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Pathology block 1 > Adaptation, injury, and approach to disease (notes) > Flashcards

Adaptation, injury, and approach to disease (notes) Flashcards

1
Q

reversible deficiency of blood flow for the metabolic needs of the tissue (4 minutes for brain, 20 minutes for heart, 2 hours for liver).

A

Ischemia

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2
Q

ischemic death of tissue usually due to arterial occlusion by a blood clot that formed at the site (thrombosis) or traveled there (thromboembolism).

A

Infarction

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3
Q

the appearance a dead organ or tissue takes on in a person who remains alive.

A

Necrosis

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4
Q

programmed cell death, a pathway induced by a tightly regulated intracellular program of activating enzymes that degrade the cell’s own parts.

A

Apoptosis

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5
Q

a localized area of liquefactive necrosis, usually due to acute necrotizing infection, usually best treated by draining the infected liquid.

A

Abscess

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6
Q

A single diagnosis that explains all of a patient’s symptoms, signs and other manifestations of disease is most likely the correct diagnosis.

A

Occam’s razor

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7
Q

Disease has a spectrum of effects on a person. Define adaptation

A

set of physiologic and morphologic changes, modulating the function of a person, organ or cell, bringing her or him or it to a new altered steady state of homeostasis, which can usually be sustained indefinitely

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8
Q

What type of disease allows adaptation?

A

mild disease

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9
Q

Describe moderate disease wrt adaptation

A

Moderate disease causes injury because it exceeds the ability to adapt.

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10
Q

Define injury

A

the reversible pathophysiologic and morphologic response to a stress or noxious stimulus exceeding the capacity to adapt, but not enough to kill the cell, organ or person.

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11
Q

What disease causes injury too great for a cell, organ or person to survive?

A

severe disease

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12
Q

Describe the result of slow chronic loss of small amounts of blood from the gastrointestinal tract causes a person’s blood-making organ, the bone marrow, to adapt and make more blood.

A

anemia

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13
Q

Describe the result to blood loss that is simply too much or too rapid,

A

the injury to vital organs is irreversible and incompatible with life.

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14
Q

Describe the spectrum from adaptation through injury to death

A

occurs at the level of tissues (less than a whole organ) and the individual cells that make up tissues and organs.

As a general principle, vital organs have a large reserve capacity

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15
Q

T/F Disease commonly uses up an organ’s reserve capacity silently until it is too late

A

true

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16
Q

The same spectrum of response to disease occurs at the level of individual body organs. Describe it wrt blood loss and the kidney

A
  • If the blood supply to a kidney becomes inadequate, the kidneys adapts by doing less work. It makes less urine.
  • If inadequate blood supply to a kidney becomes chronic, it shrinks; this is the process of atrophy.
  • If the inadequacy of blood supply is too severe, the kidney dies.
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17
Q

Death of an organ is called

A

necrosis

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18
Q

Describe the disease process of atherosclerosis

A
  • atherosclerosis gradually narrows the lumen of critical blood vessels in the heart
  • suddenly something (like severe exertion) demands more blood flow than can be delivered
  • or something (like a blood clot) reduces blood flow below the minimum needed at rest
  • the person dies suddenly.
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18
Q

Disease causes visible manifestations in what? What is the other name for visible manifestations of disease?

A

cells, tissues, organs and people

morphology

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19
Q

What is the appearance of disease without the aid of a microscope?

A

gross morphology

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20
Q

What is a term for a discrete visible manifestation of disease?

A

Lesion

most commonly used for a well circumscribed visible manifestation of a disease

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21
Q

cause of a disease is commonly referred to as what?

A

etiology

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22
Q

What is normal function?

What is abnormal function, rendered abnormal by disease?

A

Physiology

Pathophysiology

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23
Q

Describe pathogenesis

A

the sequence of events in the response of the person, organ or cell to the etiologic agent of a disease, from the initial stimulus to the ultimate manifestation of the disease

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24
Q

Name the classifications of the categories of disease

A
  1. V for Vascular
  2. I for Infectious
  3. T for Toxic
  4. A for Autoimmune
  5. M for Metabolic
  6. I (second one) for Idiopathic (to include degenerative)
  7. N for Neoplastic
  8. D for Developmental (to include genetic)

VITAMIN D

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25
Q

T/F Inflammation is a classification of the categories of disease

A

False, it is present in a lot of diseases but not a specific category

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26
Q

Describe what is included in infectious diseases

A
  • generally recognized as communicable or transmissible
  • includes any disease caused by a virus, a bacterium, a prion, a fungus, protozoon or a parasite
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27
Q

Describe the category of toxic diseases

A
  • a group of diseases due to a poison, toxin, or other noxious substance, commonly manifesting the symptoms of infection
  • includes alcohol, radiation injury, natural toxins and therapeutic drugs
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28
Q

Describe autoimmune diseases

A

those in which the body’s immune system causes illness by attacking its own cells, tissues or organs.

