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Pathology Quiz 1 > Quiz 1_Learning Objectives Part 1_Spencer > Flashcards

Quiz 1_Learning Objectives Part 1_Spencer Flashcards

1
Q
  1. Distinguish reversible from irreversible cell injury.
A

Example: Steatosis arises from exposure of hepatocytes to EtOH. The EtOH is metabolized to acetate, and also stimulates triglyceride synthesis and inhibits fatty acid oxidation. VLDL secretion is also inhibited. Thus, hepatocytes build up fat stores. If you then abstain from EtOH, the steaotosis will reverse and the hepatocyte will be normal.

Mallory’s hyaline arises from exposure of hepatocytes to EtOH which then causes aggregation of cytokeratin filaments. Histologically this appears as a dense rope like body in the cytoplasm of hepatocytes.

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2
Q
  1. Identify the cytological changes that are associated with irreversible injury.
A

Decrease basophilia, nuclear changes, cytoskeleton alterations.

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3
Q
  1. Explain how steatosis occurs due to alcohol ingestion.
A

EtOH is converted to acetaldehyde which is converted to acetate. The increased NADH/NAD ratio favors TAG synthesis and inhibits FAO. The ethanol also inhibits release of VLDLs, so TAGs build up inside hepatocytes even more. Decrease lipoprotein synthesis so you can’t export it.

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4
Q
  1. Name and distinguish 4 types of pathological necrosis.
A

Coagulative is the most common and involves denaturation of cell proteins. Hallmarks: look for “ghosts”, loss of basophilia. Liquefactive involves extensive acute inflammation and is secondary to bacterial or fungal infections. Caseous is a combination of those two types and has a “cheese” appearance both grossly and histologically (partly from cavitation). Example is TB. Gangrenous is when bacteria colonize an already-necrotic tissue.

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5
Q
  1. Explain the relationship between hemochromatosis and cirrhosis.
A

Hemochromatosis (disease) is iron overload from a genetic abnormality. The iron overload causes cirrhosis (reversible). Hemosidderosis = observable symptoms.

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6
Q
  1. Diagram the mechanisms active in cellular apoptosis.
A

Intrinsic: cell injury occurs and this triggers the Bcl-2 family sensors. The Bcl-2 effectors induce cytochrome c and other pro-apoptotic proteins to initiate caspases. Executioner caspases then cause DNA fragmentation and exocytose apoptotic bodies for ingestion by phagocytes.
Extrinsic: receptor-ligand interactions occur (Fas, TNF receptor) and activate adapter proteins. These activate the same initiator/executioner caspase pathway described above.

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7
Q
  1. Name four features of cellular injury that are reversible.
A

Metabolic/oxidative phosphorylation activity, cellular pH, influx of Ca/etc, phospholipid metabolism

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8
Q
  1. Describe the electrolyte shifts that occur in ischemic cell injury leading to cell death.
A

There is an influx of Ca2+, H2O, Na+, and an efflux of K+. These shifts are mainly modulated through the decreased ATP available intracellularly.

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9
Q
  1. Explain the role of Ca++ ions in irreversible cell injury.
A

The increased Ca++ in the cytosol causes increased ATPase activity, decreased phospholipids, disruption of membrane proteins (via increased protease activity), and increased endonuclease activity.

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10
Q
  1. Name seven categories of causes of cell injury. One example is toxic chemicals.
A

Anoxia, immune/autoimmune, microbiologic, nutritional, physical agents (eg trauma, fever), toxic chemicals

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11
Q
  1. Explain the difference between etiology and mechanism in cell injury.
A

Etiology is cause, mechanism is pathogenesis.

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12
Q
  1. Explain the mechanism of cellular ATP deficit caused by anoxia, carbon monoxide poisoning, and cyanide poisoning.
A

Anoxia is just less oxygen reaching tissues. CO poisoning is due to competitive inhibition for O2 binding on Hb. CN blocks oxidative phosphorylation in mitochondria

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13
Q
  1. State the molecular mechanism for CCl4 toxicity, and explain why gut lining cells escape toxic effects of CCl4.
A

CCl4 → CCl3 + Cl. CCl3 is a free radical and it causes cell injury. Gut lining escapes because CCl4 is activated in cytochromes in the liver.

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14
Q
  1. State the critical feature of molecular structure of a free radical.
A

Free electron.

