Unit 1 Flashcards

Question

What is the difference between exertional heat stroke and classic heat stroke?

Answer 1

Exertional heat stroke: hot, dry skin, usually (not always) there is cessation of sweating. Usually lactic acidosis. May lead to rhabdomyolysis (breakdown of skeletal muscle fibers), AKI, disseminated intravascular coagulation (DIC), multi organ failure. Classic heat stroke - young, elderly, obese in hot humid weather. Hot, dry skin. No lactic acidosis, but respiratory alkalosis. Hypotension, coma. AKI and DIC are very uncommon.

Answer 2

In alcoholic hepatitis, we see swollen hepatocytes, death of occasional hepatocytes, an infiltrate of PMNs, and a ropy, eosinophilic material within the cytoplasm of some hepatocytes called “alcoholic hyaline” (representing aggregates of cytokeratin filaments).

Answer 3

Oxygen therapy Acute inflammation (PMNs have myeloperoxidases) Reperfusion (Xanthine oxidase, which is produced from proteolysis during hypoxia)

Answer 4

Superoxide dismutase (SOD) gets rid of superoxide (O2-) by converting to hydrogen peroxide Glutathione peroxidase is a very important enzyme – catalyzes: o GSH is a reducing agent in the cell that gets rid of radicals Antioxidants (uric acid, Vitamin E) can eliminate radicals

Answer 5

Chronic reflux esophagitis leads to replacement of the stratified squamous epithelium along the distal esophagus by a columnar type of intestinal epithelium. Stratified squamous --> columnar

Answer 6

Replacement of the pseudostratified columnar epithelium of the bronchus by stratified squamous epithelium Columnar --> stratified squamous

Answer 7

↓ Na pump ↑ influx of Ca and Na ions & water ↑ efflux of K ions leads to cellular swelling

Answer 8

Dead cell remains a ghost-like remnant of its former self – classically seen in an MI Pyknosis Nucleus is intensely dark staining and shrunken --> seen in a necrotic (dead) cell Karyorrhexis Fragmentation of pyknotic nucleus Karyolysis Extensive hydrolysis of the pyknotic nucleus with loss of staining. Represents breakdown of the denatured chromatin.

Answer 9

The dead cell undergoes extensive autolysis, caused by the release of lysosomal hydrolases (proteinases, DNases, RNases, lipases, etc.) Seen classically in the brain and spleen following infarction All of the dead tissue is liquefied

Answer 10

Seen in TB (mycobacterium tuberculosis) Type of necrosis seen within infected tissues characterized as soft, friable, whitish-grey (resembles the milk protein casein)

Answer 11

Leakage of lipases from dead cells attack triglycerides in surrounding fat tissue and generate free fatty acids and calcium soaps. These soaps have a chalky-white appearance Seen in the pancreas following acute inflammation

Answer 12

Ultra-filtrate of plasma Etiology = ↑ hydrostatic pressure/reduced oncotic pressure **More glucose**

Answer 13

Protein-rich content; cells Protein >1.02 g/mL, fibrin Etiology = inflammation Less glucose = if you have a bacterial infection, the bacteria will use up a lot of that glucose, so there’ll be less in the exudate than transudate Leukocytes

Answer 14

ACUTE: PMNs CHRONIC: Macrophages, lymphocytes, plasma cells, eosinophils, BOTH: Mast cells/basophils, platelets

Answer 15

A group of giant cells that have come together

Answer 16

Too much iron in the body = iron overload The organs involved are the liver, heart, pancreas, pituitary, joints, and skin Excess iron is hazardous, because it produces free radical formation

Answer 17

Native macrophages within tissues

Answer 18

Anywhere, but usually in non-confined space PMNS predominate Infectious: bacterial, fungal

Answer 19

Within parenchyma/confined space (brain, lung, liver). PMNs predominate Infectious: bacterial, fungal

Answer 20

Within an anatomic cavity or space: pleural, subdural, etc. Early PMNs, then macrophages & lymphocytes Infectious: bacterial & fungal

Answer 21

Skin (epidermis, dermis, subq) Fascia/deep CT Infectious (bacterial: Staph, Strep) Inflammatory Neutrophils early... mononuclear later on Into fascia: necrotizing fasciitis

Answer 22

Usually within parenchyma (lung, lymph node, liver, spleen) Rounded, nodular appearance. Often mineralized, so visible on CT/X-ray Macrophages, lymphocytes, and plasma cells

Answer 23

Gallstone(s)

Answer 24

Inflammation of the gall bladder

Answer 25

Gallstone(s) in the common bile duct

Answer 26

Collateral damage occurs because of: - Neutrophils that die 1-2 days after migration --> cellular contents released - Macrophages - Inflammatory mediators (reactive O2 species, NO) - Enzymes, proteases, acid hydrolases from immune cells Clinical examples: - Loss of septae in pneumonia – PMNs chewed their way through the CT - Rheumatoid arthritis --> chronic inflammatory cells attack synovial joint space; erode through cartilage

Answer 27

Histamine, serotonin, and lysosomal enzymes

Answer 28

Prostaglandins, leukotrienes, platelet-activating factors, activated O2 species, NO, and cytokines

Answer 29

The liver makes Factor XII (Hageman) factor --> bradykinin, coagulation; activates complement

Answer 30

Mast cells, basophils, platelets

Answer 31

Neutrophils, macrophages

Answer 32

Hydrostatic pressure “pushes” fluid from the capillary into the interstitial space at the arterial end.