  • includes systematic lupus erythematosus and rheumatoid arthritis
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30
Q

What is an autonomous growth of cells uncontrolled by the normal controls on cell proliferation (a tumor)?

A

neoplasm

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31
Q

What is included in the neoplasm classification of disease?

A

includes benign neoplasms, malignant neoplasms and carcinoma in situ (malignant, but without visible invasion)

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32
Q

What is included in genetic diseases?

A

nclude autosomal dominant disorders such as polycystic kidney disease, recessive disorders such as cystic fibrosis, and cytogenetic disorders involving autosomes like trisomy 21 and sex chromosomes such as Turner syndrome.

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33
Q

Name the systematic study of disease wrt its divisions

A
  1. Definition
  2. Epidemiology
  3. Pathogenesis
  4. Gross Pathology
  5. Microscopic Pathology
  6. Symptoms
  7. Signs
  8. Diagnosis
  9. Treatment
  10. Prognosis
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34
Q

Describe the 1 and 2 steps of knowing a disease

A
  1. first step in knowing a disease is having a precise definition of it
  2. next step is knowing the epidemiology of it. The first step in knowing the epidemiology is knowing how common it is
  3. The next step in knowing the epidemiology of a disease is knowing its distribution in different age groups, genders and races.
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35
Q

T/F All diseases occur with different frequencies on the continuum of age and some are unique to a gender, race or ethnic group

A

true

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36
Q

Describe the differential Dx of a disease

A

Once you have settled on a diagnosis, the differential diagnosis refers to everything else that might be the right diagnosis if you are wrong

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37
Q

What are the medically important electrolytes? Name them in order of importance

A
  1. potassium (K),
  2. sodium (Na),
  3. bicarbonate (HCO3),
  4. chloride (Cl),
  5. calcium (Ca)
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38
Q

What electrolyte is important due to abnormal levels impair the heart’s electrical signaling mechanism for the synchronized contraction essential to pumping blood?

A

potassium

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39
Q

What will a decrease in levels of potassium cause?

A

produce a disturbance in the heart’s signaling rhythm (an arrhythmia, a spelling challenge)

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40
Q

What is the cause to interfere with the contractility of skeletal muscle, causing weakness, myalgias (muscle aches) and fatigue, commonly first symptomatic in the leg muscles?

A

Low potassium

hypokalemia

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41
Q

Hypokalemia also causes what?

A

hypocontractility of smooth muscle, causing loss of the normal peristalsis (squeezing motion) of the intestines

  • resulting mechanical shutdown and dilatation, a condition referred to as ileus or adynamic ileus or paralytic ileus.
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42
Q

Describe a patient with hypokalemia typically presenting with

A

irritability and develops a rapid heart rate (tachycardia)

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43
Q

More severe hypokalemia may cause respiratory muscle weakness manifested as shallow respirations. Muscle weakness progresses to paralysis. What electrolyte has an imbalance?

A

potassium

hypokalemia

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44
Q

What does high potassium or hyperkalemia interfere with? What does it cause?

A

interferes with muscle function and produces similar

Hyperkalemia causes mental malfunction typically manifested by confusion and nerve malfunction manifested by numbness, tingling and loss of deep tendon reflexes

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45
Q

A patient with hyperkalemia typically has what?

A

a slow heart rate (bradycardia), progressive muscle weakness, paralysis and then cardiac arrest.

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46
Q

Which is much more likely to cause a fatal cardiac arrhythmia, hypokalemia or hyperkalemia?

A

hyperkalemia

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47
Q

What electrolyte is crucial in maintaining the tonicity (osmolality) of the body fluids?

A

sodium

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48
Q

What causes water to enter cells in excess, with resultant cellular swelling?

A

Low levels of sodium in blood (hyponatremia)

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49
Q

Where is hyponatremia most dangerous?

