Patho 1 | Cellular Response To Injury

Front 1

Increase in size of cells due to increase in functional demand

Back 1

Hypertrophy

Front 2

Stimulus for physiologic hypertropy of the uterus

Back 2

Estrogen

Front 3

2 organs which undergo both physiologic hypertrophy and hyperplasia

Back 3

Uterus

Breast during puberty

Front 4

Increase in number of cells

Back 4

Hyperplasia

Front 5

Decrease in cell size and number due to decreased protein synthesis

Back 5

Atrophy

Increased protein degradation (ubiquitin-proteasome) and autophagy

Front 6

3 types of metaplasia

Back 6

1. Columnar to squamous - smokers, Vitamin A deficiency

2. Sq to colum - Barrett esophagus, cervical cancer

3. Connective tissue - myositis ossificans

Front 7

First manifestation of reversible cell injury

Back 7

Cellular swelling

Hydropic changes

Vacuolar degeneration

Front 8

Histologic findings of necrosis

Back 8

Increased eosinophilia

Discontinuities in plasma membrane

Front 9

Whorled phospholipid precipitates derived from damaged cell membranes

Phagocytized or degraded into fatty acids

Calcium soap formation

(*necrosis)

Back 9

Myelin figures

Front 10

3 types of nuclear changes in necrosis

Back 10

Karyolysis

Pyknosis

Karyorrhexis

Front 11

Basophilia of the chromatin may fade or dissolve

*necrosis

Back 11

Karyolysis

Front 12

Nuclear shrinkage and increased basophilia

*necrosis

Back 12

Pyknosis

Front 13

Pyknotic nucleus undergoes fragmentation

Back 13

Karyorrhexis

Front 14

Localized area of coagulative necrosis

Back 14

Infarct

Front 15

Digestion of dead cells resulting in transformation of the tissues into liquid viscous mass

Back 15

Liquefactive necrosis

+ brain, abscess, pleural effusion

Front 16

Coagulative necrosis involving multiple tissue planes usually applied to the limb

Back 16

Gangrenous necrosis

Front 17

Collection of fragmentes or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border

Back 17

Granuloma formation

Front 18

4 disease which cause caseation necrosis

Back 18

Syphilis

Coccidioidomycosis

Cryptococcus

Histoplasmosis

*systemic mycoses

Front 19

Fatty acids combine with calcium to produce grossly visible chalk-white areas

Back 19

Saponification

ex. acute pancreatitis

Front 20

Electrolyte abnormality that occurs in acute pancreatitis due to saponification

Back 20

Hypocalcemia

Front 21

Complexes of antigens and antibodies are deposited in the walls of arteries

Immune complexes + fibrin

Back 21

Fibrinoid necrosis

Front 22

3 characteristics of necrosis vs apoptosis

Back 22

+ cellular swelling

+ nuclear changes (pyknosis etc)

+ disrupted cell membrane

+ enzymatic digestion

+ inflammation

Front 23

Membrane bound organelles that undergo apoptosis after completing their function

("suicide bags of cells")

Back 23

Lysosomes

Front 24

3 examples of physiologic apoptosis

Back 24

Embryogenesis

Involution after hormone withdrawal

Elimination of self-reactive lymphocytes

Front 25

Most characteristic histologic feature of apoptosis

Back 25

Chromatin condensation

Front 26

Found in apoptosis

Composed of cytoplasm and tightly packed organelles w/ or w/o nuclear fragments

Back 26

Apoptotic bodies

Front 27

Anti-apoptotic gene that triggers cell injury

Back 27

Bcl-2

*Bax, Bak - inhibition of these pro-apoptotic gene

Front 28

Markers for cell undergoing apoptosis

Back 28

Caspases

Front 29

Fatty change which indicates accumulation of triglycerides

Back 29

Steatosis

Front 30

Stain using Sudan IV or oil Red-O

Back 30

Steatosis

Front 31

Organ which displays fatty change of uniform/alternating bands of yellow and red (tigered effect)

Back 31

Heart

Front 32

Cholesterol deposits along the tendon

Back 32

Xanthoma

Front 33

Strawberry gallbladder is seen in?

