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KN-Pathology Block 1 > Adaptation, Injury, Death and Systematic Approach to Disease - Prestudy > Flashcards

Adaptation, Injury, Death and Systematic Approach to Disease - Prestudy Flashcards

1
Q

What is ischemia?

A

REVERSIBLE injury due to inadequate blood supply

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2
Q

What is infarction?

A

IRREVERSIBLE necrosis due to ischemia not relieved in time

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3
Q

How should liquefactive necrosis be treated?

A

drainage

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4
Q

How should caseous necrosis be treated?

A

anti-fungal and anti-TB treatments

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5
Q

How should gangrenous necrosis be treated?

A

amputation

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6
Q

What things is pathologic apoptosis important in?

A

certain cancers, chemotherapy, radiation, and transplant rejection

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7
Q

Define etiology

A

doctorspeak for “cause”

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8
Q

define morphology

A

pathologistspeak for “visible manifestation”

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9
Q

Define “gross”

A

pathologistspeak for “visible without a microscope”

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10
Q

What is the difference between adaptation and injury?

A

Adaptation - body responds and develops a new homeostasis in which it can survive

Injury - reversible pathophysiologic and morphologic response to stress that exceeds the capacity of a cell/tissue to adapt, but is not lethal.

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11
Q

Define hypereosinophilia

A

excess of eosinophils, a type of granular containing white blood cells.

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12
Q

What happens to cellular ATP and ROS levels during mitochondrial damage? What would Ca do? What else occurs?

A

ATP drops and ROS (reactive oxygen species) increases. Ca2+ enters the cell cell in excess.

Protein misfolding and membrane degradation

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13
Q

During ischemia, mitochondrial activity decreases, resulting in low ATP levels. How does this affect Na+, Ca2+, and H20 levels?

A

Na+ pump doesn’t have energy to run so Na can not be pumped out and it builds up inside the cell. Similarly, K+ is no longer being forced into cell so K+ effluxs out.
Ca2+ will begin to influx into the cell.

Net ion concentration increases and cell begins to swell with H20.

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14
Q

What change would you expect in pH in an ischemic cell?

A

pH will drop and become more acidic because of anaerobic glycolysis, which produces lactic acid.

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15
Q

What are the effects of increased cytosolic Ca2+?

A

activation of proteases, phospholipases, and endonucleases cause membrane and nuclear damage.

ATPase activation (as well as the influx of Ca2+ from the cytosol to the mitochondria) will decrease ATP production, causing further damage.

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16
Q

How can reperfusion (the restoration of blood to ischemic cells) cause further injury?

A

The newly restored blood brings oxygen, which is necessary, but can be converted to ROS which can cause further damage.

New blood can also increase Ca2+ levels, causing further inappropriate enzyme activation and mitochondrial permeability.

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17
Q

The presence of amylase in blood is indicative of what?

A

necrosis of pancreatic, duedenal, or salivary gland cells

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18
Q

The presesnce of lipase in retroperitoneal fat is indicative of what?

A

pancreatitis (pancreas necrosis)

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19
Q

What compound would you expect to find in the blood after myocardial injury?

A

CPK MB fractions (creatine phosphokinase M and B dimers)

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20
Q

What are troponins? When would you find them in the blood stream?

A

proteins that regulate Ca-mediated contraction of cardiac and skeletal muscle.

Can be released into blood after myocardial injury

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21
Q

What is ALT? What does it do? When would its blood concentration increase significantly?

A

ALT is alanine aminotransferase, a transaminase that converts Glu to Ala.
Release into blood after liver injury.

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22
Q

What is AST? What does it do? When would its blood concentration increase significantly?

A

AST is aspartate aminotransferase, which converts Glu and Asp.

It is released after muscle, liver and other organ injury.

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23
Q

What would be released more after liver injury: ALT or AST?

A

ALT

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24
Q

What is ALP? What does it do? What pathologies would cause it to be released into blood?

A

ALP is alkaline phosphatase, which transfer P04 from donors to receptors at basic pHs.

It is released into blood by liver, bone, especially biliary obstruction or hepatic space-occupying disease. Cholestasis

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25
Q

What is GGT? What does it do? What pathologies would cause it to be released into blood?