A

the brain

The swollen brain cells begin malfunctioning.

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50
Q

What are the results of hyponatremia?

A

This results in confusion, followed by progressive lethargy, obtundation, stupor, coma, seizures and death.

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51
Q

What are the early stages of hyponatremia?

A

In the early stages of hyponatremia, a patient may experience headache, nausea and malaise

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52
Q

What does high sodium or hypernatremia interfere with?

A

brain function, leading to confusion, disorientation, progressive lethargy, obtundation and coma.

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53
Q

What does severe hypernatremia do?

A

depresses the respiratory center in the brain, which supplies the drive to breathe

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54
Q

T/F The lungs do not work w/o stimulus from the brain

A

true

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55
Q

What electrolyte is created in the body by renal metabolism?

A

bicarbonate

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56
Q

What is the most important substance in the blood buffering this acid as it is carried to the kidney for excretion?

A

bicarbonate

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57
Q

A deficiency of bicarbonate results in what?

A

a buildup of acid within the body, acidosis.

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58
Q

What is the most common cause of acidosis? What is the result?

A

renal failure

diminishing the body’s ability to get rid of the acid continuously produced by normal metabolism

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59
Q

Other than a deficiency of bicarbonate, describe another cause of excess acid production wrt to anaerobic metabolism

A

excess acid production due to inadequate oxygen supply to large parts of the body, such as the legs, which makes them resort to anaerobic metabolism, generating lactic acid

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60
Q

Respiratory failure also produces acidosis because of what reason?

A

the carbon dioxide the lungs fail to excrete as a gas combines with water to form carbonic acid (H2CO3)

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61
Q

T/F Unlike hypokalemia and hyponatremia, acidosis does not have a single distinct clinical syndrome

A

true

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62
Q

Respiratory failure leads to what?

Hyperventilation leads to what?

A

acidosis

alkalosis

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63
Q

What are the causes of alkalosis? Which one will also deplete potassium?

A

hyperventilation

vomiting => will deplete potassium

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64
Q

Describe how vomiting causes alkalosis

A

The expulsion of the hydrochloric acid in gastric juice can leave behind an excess of bicarbonate

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65
Q

T/F alkalosis in general and bicarbonate excess in particular do not have distinct clinical syndromes

A

True - Acidosis does not have a single distinct clinical syndrome.

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66
Q

How is bicarb measured?

A
  • estimated on the basis of measurement of a related substance
  • sample of blood is treated with a strong acid, which breaks down the bicarbonate and liberates its components, including the gas carbon dioxide
  • This CO2 is measured and reported as a surrogate for bicarbonate.
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67
Q

What are the other sources of CO2? Which could change the reading of bicarbonate?

A

Other sources include carbonic acid, carbonates and carbamino compounds

carbonic acid is about 5% of this CO2 is normally from carbonic acid and with respiratory failure, this can double.

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68
Q

How would you improve the accuracy of the test for bicarb in the blood?

A
  • reduced any excess carbonic acid (due to respiratory failure) by exposing the blood sample to an atmosphere with 40 mm Hg of CO2, the average normal partial pressure of CO2 dissolved in the blood and then reported it as “CO2 combining power” or “alkaline reserve”.
  • To further improve the surrogacy of the CO2, some medical laboratories have also added oxygen to fully oxygenate the hemoglobin (also a buffer) and run the test at 37 degrees C.
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69
Q

Describe pCO2

A

the partial pressure of dissolved CO2 in the blood determined as part of the “blood gases”.

The pCO2 reflects the exhalation of CO2, respiratory function, whereas the bicarbonate reflects the acid-base balance from metabolism.

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70
Q

There are many causes of injury to a person, an organ or a cell. Perhaps the most common is an inadequacy of blood supply, which is termed what?

A

ischemia

71
Q

If the heart stops pumping blood, the person as a whole experiences ischemia, but not for long because why?

A

total body ischemia soon causes loss of consciousness

72
Q

If the artery bringing blood to an organ or part of an organ (tissue) is blocked, the result is what?

A

localized ischemia

73
Q

If ischemia goes on too long, the result is beyond injury; What is the result?

A

it is the death of the tissue or the organ (termed infarction) or death of the person

74
Q

Internal organs that are ischemic, but not yet infarcted tend to have what common characteristic?

