudate: protein poor, translucent, exception: peritoneal effusion due to lymph block (has lipids)
Exudative: protein rich

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10
Q

Hyperemia vs congestion

A

Hyperemia: active process from augmented tissue inflow due to arteriolar dilation; tissues turn red (engorged oxygenated blood); skeletal muscle during exercise (inc blood flow)

Congestion: passive process from impaired outflow of blood; inc hydrostatic pressure; red-blue (deoxy blood accumulation andred cell stasis); cardiac failure (systemic) and isolated venous obstruction (localized)

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11
Q

Chronic passive congestion

A

Chronic hypoxia -> ischemic tissue injury and scarring

Capillary rupture -> hemorrhagic foci + RBC catabolism

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12
Q

Acute pulmo congestion vs chronic pulmo congestion

A

Acute: blood-engorged alveolar capillaries, alveolar septal edema, focal intraalveolar hemorrhage

Chronic: CHF; thick and fibrotic septa; hemosiderin-laden macrophages in alveoli

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13
Q

Acute hepatic congestion vs chronic hepatic congestion

A

Acute: distended CV and sinusoids w blood; centrilobular hepatocyte = ischemic necrosis, periportal hepatocytes = better O2

Chronic: right sided heart failure (CHF); red-brown centrilobular regions; tan colored parenchyma

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14
Q

Hemorrhage clinical correlates

A
  1. Hematoma accumulation (bruise, retroperitoneal hematoma, rupture of aneurysm)
  2. Intracranial hemorrhage = compromises blood supply and herniates brain
  3. Chronic/recurrent external blood loss -> iron loss -> iron deficiency anemia
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15
Q

Defects in primary hemostasis

A

Bleeds in skin/mucosal membranes

Petechiae
Purpura
Epistaxis (nosebleeds)
GI bleeding
Menorrhagia
Intracerebral hemorrhage
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16
Q

Petechiae vs purpura

A

Petechiae: 1-2 mm; low platelet (thrombocytopenia),defective platelet function in uremia (elevation of BUN & creatinine); clotting deficits, locally increased intravascular pressure

Purpura: 2º to trauma, vascular inflammation (vasculitis), increased vascular fragility (amyloidosis)

17
Q

Defects of secondary hemostasis

A

From coagulation factor defects

Bleeds into soft tissues (muscle) or joints

18
Q

Generalized effects

A

Hematoma

Palpable purpura
Ecchymoses: >1-2 cm subcutaneous hematomas

19
Q

Function of normal hemostasis

A

Maintain blood in a fluid, clot-free state in normal vessels

Induce rapid and localized hemostatic plug at site of vascular injury

20
Q

Normal hemostasis 1 vasoconstriction

A

Reflex neurogenic mechanisms -> vasoconstriction

Endothelin: vasoconstrict

21
Q

Normal hemostasis 2 primary hemostasis

A 
Subendothelial ECM: platelet adherence and activation, Platelets-Glycoprotein Ib receptors-VWF
Platelet activation (disc -> plate)
Secretory granule release: ADP, Thromboxane A2

Form reversible hemostatic plug (no fibrin)

22
Q

Normal hemostasis 3 secondary hemostasis

A

Tissue factor (Factor III + thromboplastin) -> coagulation cascade 0> activate thrombin

Thrombin: converts fibrinogen to fibrin -> create fibrin meshwork + platelet recruitment

23
Q

Normal hemostasis 4 Thrombus and anti-thrombotic effects

A

Fibrin + platelet = permanent (platelet) plug

Tissue plasminogen activator: activates plasminogen -> plasmin; fibrinolysis, clot resorption and tissue repair
Thrombomodulin: blocks coagulation cascade

24
Q

(antithrombotic properties) Antiplatelet effects

A

Prostacyclin (PGI2) and NO: vasodilators and inhibit platelet aggregation
Adenosine diphosphatase: degrades ADP -> inhibit platelet aggregation

25
Q

(antithrombotic properties) Anticoagulant molecules

A

Heparin-like molecules: with antithrombin III = inactivate thrombin, factor Xa, etc.
Thrombomodulin: binds to thrombin to make it into anticoagulant via activation of protein c
Protein c: inhibits clotting, cleaves factor Va and VIIIa
Protein s: cofactor for protein c and TFPI
TFPI: inhibits factor VIIa and Xa

26
Q

(antithrombotic properties) Fibrinolytic effects

A

Tissue-type plasminogen activator

27
Q

(prothrombotic properties) Platelet effects

A

VWF: platelet adhesion to ECM

28
Q

(antithrombotic properties) procoagulant effects

A

Tissue factor: extrinsic clotting cascade

29
Q

(antithrombotic properties) antifibrinolytic effects

A

PAIs: inhibit fibrinolysis and favors thrombosis

30
Q

Platelet cytoplasmic granules

A

a-granules: has P-selectin, for coagulation (fibrinogen, factor B, factor VIII, VWF)

d-granules: contain ADP and ATP (platelet aggregation), Ca (coagulation cascade), histamine, serotonin, epinephrine

31
Q

Platelet adhesion

A

platelet - GpIIb-IIIa - fibrinogen - GpIIb-IIIa - platelet - GpIb - VWF

Bleeding disorders:
no VWF: von willebrand disease
no GpIb: bernard-soulier syndrome
no GpIIb-IIIa: Glanzmann thrombasthenia

32
Q

Platelet shape change

A

Altered GpIIb-IIIa = inc affinity of platelets to fibrinogen

Translocation of neg phospholipids (to prevent Ca binding and coagulation cascade)

33
Q

Platelet secretion

A

Thrombin: activate platelet with protease-activated receptor (PAR)
Release of granule contents: ADP and TxA2 (inc platelet recruitment)
Aspirin: inhibit cyclooxygenase (for synthesis of TxA2) -> inhibit platelet aggregation
Pro-inflammatory effects of thrombin: PAR -> proinflamm effects

34
Q

Platelet aggregation

A

GpIIb/IIIa: ADP activation -> fibrinogen binding
Thrombin: fibrinogen -> fibrin

further platelet activation and aggregation -> platelet contraction -> secondary plug

03 BP1 (18 decks)

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