Back 33

Cholesterolosis

Front 34

Histo: seen in multiple myeloma, excess of immunoglobulin

Back 34

Russell bodies

Front 35

Condition where carbon deposition blackens the tissues of the lungs

Back 35

Anthracosis

Front 36

Wear and tear pigment

Back 36

Lipofuschin

Front 37

Clinical condition where lipofuscin accumulates in the colon after prolonged use of senna (anthraquinone)

Back 37

Melanosis coli

Front 38

Triad of hematochromatosis

Back 38

Micronodular cirrhosis

Skin pigmentation

DM

Front 39

Endogenous pigment visualized by using Prussian Blue

Back 39

Hemosoderin

Front 40

Type of calcification found in necrosis

Formation of crystalline calcium phosphate

Back 40

Dystrophic calcification

Front 41

4 conditions with Psammoma bodies

Back 41

Papillary thyroid CA

Serous cystadenoCA, ovaries

Meningioma

Mesothelioma

Prolactinoma

Front 42

Metastatic calcification occurs in tissues due to

Back 42

Hypercalcemia

Front 43

Lung cancer which causes paraneoplastic hypercalcemia

Back 43

Squamous cell

Front 44

Terminally nondividing state

Back 44

Senescence

Front 45

First crucial step in inflammation

Back 45

Recognition

Front 46

Hallmark of acute inflammation

Back 46

Increased vascular permeability

Front 47

Function of platelet-activating factor

Back 47

Vasoconstriction

Pro-inflammatory

Front 48

4 derivatives of arachidonic acid

Back 48

Thromboxane

Prostaglandin

Prostacycline

Leukotriene

Front 49

Substrates which cause fever

Back 49

TNF

IL-1

Front 50

Substrates which cause vasodilation

Back 50

Histamine

NO

Front 51

5 conditions which present with increased ESR

Back 51

Infections

Inflammation

Cancer

Pregnancy

SLE

Front 52

3 conditions with decreased ESR

Back 52

Sickle cell anemia

Polycythemia

CHF

Front 53

Morphologic patterns of acute inflammation

Back 53

Dilation of small blood vessels

Slowing of blood flow

Accumulation of leukocytes

Front 54

Inflammation where outpouring of effusion derived from plasma/secretions of mesothelial cells

Back 54

Serous

Front 55

Most common variant of porphyria

Back 55

Porphyria cutanea tarda

Deficient in uro decarboxylase

Front 56

Inflammation with bread and butter appearance

Back 56

Fibrinous

Front 57

Type of Fibrinous inflammation causing pericarditis post-MI

Back 57

Dressler's syndrome

Front 58

Localized collections of purulent inflammatory tissue

Central region has necrotic WBCs and tissue cells

Back 58

Abscess

Front 59

Local defect or excavation on the surface of an organ

Sloughing off of inflammed necrotic tissue

Back 59

Ulcer

Front 60

Inflammation seen in acute appendicitis

Back 60

Suppurative

Front 61

Inflammation seen in peptic ulcer disease

Back 61

Ulcerative

Front 62

MC complications of PUD?

Back 62

Bleeding*

Perforation

Obstruction

Front 63

Inflammation with bacterial-toxin induced damage of the mucosal lining

Shaggy membrane of necrotic tissue

Back 63

Pseudomembranous

Front 64

Cytokines which promotes production of IFN-gamma

Back 64

IL-12

Front 65

Cytokine for activation of macrophage

Back 65

IFN gamma

Front 66

Cytokine for recruitment of neutrophils and monocytes

Back 66

IL-17

Front 67

3 features of chronic inflammatim

Back 67

Mononuclear cells

Tissue destruction

Angiogenesis and fibrosis

Front 68

DMARD drug which can cause reactivation of latent tuberculosis infection

Back 68

Infliximab

*do PPD

Front 69

4 infectious causes of granulomatous infection

Back 69

TB

Leprosy

Cat-scatch disease (Bartonella)

Syphilis 3

Systemic mycoses

Front 70

3 non-infectious causes of granulomatous infection

Back 70

Sarcoidosis

Chron's disease

Berylliosis

Front 71

Only protein that does not undergo final modification in the RER

Back 71

Collagen

Front 72

Collagen lacking in osteogenesis imperfecta

Back 72

Type 1

Front 73

Collagen needed in late wound repair

Back 73

Type 1

Front 74

Collagen found in the vitreous body and nucleus pulposus

Back 74

Type 2

Front 75

Collagen needed in early wound repair

Back 75

Type 3

Front 76

Collagen deficiency in Ehlers-Danlos

Back 76

Type 3 and 5

Front 77

Collagen deficiency in Alport syndrome

Back 77

Type 4

Front 78

Hallmark of tissue repair

Back 78

Granulation tissue

Front 79

Most important event in wound healing

Back 79

Hemostasis for clot formation

Front 80

Cells which cause wound contraction

Back 80

Myofibroblasts

Front 81

Difference between healing by primary vs secondary intention

Back 81

Wound contraction

> increased granulation tissue, larger fibrin clot, more intense inflammatory reaction

Front 82

Hemodynamic Disorders

Morphology: clearing and separation of ECM and subtle cell swelling

Back 82

Edema

Front 83

Hemodynamic Disorders

Affected tissues turn red due to engorgement of vessels with oxygenated blood

Back 83

Hyperemia

Front 84

2 causes of cyanosis

Back 84

Red cell stasis

Accumulation of deoxygenated hemoglobin

Front 85

Congestion vs hypermia - differences?