A

congested with excess blood in the veins and swollen with fluid leaked from the blood vessels

75
Q

What is often the earliest gross pathologic change?

A

a darkening of color

76
Q

The intestines are normally tan and become brown or red during what disease state?

A

ischemia

77
Q

Describe an ischemic kidney

A

the medulla (inner portion) becomes congested

  • cortex (outer portion) becomes pale
78
Q

Injured cells release some of their contents into the bloodstream. It is common in muscle but cannot take place in the brain. Why?

A

The blood brain barrier prevents debris from cerebral ischemia from entering the blood. You will need to do a lumbar puncture.

79
Q

Blood testing is often used for diagnosing injury what?

Blood testing cannot be done for what organ? Why?

A

heart, pancreas and liver

kidneys

  • renal cells do not have unique cellular contents like the pancreatic enzymes
  • the kidneys are relatively small organs so that a small injury to a larger organ cannot be differentiated from a large injury to the kidneys
80
Q

How is kidney damage monitored?

A

Renal injury is diagnosed by monitoring the output of its liquid product and the buildup of waste products in the bloodstream from the failure of renal function

(blood urea nitrogen and creatinine)

81
Q

Other than the kidney, what other organ besides the kidney does not have a unique cellular contents? How is the damage diagnosed?

A

lung injury is diagnosed by functional assessment

82
Q

T/F stomach has some unique cellular contents

What occurs when this happens?

A

true

generally pepsin, released into the lumen rather than the bloodstream

83
Q

The diagnosis of gastric injury is done by what?

A

causes bleeding into the lumen, so passing a tube through the nose into the stomach (nasogastric intubation) and aspiration of the gastric luminal contents allows detection of gastric injury by assessing the nasogastric aspirate for blood

84
Q

How can the colon be diagnosed?

A

colon usually causes bleeding into the lumen (or at least diarrhea) so examining the stool for blood can serve as a screening test for colonic injury

85
Q

How do you diagnose the small intestine? Which part is usually damaged? Which can be viewed by endoscopy?

A

jejunum is usually damaged => the difficulty diagnosing injury to the jejunum, it is commonly fatal before it is diagnosed.

duodenum and terminal ileum can be viewed

endoscopy and capsule film,

86
Q

Amylase is an enzyme that digests carbohydrates. What secrets it?

A

pancreas and salivary glands

87
Q

Lipase is an enzyme that digests fats. What organ releases amylase and lipase upon damage?

A

pancreas

88
Q

Describe how alcohol damages the pancreas

A

alcohol causes inflammation of the pancreas because the release of enzymes designed to digest our hamburger begins digesting us instead.

causes necrosis that elicits an inflammatory response, acute pancreatitis

89
Q

Even if no physical or radiological damage is seen in the pancreas, how can it be determined if the pancreas is damaged?

A

elevated amylase and lipase

90
Q

T/F amylase is excreted in the urine.

Why?

A

true

small enough to pass through renal glomerulus but amylase can

renal failure causes an increased serum level of amylase

91
Q

What can be the cause of elevated amylase?

A
  1. salivary gland inflammation
  2. tumors of lung and ovary
  3. ruptured ectopic pregnancy
  4. diabetes meliitus
  5. acute appendicitis
92
Q

Most of the lipase in serum is produced by what? What are secondary secretors of lipase?

Where else is lipase present?

A

pancreas

lingual salivary glands, gastric mucosa, intestinal mucosa, pulmonary mucosa

present in leukocytes and adipose tissue cells

93
Q

Describe acute pancreatitis wrt lipase and amylase

A

serum lipase levels remain elevated longer than amylase levels, commonly for 8 to 14 days.

90% of patients with acute pancreatitis have elevated levels of amylase and lipase, so these tests have a 90% sensitivity for this diagnosis

40% of patients with elevated lipase do not have acute pancreatitis, so this test is only 60% specific for acute pancreatitis

94
Q

Spontaneous non-traumatic gas gangrene is usually associated with underlying diseases. What is especially associated?

A

diabetes mellitus, hematological malignancy and colon cancer

95
Q

Other than the heart, the organ that uses blood testing to diagnose is what?

What will help diagnose this organ?

A

liver

leaked hepatocyte contents in the bloodstream for the diagnosis of hepatic injury

96
Q

The enzymes used to diagnose tissue injury include what?