A

GGT is gammaglutamyl-transferase, an outer cell membrane enzyme that transports AA’s into cells.

Released by liver injury (especially toxic injuries)

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26
Q

What is LDH? What does it do? What pathologies would cause it to be released into blood?

A

LDH is lactate dehydrogenase, which converts lactate to pyruvate by removing two hydrogens.

Released by injury to blood cells, liver, muscle, or other organs.

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27
Q

Define coagulative necrosis.

A

Morphological manifestation of irreversible injury to cell, tissue or organ due to ischemia (except in brain)

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28
Q

Which organ is most vulnerable to ischemia? What timeframe before infarction?

A

The brain. Infarction after 3 min.

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29
Q

Approximately how long can the heart withstand ischemia?

A

20 min

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30
Q

Approximately how long can the liver withstand ischemia?

A

2 hours

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31
Q

What features would you expect to find in tissue that has undergone coagulative necrosis?

A

preservation of the ghost cell outline.
increase in pink eosinophilia in cytoplasm.
pyknosis of nucleus (increased blue basophilia and shrinkage).
Nucleus Karyorrhexis (fragmentation)
Nucleus Karyolysis (fading away)
Acute inflammatory response

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32
Q

Which is more likely to be damaged by ischemia: renal tubules or glomeruli? Why?

A

The renal tubules are much more susceptible to ischemic injury and necrosis because the glomeruli recieve blood first, then it passes to the renal tubules.

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33
Q

Ischemia is not relieved in brain. What type of necrosis will likely occur?

A

liquefactive necrosis

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34
Q

Ischemia in tissue outside the brain is not relieved; what type of necrosis will likely occur?

A

coagulative necrosis

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35
Q

Severe infection damages tissue; what type of necrosis is likely?

A

liquefactive necrosis or caseous necrosis

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36
Q

What is an abscess?

A

localized area of liquefactive necrosis

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37
Q

A micronecrosis is eosinophilic and lacks ghost cell outlines. What type of necrosis is it?

A

Caseous. Lack of ghost cell outlines.

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38
Q

Describe gangrene

A

a type of coagulative necrosis where the tissue turns black and shrinks

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39
Q

What is fat necrosis?

A

adipose tissue digested by pancreatic lipase or from trauma causing chalky white deposits of Ca and FA soaps.

40
Q

What is the common mechanistic point in extrinsic and intrinsic apoptosis?

A

Initiator capsases, which lead to executioner capsases

41
Q

What things can initiate the mitochondrial (intrinsic) death pathway?

A

growth factor withdrawal, DNA damage, protein misfolding

42
Q

What is the extrinsic apoptosis pathway?

A

Death receptor pathway involving Fas and TNF receptor, which then activate adaptor proteins and activate initiator capasases and the rest of the breakdown pathway.

43
Q

Describe the steps of the intrinsic apoptosis pathway.

A

Cell injury is detected by Bcl-2 family sensors which activate Bcl-2 family effectors (Bax and Bak). These alter the mitochondria and cause activation of cytochrome C and and other pro-apoptotic proteins which leads to activation of initiator capasases and the rest of the degradation process.

44
Q

Describe the common apoptosis pathway.

A

The first common step is initiator capsases, which activate executioner capsases, which cause breakdown of cytoskeleton and activation of endonucleases to breakdown nucleus. The cell shrinks and becomes an apoptotic body, which is then digested by phagocytes.

Cellular membrane remains intact to prevent cellular leakage into surroundings.

45
Q

How does a cell adapt to high misfolded protein levels?

A

decreases protein synthesis and increases chaperone synthesis

46
Q

What are the features of a cell undergoing apoptosis?

A 
cell shrinkage
cytoplasmic hypereosinophilia
chromatin condensation (pyknosis)
karyorrhexis (nuclear fragmentation)
phagocytosis by macrophages
47
Q

What happens to the cell membrane in necrosis? What happens to it in apoptosis?

A

Necrosis - membrane ruptured and contents leak.

Apoptosis - membrane remains intact and no inflammatory response.

48
Q

Define lesion.

A

discrete visible manifestation of disease (wounds, injury sites, etc)

49
Q

Define pathogenesis.

A

Sequence of events in response to etiological event to the ultimate manifestation of disease

50
Q

What are the categories of disease?

