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Erwin Personal Flash Cards > Tissue Repair & Hemodynamic Disorders > Flashcards

Tissue Repair & Hemodynamic Disorders Flashcards

1
Q

Regeneration and Scar formation

A

Repair

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2
Q

Extensive deposition of collagen

A

Fibrosis

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3
Q

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

A

Labile cells

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4
Q

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

A

Stable cells

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5
Q

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

A

Permanent cells

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6
Q

Most abundant protein

A

Collagen

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7
Q

Only protein that undergo final modification in the RER

A

Collagen

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8
Q

Modification of collagen occurs in this part of the cell

A

RER

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9
Q

Most abundant amino acid

A

Glycine

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10
Q

Type 1 collagen

A

Bone
Skin
Tendon (elastic, fibrocartilage)

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11
Q

Type 2 collagen

A

Hyaline cartilage

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12
Q

Type 3 collagen

A

Reticulin

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13
Q

Collagen type 4

A

Basement membrane or basal lamina

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14
Q

Most important cause of delay in healing

A

Infection

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15
Q

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

A

Keloid formation

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16
Q

What percentage of body weight is in the interstitial fluid compartment

A

15% Interstitial fluid compartment

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

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17
Q

Type of edema

Protein: High
Cell: normal
Pressure response: nonpitting

A

Lymphedema (eg. Elephantiasis)

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18
Q

Type of edema

Protein: High
Cell: High
Pressure response: nonpitting

A

Exudate (eg. Ascites in CLD)

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19
Q

Type of edema

Protein: low
Cell: low
Pressure response: ptting

A

Transudate (eg. Leg edema in CHF)

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20
Q

Type of edema

Protein: Normal
Cell: normal
Pressure response: nonpitting

A

GAGs (eg. Pretibial myedema in graves dse.)

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21
Q

Drug used for treatment of cerebral edema

A

Mannitol (osmotic diuresis)

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22
Q

Catastrophic complications of cerebral edema

A

Tonsillar herniation (compressing CN III)

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23
Q

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

A

Hyperemia

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24
Q

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

A

Congestion

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25
Q

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

A

Chronic pulmonary congestion

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26
Q

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

A

Acute pulmonary congestion

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27
Q

Type of hepatic congestion with ischemic centrilobular hepatocytes with periportal steatosis

A

Acute hepatic congestion

28
Q

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

“Nutmeg Liver”

A

Chronic passive hepatic congestion

29
Q

Accumulation of blood within tissues

A

Hematoma

30
Q

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

A

Petichiae

31
Q

=/> 3mm hemorrhages

Trauma, vasculitis, vascular fragility

A

Purpura (henoch schonlein purpura)

32
Q

> 1-2cm subcutaneous hematoma

A

Ecchymoses

33
Q

> 20% blood loss

A

Hemorrhagic shock

34
Q

Physiologic process of rapid clot formation at site of vascular injury

A

Hemostasis

35
Q

Pathologic clot formation in intact vessels

A

Thrombus

36
Q

Product of primary hemostasis

A

Platelet plug

37
Q

Initiates coagulation cascade in secondary hemostasis

A

Tissue factor
Factor XII

Culminates in thrombin generation that cleaves fibrinogen into insoluble fibrin (fibrin meshwork)

38
Q

Amplifies platelet aggregation in primary hemostasis

A

Thromboxane A2

39
Q

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

A

Abciximab
Eptifibatide
Tirofiban

(Glycoprotein IIb-IIIa inhibitors)

40
Q

Virchow’s triad

A

Endothelial injury
Hypercoagulability
Abnormal blood flow

41
Q

Most common primary hypercoagulable state

A

Facto V Leiden mutation

42
Q

Treatment for heparin induced thrombocytopenia

A

Lepirudin
Argatroban
(Direct thrombin inhibitors)

43
Q

Signify thrombus formed in flowing blood.

distinguishes antemortem thrombosis

A

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

44
Q

Gelatinous with dark r d dependent portion and yellow”chicken-fat” upper portion

Lines of Zahn are absent.

A

Postmortem thrombosis

45
Q

Settling of blood in the dependent portion of the body

20mins-3hrs after death

A

Livor Mortis/ Post-mortem Lividity/ Suggilation

46
Q

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

A

Arterial thrombosis

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

47
Q

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

A

Venous thrombosis

48
Q

Most common site of DVT

A

Calf veins

49
Q

Sterile verocous endocarditis in SLE patients

A

Libman-Sacks endocarditis (mitral valve)

50
Q

Sudden or insidious onset widespread fibrin thrombi in the microcirculation

A

DIC (consumptive coagulopathy)

51
Q

Most common symptom of pulmonary embolism

A

Dyspnea

52
Q

Most common sign of pulmonary embolism

A

Tachypnea

53
Q

Classic signs of Pulmonary embolism

A

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

54
Q

Common ECG manifestation in Pulmonary Embolism

A

Sinus tachycardia

55
Q

Gold standard for the diagnosis of pulmonary embolism

A

Pulmonary angiography

56
Q

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

A

Phlegmasia alba dolens

57
Q

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

A

Phlegmasia cerulia dolens

58
Q

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

A

Paradoxical embolism

59
Q

Minimum amount of air embolism that can produce a clinical effect

A

100cc

60
Q

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

A

Caisson disease

61
Q

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

A

Infarct

62
Q

Dominant histologic characteristic of infarction

A

Ischemic coagulative necrosis (except in brain- liquefactive necrosis)

63
Q

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

A

Tricuspid valve endocarditis

64
Q

Common Etiologic agent in Tricuspid valve endocarditis

A

Staphylococcus aureus

65
Q

The most severe form of meningococcimia

A

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

66
Q

GpIb deficiency(platelet disorder)

A

Bernard-Soulier syndrome

67
Q

Proliferation of cells to replace lost structures

A

Regeneration

Erwin Personal Flash Cards (16 decks)

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