A
  1. alanine aminotransferase (ALT),
  2. aspartate aminotransferase (AST),
  3. alkaline phosphatase (ALP or “alk phos”),
  4. gamma-glutamyl-transferase (GGT),
  5. lactate dehydrogensase (LDH),
  6. creatine phosphokinase [CPK],
  7. amylase
  8. lipase
97
Q

Which enzymes atalyze the interconversion of amino acids? Describe their specificity to the AA

A

ALT => glutamate and alanine

AST => glutamate and aspartate

98
Q

T/F Most cells need these transaminases to convert amino acids as needed for making different proteins

A

false, ALL cells

but different cell types have different amounts of each

99
Q

T/F Although there is more AST than ALT in hepatocytes, the relative amount of AST is much lower than in other organs

A

true

100
Q

T/F Liver injury is more likely to elevate the ALT out of proportion to the AST than injury to any other organ.

A

true

101
Q

Elevation of the amount of ALT in the blood is more specific for what?

A

liver injury than elevation of AST

102
Q

What is the de Ritis ratio and what is normal ratio? Why is it important?

A

ratio of AST over ALT => ratio of 1.15

sometimes helpful in differentiating among the causes of hepatic injury

103
Q

Acute hepatic injury will result in what to the de Ritis ratio? Chronic hepatic injury?

A

acute=> decrease to less than 1

chronic => ratio greater than 1

104
Q

Many liver diseases cause an elevated level of a key excretory product of the liver. What is this product?

A

bilirubin

105
Q

When elevations of AST and ALT are associated with hyperbilirubinemia due to biliary ductal obstruction outside the liver, the de Ritis ratio is generally?

A

less than 1.5

106
Q

With intrahepatic biliary obstruction, the ratio is generally?

A

greater than 1.5

107
Q

Alcoholic liver disease is associated with a high de Ritis ratio is generally?

A

range of 2-9

108
Q

T/F high de Ritis ratio of AST/ALT is adequate to distinguish alcoholic liver disease from the other causes of hepatic injury

A

false, it is nowhere near

109
Q

What enzyme is located on the outer cell membranes of nearly all our cell types and functions to transport amino acids into cells?

A

Gamma-glutamyltransferase (GGT)

110
Q

Why is GGT present more in hepatocytes than any other organ?

A
  • hepatocytes have the job of taking in amino acids from the blood carried to them from the intestines (the portal circulation) and making new proteins out of these amino acids
111
Q

Acute hepatic injury due to viral infection or acetaminophen (Tylenol) overdose causes an elevation in what?

A

elevation in GGT

much higher elevation in ALT and AST

112
Q

Diseases causing the backup of bile in the liver (cholestasis) have an elevation of what enzymes? What is a disease that is most present in?

A

higher levels of GGT than ALT or AST

extrahepatic biliary obstruction

113
Q

Alcoholic liver disease also causes elevation of what? Why?

A

elevation of GGT out of proportion to ALT and AST

  • alcohol=>potent inducer of GGT synthesis by the hepatocytes
  • too much overlap between the levels seen in alcoholic liver disease and other liver diseases for GGT to reliably distinguish them
114
Q

What is an enzyme made of multiple phosphatases that transfer inorganic phosphate from donor to receptor molecules at an alkaline pH?

A

Alkaline phosphatase (ALP)

115
Q

In normal adults, most of the ALP in serum is from what?

A

liver or bone

116
Q

Cholestatic liver diseases cause elevated in what?

A

elevated ALP out of proportion to ALT and AST

117
Q

T/F Alcoholic liver disease causes less elevation of ALP than GGT

A

true

118
Q

T/F Malignant tumors in the liver cause more elevation of ALP than GGT

A

true

119
Q

What else will show an increase in ALP?

A

Paget’s disease of bone

normal puberty

normal pregnancy

malignant tumors produce ALP of placental type that gets into the blood to elevate ALP levels

120
Q

What enzyme catalyzes the conversion of lactate to pyruvate by removing two hydrogens?

A

lactate dehydrogenase (LDH)

121
Q

What disease states generally force cells to generate lactic acid?

A

all sorts of cells generate lactate especially when ischemia or hypoxia forces them to resort to anaerobic energy metabolism

122
Q

The buildup of lactate is thought to mediate what?

A

the muscle pain caused by exercise

123
Q

What causes an increase in LDH?