Back 85

Passive vs active

Oxygenated vs deoxygenated

Front 86

Hemodynamic DisordersMorphology: engorged alveolar capillaries with alveolar septal edema and focal intra-alveolar hemorrhage

Back 86

Acute pulmonary congestion

Front 87

Hemodynamic DisordersMorphology: septa are thickened and fibrotic, heart failure cells

Back 87

Chronic pulmonary congestion

Front 88

Hemodynamic DisordersMorphology: hemorrhagic centrilobar hepatocytes accentuated against uncongested tan liver

Back 88

Nutmeg liver

Chronic liver congestion

Front 89

Bleeding disorder with fragility of blood vessels, platelets, coagulation cascade

Back 89

Hemorrhagic diathesis

Front 90

3 conditions causing hemorrhage

Back 90

Chronic congestion

Bleeding diasthesis

Rupture of large artery or vein

Front 91

Accumulation of blood within tissues

Back 91

Hematoma

Front 92

Color changes in ecchymoses

Back 92

Hemoglobin

Bilirubin (blue-green) 5-10 days

Hemosiderin (gold-brown) >10 days

Front 93

Normal hemostasis

Created when thrombin cleaves circulating fibrinogen into fibrin creating a fibrin meshwork

Back 93

Secondary hemostatic plug

Front 94

Normal hemostasis

Platelet adherance and activation leads to platelet aggregation

Back 94

Primary hemostatic plug

Front 95

Substrate which amplifies platelet aggregation leading to primary hemostasis

Back 95

Thromboxane

Front 96

Virchow's triad

Back 96

Endothelial injury

Hypercoagulability

Abnormal blood flow

Front 97

Most common primary hypercoaguable state

Back 97

Factor V Leiden mutation

Front 98

4 high risk acquired hypercoaguable states

Back 98

Prolonged immobilization

Myocardial infarction

Atrial fibrillation

Tissue injury

Cancer

Front 99

3 low risk hypercoagulable states

Back 99

Nephrotic

OCP use

Sickle cell anemia

Smoking

Front 100

Treatment for heparin-induced thrombocytpenia

Back 100

Direct thrombin inhibitors

ex. Lepirudin, Argatroban

Front 101

Antibodies lacking in APAS

Back 101

Anticardiolipin

Lupus anticoagulant

Front 102

Laminations with pale platelet and fibrin deposits alternating with darker red cell rich layers

Back 102

Lines of Zahn

Front 103

Lines of Zahn seen in ?

Back 103

Antemortem thrombosis

Front 104

Gelatinous with dark red dependent portion and yellow chicken fat upper portion

Back 104

Post-mortem thrombosis

Front 105

Thrombi occurring in heart chambers or in aortic lumen

Back 105

Mural thrombosis

ex. abnormal myocardial contraction

Front 106

Marantic endocarditis seen in which neoplastic condition?

Back 106

Colorectal CA

*caused by Strep. bovis

Front 107

Condition of sterile verrucous endocarditis in SLE

Back 107

Libman-Sacks endocarditis

Front 108

Consumptive coagulopathy

Sudden or insidious onset of widespread fibrin in the microcirculation

Back 108

DIC

Front 109

Gold standard for the diagnosis of PE

Back 109

Pulmonary angiography

CT scan with IV contrast

Front 110

Emboli that passes through heart defect to reach systemic circulation

Dislodged venous thrombus passes through heart defect and causes CVD

Back 110

Paradoxical embolism

Front 111

Which MI associated with increase risk of arterial thromboembolism?

Back 111

Anterior wall

*80% arise from mural thrombi

Front 112

Embolism associated with open long bone fracture

Back 112

Fat

Front 113

3 clinical presentations of decompression sickness

Back 113

Bends

Chokes

Caisson disease - ischemic necrosis of femoral heads, tibia, humerus

Tx > hyperbaric chamber

Front 114

Infusion of amniotic fluid or fetal tissue into maternal circulation

Back 114

Amniotic fluid embolism

Front 115

Dominant histologic characteristic is ischemic coagulative necrosis

Back 115

Infarction

Front 116

Valvular heart defect usually leading to septic embolism in the lungs

Back 116

Tricuspid valve endocarditis

Front 117

Infarction which occurs in venous occlusion and tissues with dual circulation (liver, lung, intestine)

Back 117

Hemmorhagic/red

Front 118

Infarction which occurs in solid organ with end arterial circulation

Back 118

Pale/white

Front 119

ECG seen in cardiogenic shock

Back 119

Low-voltage complexes

Front 120

Most severe form of meningococcemia

Back 120

Waterhouse-Friderichsen

Front 121

Effect of shock on the kidney

Back 121

Acute tubular necrosis

Front 122

All tissues may revert to normal EXCEPT

Back 122

Neurons

Myocytes