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15
Q
  1. List an example of a poison that is made toxic by metabolic alteration.
A

CCl4, benzoapyrene

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16
Q
  1. List an example of a poison that does not require metabolic activation in order to become toxic.
A

Strong acids and bases, heavy metals, CO

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17
Q
  1. Use the example of cis-platinum (a chemotherapeutic agent) in describing the various mechanisms of molecular damage/alterations that lead to cell death.
A

Cis-platinum causes DNA synthesis to shut down, cell division to stop, apoptosis, necrosis. Essentially the Pt forms a covalent bond with certain structures such as DNA.

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18
Q
  1. List a differential diagnosis for abdominal pain in a young male/female adult.
A
  1. List a differential diagnosis for abdominal pain in a young male/female adult.
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19
Q
  1. Discuss the physiological mechanism and some causes of vomiting.
A

Vomiting is caused by 1) irritation of vagal/sympathetic afferents in pharynx, heart, peritoneum, mesentery, bile ducts, stomach, bowels via the medullar reticular center, or 2) from gastric irritation, distension, intracranial pressure, metabolic disturbances, drugs, pharyngeal stimulation, emotional upset.

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20
Q
  1. Explain what information and implications derive from the following laboratory tests if 
they are abnormal:
A

bilirubin – defective bilirubin metabolism
prothrombin – monitor extrinsic pathway, monitor Coumadin therapy. Screens for liver disease, K deficiency, factor deficiency, DIC
ALT – liver disease, confirms AST is from liver
AST – acute liver injury
amylase – watch for pancreatitis/abdominal issues

21
Q
  1. Demonstrate how to use a modified Rumack-Matthew normogram for acetaminophen
A

Y axis = acetaminophen concentration, X axis = hours after ingestion. Measure below line = no toxicity, above line = probably toxicity.

22
Q
  1. Explain how acetaminophen is rendered toxic to hepatocytes.
A

Overdose → NAPQI is formed → outstrips glutathione supply → NAPQI binds to proteins and causes cell death.

23
Q
  1. State 4 mechanisms by which n-acetylcystine (NAC) prevents acetaminophen toxicity.
A
  1. Limits formation of NAPQI by helping supply glutathione (by providing cysteine which is then converted)
  2. Increases detox capacity of hepatocytes to deal with NAPQI
24
Q
  1. Name the cause of and treatment for hepatic encephalopathy.
A

Hepatic encephalopathy is confusion, altered consciousness, and coma resulting from liver failure. It is caused by accumulation of toxic substances that are normally dealt with by the liver. Treat with laxative lactulose to prevent toxic metabolic processes in the intestine.

25
Q
  1. Explain the mechanism for disseminated intravascular coagulation.
A

The liver either used up a lot of the clotting factors or stopped making them. Either way, the patient becomes more prone to bleeding and has a longer PT and PTT since systemically he lacks sufficient clotting factors. If the liver was also hoarding clotting factors, then this could have induced formation of anticlotting agents (ie fibrinolytic system, incl plasmin, tissue plasminogen activator (t-PA).

26
Q
  1. Define in histological terms:
    a. hypertrophy:
    b. atrophy:
    c. hyperplasia:
    d. metaplasia:
    e. dysplasia:
A
  1. Define in histological terms:
    a. hypertrophy: cells getting larger
    b. atrophy: opposite of hypertrophy/hyperplasia
    c. hyperplasia: cells multiplying/proliferating
    d. metaplasia: changing type of cell
    e. dysplasia: disordered growth
27
Q
  1. Describe the changes that occur in Barrett’s esophagus.
A

Acid reflux causes the epithelial lining in the esophagus to become more like the stomach/intestine too soon, so stratified squamous to columnar with goblet cells. Process goes metaplasia -> dysplasia -> neoplasia

28
Q
  1. Describe the changes occurring in “dysplasia” as a process.
A

Less differentiated higher in the epithelium; eg columnar to squamous

29
Q

physiological hyperplasia:
physiological hypertrophy:
physiological atrophy:

A

physiological hyperplasia: breasts (lactation change), prostate (BNP), normal growth
physiological hypertrophy: muscles, LVH in distance runner, endometrium
physiological atrophy: aging,

30
Q
  1. Explain the mechanism underlying the four causes of edema and give an example of each.
A

a. Increased hydrostatic eg heart failure
b. Decreased oncotic pressure eg starvation
c. Increase permeability eg burns
d. Lymphatic obstruction eg neoplasia

31
Q
  1. Distinguish a transudate from an exudate.
A

Transudate = low protein content; exudate = high protein content (ex for excellent protein)

32
Q
  1. Define hyperemia and hemorrhage.
A

Hyperemia is too much blood in a vessel; hemorrhage is leaking into outside.