A
  • skeletal muscle
  • myocardial infarction
  • pulmonary infarction and some pneumonia
  • Malignant tumors (higher in metastasizing)
  • Hepatitis
  • hemolysis (breakdown of RBCs)
    *
124
Q

To diagnose hemolysis, what can LDH be combined with?

A
  1. LDH combined with tests for haptoglobin (hemoglobin transport protein)
  2. bilirubin (Hg breakdown product)
  3. plasma free hemoglobin
125
Q

What is ischemic necrosis of an organ or tissue?

A

infarction

126
Q

What is the appearance a dead organ or tissue takes on in a person who remains alive?

A

necrosis

127
Q

T/F When a person dies, all of the organs and tissues take on a morphology is similar to necrosis

A

false, it is different from necrosis and referred to as autolysis

128
Q

What is the difference between necrosis and autolysis?

A

necrosis elicits an acute inflammatory response under most circumstances, while autolysis does not

129
Q

What s characterized by a gradual fading of the components of every cell, all at the same rate?

A

autolysis

130
Q

What are infarcts usually due to?

A

due to occlusion of an artery by a blood clot that formed at the site of occlusion (thrombosis) or traveled there (thromboembolism)

  • 99% caused by a clot occluding an artery
131
Q

Why does an occlusion in a vein rarely cause an infart?

What are the exceptions?

A

Occlusion of a vein rarely causes infarction because the body has alternative (collateral) pathways for venous outflow from most organs.

  • The testes and ovaries are exceptions.
132
Q

How can the testis and ovary cause an infarction?

A

Torsion (twisting) of either a testis or an ovary on its pedicle collapses and occludes the thin-walled veins and this creates impedance to arterial inflow

results in infarction if unrelieved

133
Q

What four factors have an influence on whether reversible ischemia becomes irreversible infarction?

A
  1. vulnerability of the tissue,
  2. rate of development,
  3. alternative blood supply
  4. blood oxygenation
134
Q

What is the most vulnerable organ to ischemia?

A

brain

135
Q

Why would a physician prescribe exercise that could cause claudication?

A

This ischemia is not life-threatening and it causes the growth of collateral arteries, which alleviates the disease.

136
Q

What are the red hemorrhagic infarcts mechanisms? (3)

A
  1. venous occlusion,
  2. dual or anastomosing blood supply
  3. reperfusion
137
Q

When an ovary twists on its meso-ovarian pedicle (torsion) cutting off the venous outflow, but not the arterial inflow, the result is what?

A

a red hemorrhagic infarct associated with the sudden onset of extreme abdominal pain

138
Q

The brain is unique in the way its infarcts evolve. If a cerebral artery is occluded, leading to ischemic necrosis, how does cerebral infarction develop? Why?

A

ends to develop liquefactive necrosis, that is, the solid tissue turns to liquid and drains away

  • a barrier between the inside of the cerebral blood vessels and the cerebral parenchyma, the blood-brain barrier
  • Behind the blood-brain barrier, the brain has glial cells that perform the roles of white blood cells.
139
Q

What cells can transform into debris-eating macrophages within a cerebral infarction and the cells that make collagen and convert infarcts in other organs into scars tend to be excluded by the blood-brain barrier?

A

microglial cells

140
Q

What enzyme is released during a myocardial infarction?

A

Creatine phosphokinase (CPK) or creatine kinase (CK)

141
Q

What is an enzyme that catalyzes the transfer of phosphate from creatine phosphate to ADP, creating ATP?

A

CPK

142
Q

What enzyme is generated in muscle and brain? What is it composed of? Describe the difference

A

CK generated in muscle and brain

composed of M and B dimers

The MB fraction is released into blood with myocardial necrosis (CK-MB) and released after about 3 hours

143
Q

When is AST released into blood with myocardial necrosis?

A

starting after 24 hours and peaking 48 hours then normalizing after 4 days

144
Q

What enzyme is released into the bloodstream with myocardial necrosis after about 24 hours then peaking at 72 hours and normalizing around 7 days?

A

LDH

145
Q

What are proteins that regulate calcium-mediated contraction of cardiac and skeletal muscle?

A

troponins

146
Q

Cardiac-specific troponins are released with myocardial necrosis, starting after and peaking when?

Which enzyme is it the same as during a myocardial infarction?

