Tissue Repair & Hemodynamic Disorders Flashcards by Erwin Corinales

Regeneration and Scar formation

Repair

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Extensive deposition of collagen

Fibrosis

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Continuously dividing cells that proliferate through out life
(Skin, oral cavity, vagina, cervix)

Labile cells

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Quiescent tissues with low level of replication
Can undergo rapid replication in response to stimulus.
(Liver, kidneys, pancreas)

Stable cells

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Non-dividing tissues, have left the cell cycle and cannot undergo mitotic division.
(Neurons, skeletal and cardiac muscle)

Permanent cells

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Most abundant protein

Collagen

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Only protein that undergo final modification in the RER

Collagen

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Modification of collagen occurs in this part of the cell

RER

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Most abundant amino acid

Glycine

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Type 1 collagen

Bone
Skin
Tendon (elastic, fibrocartilage)

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Type 2 collagen

Hyaline cartilage

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Type 3 collagen

Reticulin

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Collagen type 4

Basement membrane or basal lamina

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Most important cause of delay in healing

Infection

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Excessive formation of scar where collagen deposition goes beyond the wound edge

Keloid formation

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What percentage of body weight is in the interstitial fluid compartment

15% Interstitial fluid compartment

Breakdown:
60% TBW
40% ICF
20% ECF (5% plasma 15% int fluid compt)

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Type of edema

Protein: High
Cell: normal
Pressure response: nonpitting

Lymphedema (eg. Elephantiasis)

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Type of edema

Protein: High
Cell: High
Pressure response: nonpitting

Exudate (eg. Ascites in CLD)

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Type of edema

Protein: low
Cell: low
Pressure response: ptting

Transudate (eg. Leg edema in CHF)

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Type of edema

Protein: Normal
Cell: normal
Pressure response: nonpitting

GAGs (eg. Pretibial myedema in graves dse.)

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Drug used for treatment of cerebral edema

Mannitol (osmotic diuresis)

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Catastrophic complications of cerebral edema

Tonsillar herniation (compressing CN III)

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Active process in which arteriolar dilation leads to increase in blood flow

Hyperemia

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Passive process
From reduced outflow of blood from a tissue
Cyanosis (accumulation of deoxygenated hemoglobin)

Congestion

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Type of pulmonary congestion with presence of hemosiderin laden macrophages "heart failure cells", thickened and fibrotic septa

Chronic pulmonary congestion

Type of pulmonary congestion with engorged alveolar capillaries with alveolar septal edema and focal intra-alveolar hemorrhage

Acute pulmonary congestion

Type of hepatic congestion with ischemic centrilobular hepatocytes with periportal steatosis

Acute hepatic congestion

Type of hepatic congestion with hemorrhagic centrilobular hepatocytes accentuated against uncongested tan liver "Nutmeg Liver"

Chronic passive hepatic congestion

Accumulation of blood within tissues

Hematoma

1-2mm hemorrhages into skin, mucous membranes and serosal surfaces (thrombocytopenia, defective plt function)

Petichiae

=/> 3mm hemorrhages | Trauma, vasculitis, vascular fragility

Purpura (henoch schonlein purpura)

>1-2cm subcutaneous hematoma

Ecchymoses

>20% blood loss

Hemorrhagic shock

Physiologic process of rapid clot formation at site of vascular injury

Hemostasis

Pathologic clot formation in intact vessels

Thrombus

Product of primary hemostasis

Platelet plug

Initiates coagulation cascade in secondary hemostasis

Tissue factor Factor XII Culminates in thrombin generation that cleaves fibrinogen into insoluble fibrin (fibrin meshwork)

Amplifies platelet aggregation in primary hemostasis

Thromboxane A2

Glanzmann's theombosthenia resembles the MOA of which anti-platelet drugs

Abciximab Eptifibatide Tirofiban (Glycoprotein IIb-IIIa inhibitors)

Virchow's triad

Endothelial injury Hypercoagulability Abnormal blood flow

Most common primary hypercoagulable state

Facto V Leiden mutation

Treatment for heparin induced thrombocytopenia

Lepirudin Argatroban (Direct thrombin inhibitors)

Signify thrombus formed in flowing blood. distinguishes antemortem thrombosis

Lines of Zhan - pale platelet and fibrin deposits alternating with dark red cell-rich layers

Gelatinous with dark r d dependent portion and yellow"chicken-fat" upper portion Lines of Zahn are absent.

Postmortem thrombosis

Settling of blood in the dependent portion of the body | 20mins-3hrs after death

Livor Mortis/ Post-mortem Lividity/ Suggilation

Thrombus that begin at sites of turbulence or endothelial injury Compositin: friable meshwork of platelets, fibrin, red cells, and degenerating leukocytes

Arterial thrombosis Common site: coronary>cerebral>femoral (+) Lines of Zahn

Thrombus that begin at sit s of stasis, almost invariably occlusive. Composition: mor enmeshed RBCs and few platelets(red or stasis thrombi)

Venous thrombosis

Most common site of DVT

Calf veins

Sterile verocous endocarditis in SLE patients

Libman-Sacks endocarditis (mitral valve)

Sudden or insidious onset widespread fibrin thrombi in the microcirculation

DIC (consumptive coagulopathy)

Most common symptom of pulmonary embolism

Dyspnea

Most common sign of pulmonary embolism

Tachypnea

Classic signs of Pulmonary embolism

Low grade fever Neck vein engorgement Tachycardia Accentuated pulmonic component of S2

Common ECG manifestation in Pulmonary Embolism

Sinus tachycardia

Gold standard for the diagnosis of pulmonary embolism

Pulmonary angiography

DVT that presents as a pale painful leg with diminished arterial pulse due to a vasospasm

Phlegmasia alba dolens

DVT that presents as a cyanotic painful leg due to extensive thrombotic occlusion

Phlegmasia cerulia dolens

Dislodged venous thrombus that passes through a heart defect and causes stroke

Paradoxical embolism

Minimum amount of air embolism that can produce a clinical effect

100cc

Ischemic necrosis of femoral heads, tibia and humerus due to nitrogen bubbles from rapid ascent

Caisson disease

Area of ischemic necrosis caused by occlusion of either the arterial supply/ venous drainage

Infarct

Dominant histologic characteristic of infarction

Ischemic coagulative necrosis (except in brain- liquefactive necrosis)

Valvular heart defect that usually leads to septic embolism to the lungs

Tricuspid valve endocarditis

Common Etiologic agent in Tricuspid valve endocarditis

Staphylococcus aureus

The most severe form of meningococcimia

Waterhouse Frederichsen Syndrome (bilateral adrenal hemorrhage l/t insufficiency)

GpIb deficiency(platelet disorder)

Bernard-Soulier syndrome

Proliferation of cells to replace lost structures

Regeneration