33
Q
  1. Name six local and two systemic causes for hemorrhage
A

Local: trauma, infectious, degenerative, neoplasia
Systemic: hemorrhagic diathesis (coagulation or vascular defects)

34
Q
  1. Name the three factors determining the clinical significance of a hemorrhage.
A

Volume, rate, site

35
Q
  1. Distinguish: petechiae, hematoma, ecchymosis
A

Petechiae = small, hematoma = contained in tissue, ecchymosis = larger bruising on skin etc

36
Q
  1. Define “anemia” and give its two major causes.
A

Anemia is the reduction in volume or number of RBCs per unit volume. It is caused by either decreased production or increased loss of RBCs.

37
Q
  1. Distinguish ischemia from infarction.
A

Ischemia occurs when insufficient amount of blood is delivered to a tissue. Infarct is the actual tissue necrosis that results from insufficient oxygen.

38
Q
  1. Describe the morphology of an infarct of the heart.
A

In a myocardial infarct, you see necrosis, neutrophil infiltration, macrophages, fibroblasts and capillaries, and collagen formation.

39
Q
  1. Distinguish a thrombus from a clot.
A

Thrombus is the coagulation of blood inside a vessel or heart chamber, and a clot is coagula that form outside of blood vessels, for example in a test tube or tissue, or coagula that form in blood vessels when flow has ceased.

40
Q
  1. Define the process of thrombosis
A

Virchow’s Triad: vessel wall injury, blood coaguability, stasis

41
Q
  1. Understand the difference between thrombosis and hemostasis
A

Hemostasis is normal clotting/anticoagulant activity. Thrombosis is pathogenic, and is the inappropriate clot formation on uninjured endothelium.

42
Q
  1. Review the causes of thrombosis forming Virchow’s triad
A

The causes of thrombosis are endothelial injury, hypercoaguability, and abnormal blood flow. Of these, endothelial injury is the most important factor in thrombosis. Endothelial injury can be caused by loss of endothelial cells from hypertension, inflammation, anatomic alterations, trauma/surgery, or endothelial dysfunction. Abnormal blood flow can be caused by bedrest, dilation, venous thrombosis, and tends to bring platelets closer to the endothelial wall. Hypercoaguability can be caused by genetic factors or can be secondary to some acquired factor such as cardiac failure, OCP use, smoking, etc..

43
Q
  1. Discuss the most encountered cases of thrombosis

Venous thrombosis,

A
  1. Discuss the most encountered cases of thrombosis

Venous thrombosis,

44
Q
  1. Define the outcomes of thrombosis
A

Lysis (resolution), organization in connective tissue, propagation towards heart, embolization in lungs

45
Q 
45.	Define the process of embolism and its clinical outcomes
Pulmonary thromboembolism: 
Systemic embolism: 
Fat embolism: 
Air embolism: 
Amniotic fluid embolism
A

Pulmonary thromboembolism: most common. part of a dislodged thrombus that gets stuck in the lungs.
Systemic embolism: typically originate from heart (mural thrombi or fibrillating aria). Most lodge in lower extremities, but some lodge in brian.
Fat embolism: fat leaves fatty bone marrow tissue or fat tissue trauma or burns
Air embolism: decompression sickness, OB procedures, chest trauma,
Amniotic fluid embolism: fetal masses/amniotic fluid → mom → embolism

46
Q
  1. Discuss the types of embolism encountered in the clinic (thromboembolism, cholesterol embolism, decompression sickness, fat embolism, amniotic embolism, foreign bodies) their causes and their clinical outcomes
A
  1. Discuss the types of embolism encountered in the clinic (thromboembolism, cholesterol embolism, decompression sickness, fat embolism, amniotic embolism, foreign bodies) their causes and their clinical outcomes
47
Q
  1. Define shock as a cardiovascular disorder
A

Decreased systemic perfusion of tissues

48
Q
  1. Discuss the three progressive phases of shock pathogenesis
A 
Hypotension → impaired tissue perfusion → cellular hypoxia
Three phases:
1.	nonprogressive or compensated
2.	progressive but still reversible
3.	irreversible
49
Q 
49.	Name the types of shock encountered in the clinic and discuss the causes
Cardiogenic: 
Hypovolemic: 
Septic: 
Anaphylactic:
Neurogenic:
A
  1. Name the types of shock encountered in the clinic and discuss the causes
    Cardiogenic: MI, myocarditis, cardiac tamponade, pulmonary embolus
    Hypovolemic: Hemorrhage, diarrhea, dehydration, burns
    Septic: Severe infection
    Anaphylactic: type I hypersensitivity
    Neurogenic: brain damage & spinal cord injury

Pathology Quiz 1 (6 decks)

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