A

VITAMIN D:
Vascular, Infectious, Toxic, Autoimmune, Metabolic, Idiopathic (includes degenerative), Neoplastic, Developmental (includes genetic)

51
Q

What is a neoplastic disease?

A

autonomous growth of cells uncontrolled by the normal controls on cell proliforations (tumors)

52
Q

What is the differential diagnosis?

A

list of all the other diseases that can mimic the suspected disease by producing similar manifestations.

53
Q

What is Occam’s razor?

A

A single diagnosis that explains all of the patients symptoms is most likely the correct diagnosis (as opposed to the unlikely, simultaneous presence of 2 or 3 other diseases)

54
Q

What are the presentations of hypokalemia?

A

hypocontractility of skeletal muscle, myalgias (muscle aches), ileus (loss of peristalsis due to smooth muscle inability), and irritability.
Extreme cases can lead to shallow breathing and cardiac arrest.

55
Q

What are the presentations of hyperkalemia?

A

Mental malfunction, confusion, numbness, tingling, loss of deep tendon reflexes, slow heart rate (bradycardia), progressive muscle weakness. Extreme cases can cause cardiac arrest.

56
Q

Which is more likely to cause cardiac arrest: hypokalemia or hyperkalemia?

A

hyperkalemia

57
Q

What is hyponatremia? What are its presentations?

A

Low levels of sodium (Na) in blood, which causes water to swell into cells. This is especially dangerous in the brain and causes confusion, progressive lethargy, obtundation (loss of normal mental capacity), stupor, coma, seizures, and death.

Early presentations: headache, nausea, malaise (nonspecific symptom of simply feeling ill)

58
Q

What is hypernatremia? What are its presentations?

A

High Na, which interferes with brain function, causing confusion, disorientation, prgressive lethargy, obtundations and coma. Severe hypernatremia depresses the respiratory center in the brain, which will kill the stimulus to breathe and the patient.

59
Q

Which ion is crucial in maintaining tonicity (osmality) of the body fluids?

A

Sodium. Normal osmality is 300 mOsm/L and Na accounts for around 140 mOsm/L of that.

60
Q

How is bicarbonate created?

A

renal metabolism

61
Q

What happens if there is a deficit of bicarbonate? What can cause it?

A

acidosis (high acid levels). Can be caused by a variety of things such as inadequate oxygen to large parts of body, respiratory failure, and vomiting.

62
Q

What would hyperventilation cause?

A

alkilosis

63
Q

If a part of the bowels looks ‘dusky’ it is most likely what?

A

ischemic

64
Q

Usually tissues become darker when the are ischemic, but one organ does the opposite. What is it?

A

The kidney. When ischemic, the inner portion (medulla) becomes congested, but the cortex (outer portion) becomes pale.

65
Q

How can a blood test help test for pancreatitis? What would you look for?

A

pancreatic injury because of the leakage of pancreatic enzymes.

Amylase also, but not very specific so not quite as good.

66
Q

Why is blood testing not very useful for detecting kidney or stomach injury?

A

Renal cells do not have any unique cellular contents to differentiate between injury to them and injury to other organs. The unique stomach contents, like pepsin, would leak into the lumen rather than the blood stream.

67
Q

How would you detect injury to the kidneys?

A

measure output and urine content

68
Q

How would you detect injury to stomach?

A

nasogastric intubation, aspiration of gastric contents or gastroscopy.

69
Q

How would you detect injury to the colon?

A

Presence of blood in stool or colonoscopy.

70
Q

Why is jejunum injury important?

A

it is very difficult to diagnose and by the time it’s noticeable, it is already life-threatening.

71
Q

What else can cause hyperamylasemia?

A

high amylase serum levels are usually a result of pancreatitis, but can also be from renal failure, salivary gland inflammation, lung and ovary tumors, ruptured ectopic pregnancy, diabetes mellitus, acute appendicitis.
(NOT PAROTID GLAND INJURY)

72
Q

How would you test for liver damage?

A

blood test looking for elevated ALT, AST, ALP, GGT, LDH. The proportions of ALT to AST are very important. This can tell you which organ is likely damaged. In liver injury, ALT will elevate out of proportion to the AST of injuries from other organs.