Answer 33

Loss of fluid at the arterial end then increases the plasma protein concentration (oncotic pressure), so fluid is “pulled” back into the capillary at the venous end to balance the protein concentration.

Answer 34

Extravasion (leakage) of fluid into tissues

Answer 35

Extravasion of fluid into body cavities (e.g., ascites)

Answer 36

An active ↑ in blood flow due to arteriolar dilation Serves normal physiologic purposes, such as bringing inflammatory mediators into areas of tissue damage Provides oxygen to exercising skeletal muscle Causes red color (erythema) in the tissues due to increased mass of oxygenated RBCs

Answer 37

A pathologic accumulation of blood due to impaired outflow of venous blood Either too much pressure for the fluid to flow, or there’s a physical obstruction Congested tissue has a red-blue color due to accumulation of deoxygenated blood May have ↑ hydrostatic pressure

Answer 38

Capillaries that have broken and blood that has moved out into surrounding tissue --> red spots 1-2 mm in diameter

Answer 39

Bleeding into an enclosed space (within tissue)

Answer 40

Spots from bleeding >3 mm

Answer 41

Bruises --> spots from bleeding 1-2+ cm

Answer 42

(1) Endothelial injury (hypercholesterolemia, inflammation) (2) Hypercoagulability (inherited or acquired) (3) Abnormal blood flow (stasis, turbulence, etc.)

Answer 43

Thrombus: crazy clotting ATTACHED to a vessel wall Embolus: Free-floating, intravascular mass of gas, liquid, or solid Thromboembolus = clot that broke free!

Answer 44

Emboli in the venous/right sided system most commonly lodge in the lungs. Emboli in the arterial/left sided system can affect any organ, but most commonly travel to the legs or brain.

Answer 45

HEMORRHAGIC Venous insufficiency/occlusion Can occur after an arterial occlusion if blood flow is subsequently reestablished and damage vessels allow movement of blood into the necrotic area Dual blood supply YES to reperfusion Loose tissues --> permit movement of blood from adjacent areas into necrotic area Organs: lung, liver, intestine

Answer 46

ANEMIC ``` Arterial insufficiency Single blood supply NO to reperfusion Dense tissue type Organs: heart, kidney, spleen ```

Answer 47

Cardiogenic: Failure of the heart to pump an adequate amount of blood and/or to perfuse tissues adequately Hypovolemic: Not enough blood volume to perfuse all tissues, and so cardiac output decreases because there is low blood volume returning to the heart Both result in: Low blood pressure + low cardiac output --> vasoconstriction, ↑ heart rate, and renal conservation of fluid Patients present with cool skin, pallor, tachycardia, and ↓ urine output

Answer 48

A subtype of shock due to SIRS--> occurs when microbial infections cause high levels of inflammatory mediators in the blood everywhere in the body Leads to widespread arterial vasodilation, vascular leakage, and venous blood pooling --> Results in hypotension and ↓ tissue perfusion Patients present with warm, flushed skin, hypotension, edema, increased HR, and fever

Answer 49

Inhibits DNA synthesis via TS (thymidylate synthase)

Answer 50

Used for hematological malignancies Reversible, competitive inhibitor of DHFR - required for synthesis of purine nucleotides

Answer 51

Cross-link DNA (usually CpG) High nephrotoxicity. Ototoxicity, neurotoxicity. Inactivation via reaction with GSH

Answer 52

Produce inter-strand crosslinks in DNA Inactivated via GSH. Cells with high levels of ALDH are resistant to drug. Gonadal toxicity. Increased risk of later carcinogenesis.

Answer 53

The agents stabilize topoisomerase-DNA interactions, making the cell unable to re-ligate the DNA. Resistant: increased drug efflux, mutations in topoisomerases. Cardiotoxicity (iron chelators may provide protection). Secondary malignancies, especially AML.

Answer 54

Bind to tubulin --> depolymerization --> activates apoptosis Neurotoxicity, myelosuppression, neutropenia.

Answer 55

Treats hormonally-response cancers (breast, endometrial, prostate) Tamoxifen = estrogen receptor inhibitor

Unit 1 Flashcards

(80 cards)