A

after about 3 hours

peaking around 24 hours

Same as CK-MB

147
Q

The sensitivity of the troponin level for the diagnosis of acute myocardial infarction improves to something more like 90% if it is assayed when?

A

10 hours after the onset of chest pain

148
Q

Why is it recommended to repeat troponin determination at least once, 3-6 hours after the initial level?

A

to rule in or rule out the diagnosis of acute myocardial infarction

149
Q

For the diagnosis of acute myocardial infarction, an elevated troponin needs to be combined with at least one of the following?

A
  1. symptoms of ischemia
  2. electrocardiographic evidence of ischemia
  3. imaging evidence of ischemia
  4. identification of an intracoronary thrombus by angiography or autopsy
150
Q

What is a distinctive form of ischemic necrosis with blackening and shrinkage, typically of distal extremity, but also sometimes of gallbladder or other internal organs?

A

gangrene

151
Q

What is the treatment of gangrene?

A

surgery, amputation of the necrotic portion of an extremity or excision of the gangrenous internal organ

152
Q

What is a distinctive form of necrosis grossly resembling cheese, associated with tuberculosis, histoplasmosis and similar diseases?

A

caseous necrosis

153
Q

T/F Caseating necrosis is not a form of ischemic necrosis

A

true

154
Q

What usually causes caseating necrosis?

A

fungal infections or infections caused by bacteria resembling fungi (mycobacteria, principal among them Mycobacterium tuberculosis)

155
Q

What is tissue death with conversion of solid tissue to liquid due to severe acute necrotizing infection, toxicity or (in brain only) ischemia?

A

Liquefactive necrosis

156
Q

What is a localized area of liquefative necrosis. Necrotizing infections are the most common cause of abscesses?

A

abscess

157
Q

Why aren’t antibiotics brought into abscesses by blood vessels?

A

the blood vessels are destroyed within an abscess

158
Q

What are the most common cause of abscesses?

A

Necrotizing infections

159
Q

What is the usual treatment for an abscess? Why?

A

Because an abscess is liquid, however, it can be drained away with an aspirating needle and syringe

160
Q

What is the form of tissue death when fat digested by pancreatic lipase, releases fatty acids, which bind calcium, creating chalky white soap-like material (saponification)?

A

fat necrosis

161
Q

The type of necrosis determines treatment. What is the Tx for gangrene? caseous necrosis? abscesses?

A

gangrene => surgery

caseous necrosis => antifungal, antituberculous

abscess => drainage

162
Q

What is the condensation, shrinkage and hyperbasophilia of a dead cell nucleus? When is this seen?

A

Pyknosis

seen in apoptosis and sometimes necrosis

163
Q

What is the fragmentation of pyknotic dead nucleus?

A

karyorrhexis

164
Q

What is the fading away of a dead nucleus?

A

karyolysis

165
Q

What is a term for the microscopic pathology of the most common form of necrosis because it makes the dead cell look like a tiny condensed fibrin blood clot?

A

coagulative necrosis

166
Q

T/F Cells that had died of ischemia do not show it immediately

When do they show it?

A

true

Coagulative necrosis of cardiac myocytes=> 4-12 hrs

ischemic necrosis of neurons => 12-24 hrs

167
Q

Describe apoptosis

A
  • a pathway of cell death induced by a tightly regulated intracellular program of activating enzymes
  • degrade the cell’s own DNA and proteins

programmed cell death

168
Q

T/F Apoptosis can be either physiologic or pathologic

A

true

169
Q

Describe physiologic apoptosis

A
  • occurs in embryogenesis, involution, ending inflammation, and deleting self-reactive lymphocytes
170
Q

Describe the pathologic apoptosis

A

occurs in injury due to hypoxia, heat, radiation or chemotherapy, in certain viral diseases, in duct obstruction, transplant rejection and in tumors

171
Q

Both intrinsic and extrinsic pathways in pathogenesis of apoptosis activate what?

A

caspases

172
Q

T/F apoptosis is the death of a single cell or clusters of cells. They are retained in an intact cell membrane

A

true

173
Q

What prevents cells undergoing apoptosis to create an inflammatory response?

A

Apoptosis causes the cell to be targeted for phagocytosis

single mac comes and eats the shrunken apoptotic cell

There is no acute inflammatory (neutrophilic) response

174
Q

What is the standard blood test for acute myocardial infarction?

A

troponin blood test

Pathology block 1 (24 decks)

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