73
Q

What is de Ritis ratio?

A

ratio of AST:ALT

74
Q

Which has a higher concentration in liver tissue: AST or ALT?

A

AST

75
Q

What would you expect the de Ritis ratio to be in a patient with acute hepatic injury? What would it be in a healthy individual?

A

Below one. (normal value is 1.15, meaning 15% more AST than ALT)

76
Q

What would you expect the de Ritis ratio to be in a patient with chronic hepatic disease?

A

greater than 1

77
Q

A patient has a de Ritis ratio near 9. What is a possible cause of this?

A

Liver damage from alcoholism (can not rule out other causes though)

78
Q

A patient presents with elevated GGT levels out of proportion to ALT and AST. What is a likely cause?

A

Cholestasis (backup of bile in liver) or alcoholic liver damage

79
Q

A patient has a de Ritis ratio of 1.2 and hyperbilirubinemia. Assuming they have a billiary obstruction, is it likely intrahepatic or outside the liver?

A

Hyperbilirubinemia and de Ritis below 1.5 suggests biliary ductal obstruction outside the liver. Intrahepatic usually has de Ritis ratios greater than 1.5.

80
Q

What are sources of elevated LDH?

A

skeletal muscle injuries, malignant tumors, myocardial or pulmonary infarction, and hemolysis. Because it is present in so many things, elevated serum levels are really only useful if combined with other tests to confirm a diagnosis.

81
Q

What degradation process occurs after death?

A

autolysis. The gradual fading of components of every cell all at the same rate. This is not the same as necrosis, which causes inflammation

82
Q

Why do occlusions of veins rarely cause infarctions?

A

The body usually has collateral pathways for drainage, except in the testes and ovaries which only have one pathway and occlusion will cause infarction

83
Q

What causes 99% of infarctions?

A

thrombosis

84
Q

What factors influence the progression of ischemia to infarction?

A

vulnerability of the tissue
rate of development
alternative blood supplies
blood oxygenation

85
Q

What is claudication?

A

pain of leg ischemia caused by walking or exercise. Used to treat let ischemia

86
Q

What type of infarct would you expect in a solid organ with end-arterial circulation?

A

white anemic infarcts

87
Q

What are the common causes of red hemmorrhagic infarcts?

A
  1. venous occlusion
  2. dual or anastomosing blood supply
  3. reperfusion
88
Q

Why is necrosis in the brain liquefactive instead of coagulative?

A

Behind the blood-brain barrier there are many glial cells that perform the role of white blood cells and break down debris. Also, cells that make collagen and scar tissue in other infarcts are not present beyond the blood-brain barrier

89
Q

What enzyzmes would be present in the blood after myocardial infarction?

A

CPK MB fractions, AST, LDH

there will also be troponins, but these are not enzymes

90
Q

Why would a patient who exhibits the symptoms of myocardial infarction not have elevated CPK levels an hour after the heart attack?

A

It takes 3 hours for CPK levels to start rising after myocardial infarction.
On the opposite end, after 48 hrs, CPK returns to normal so you have to test within this window.

91
Q

What would you look for in a blood sample of a patient who had a myocardial infarction 3 days ago?

A

AST. Elevates after 24 hrs, peaks at 48 hrs and normalizes after 4 days.
ALSO
LDH. starts after 24 hrs, peaks at 72 hrs and normalizes after 7 days.

92
Q

What is pyknosis?

A

The condensation, shrinkage and hyperbasophilia of a dead cell nucleus seen in apoptosis and sometimes necrosis.

93
Q

What is karyorrhexis? Karyolysis?

A

Karyorrhexis - fragmentation of dead nucleus

Karyolysis - fading away of dead nucleus

94
Q

If a patient with acute pancreatits and elevated ALT, what does he likely have?

A

95% specificity and 50% sensitivity for gall stones.

95
Q

A patient has a broken bone, what enzyme would you expect to be elevated in blood?

A

ALP

96
Q

What 3 things would you look for in a blood sample when testing for liver damage?

A

ALT, AST, GGT

97
Q

What is acute mesenteric ischemia

A

mesenteric arteries are cut off so gut, kidney, liver and pancreas become ischemic

KN-Pathology Block 1 (11 decks)

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