Cell Injury Flashcards
1
Q
What is necrosis?
A
Death of cells, tissue, or organs
2
Q
What is ischemia?
A
Reversible injury due to inadequate blood supply (REVERSIBLE!)
3
Q
What is infarction?
A
Irreversible necrosis
4
Q
Definitions of etiology & morphology?
A
etiology = cause Morphology = visible manifestation
5
Q
What does reserve capacity have to do with adaption?
A
Most vital organs hace a large reserve capacity to survive (don’t need it all to live, but do to maximize survival).
6
Q
What is the danger of reserve capacity?
A
Common disease uses up reserve capacity silently until it is too late to fix.
7
Q
Artherosclerosis
A
Narrowing of the lumen of blood vessels.
8
Q
Pulmonary Emphysema
A
irreversible enlargement of airspaces due to destruction of the alveolar walls.
9
Q
Dyspnea
A
SOB
10
Q
Injury is defined as
A
reversible pathophysiologic and morphologic response to stress and noxious stimulus (exceeding capacity of cell/tissue/organ to adapt, but not enough to be lethal)
11
Q
Reactive Oxygen Species (ROS) examples
A
superoxide, OH, radicals, and ONOO-
12
Q
Amylase function
A
digests CHO
13
Q
What secretes amylase?
A
pancreas (to duodenum) & salivary glands (to saliva)
14
Q
Lipase is supposed to be release by what into what?
A
Pancreas secretes into duodenum
15
Q
Lipase is not normally found in the
A
retroperitoneal peri-pancreatic fat
16
Q
Pancreatitis causes
A
lipase to leak out into the retroperitoneal peri-pancreatic fat
Amylase & lipase to leak into blood stream
17
Q
Creatine phosphokinase (CPK) AKA
A
Creatine kinase
18
Q
Creatine Kinase concentrated in which organs?
A
Muscle: MM
Brain: BB
Heart: MB
19
Q
Myocardial infarction releases what into blood stream?
A
Troponin
MB Creatine Kinase
20
Q
What is the gold standard serum test for myocardial infarction?
A
Troponin
21
Q
What do troponins do?
A
regulate calcium mediated contraction of all muscle.
22
Q
Alanine Aminotransferase (ALT) formula
A
glutamate + pyruvate ⇌ α-ketoglutarate + alanine
23
Q
Which is more specific for liver injury? ALT or AST?
A
ALT (even though there is much more AST in the liver and other organs)
24
Q
Aspartate Aminotransferase (AST) formula
A
Aspartate (Asp) + α-ketoglutarate ↔ oxaloacetate + glutamate (Glu)
25
AST located where?
Liver, muscle, and other organs (general)
26
Alkaline Phosphate (alk phos) is released by liver when?
BIliary obstruction or hepatic space occupying lesion (general for abnormality).
27
Gamma-glutamyl-transferase (GGT) does what?
outer cell membrane enzyme that transports amino acids into cells
28
When is GGT released?
Toxic liver injuries
29
Lactate dehydrogenase converts what to what?
Lactate to pyruvate (removes 2 hydrogens)
30
When is LDH released?
Injury to RBC, liver, muscle, and other organs
31
What is coagulative necrosis?
morphologic, irreversible injury to a cell caused by ischemia (except brain!)
32
What is the maximum period of time the brain, heart, and liver can experience ischemia without major damage?
Brain: 3 minutes
Heart: 20 minutes
Liver: 2 hours
33
Ischemia not relieved in time leads to
infarction and irreversible necrosis
34
Coagulative necrosis features
eosinophilic cytoplasm (pink)
Nucleus is pyknosis, karyorrhexis, karyolysis
acute inflammatory response
35
Pyknosis
condensation, shrinkage, and hyperbasophilia of dead cell nucleus.
Apoptosis or necrosis
36
Karyorrhexis
fragmentation of dead nucleus
37
karyolysis
fading away of dead nucleus
38
Liquefactive necrosis
conversion of solid tissue to liquid
39
Causes of liquefactive necrosis
severe infection, toxicity, or ischemia in brain (exception)
40
What is an abscess?
localized liquefactive necrosis
41
Caseous Necrosis is what type of necrosis and looks like this?
Coagulative necrosis
| Cheese
42
Gangrene is progressed?
Ischemia --> necrosis (specifically coagulative)
43
Fat Necrosis results from
Pancreatic lipase melting fat which reacts with calcium to form chalky white saponifications (soap)
44
What are features of apoptosis? (4)
1: cell shrinkage
2: hypereosinophilia
3: chromatin condensation and karyorrhexis
4: phagocytosis by macrophages
45
Apoptosis has which feature about it?
Halo
46
2 differences between Apoptosis and Necrosis?
Necrosis has an inflammatory response.
| Apoptosis keeps its cell membrane intact.
47
What are the 5 electrolytes involved with adaptation?
Potassium, Sodium, Bicarb, Cl, Calcium
48
Why is Potassium the most important?
Abnormal levels impair the heart's electrical signaling for synchronized contraction.
49
Hypokalemia signs and symptoms
Muscle contraction interference (weakness and myalgias: muscle aches) in leg first.
Digestion shutdown (low peristalsis)
Tachycardia (irritable) and SOB
50
Hyperkalemia signs and symptoms
Confusion and nerve malfunction (tingling and loss of reflex)
Bradycardia
Muscle weakness and myalgias
51
Which is more likely to cause fatal cardiac arrhythmia? Hypo- or hyper- kalemia?
Hypokalemia
52
Sodium's role in the body?
Maintain tonicity of the bodily fluids (osmolality)
53
Hyponatremia of blood and fluids causes the cell to do what?
S&S?
Water enters the cell (because Na content outside the cell is less)
If brain swells due to hyponatremia, leading to HA, confusion, malaise, coma, seizure, and death
54
Severe Hypernatremia causes?
Depression of respiratory center in brain
55
Bicarbonate influences?
Body pH blood buffer
CO2 + H2O H2CO3 HCO3- + H
56
If low bicarb, what results?
Acidosis: too much acid or too little buffer.
Renal failure limits acid elimination or lactic acid build up.
57
Respiratory failure would cause?
Acidosis in form of carbonic acid.
58
What 2 things cause alkalosis?
Hyperventilation (opposite as resp failure)
| Vomiting (leaves too much bicard around)
59
Which enzyme passes the kidney tubules and is excreted?
Amylase.
If renal failure, increased serum amylase levels
60
90% of acute pancreatitis cases have elevated lipase and amylase. What is the sensitivity for these combined tests?
90%
61
Sense and Specif example:
40% of patients with elevated lipase do not have acute pancreatitis. What is the specificity of elevated lipase for acute pancreatitis?
60%
62
What is the di Ritis ratio? Normal
AST over ALT
| 1.15 (15% higher)
63
Acute hepatic injury leads to which di Ritis ratio? Chronic?
Acute: under 1
Chronic: over 1
64
Bilirubin is
breakdown of heme excreted in urine and bile. Biliary function can be influenced by obstruction.
65
Hyperbilirubinemia and a di Ritis of less than 1.5 indicates
biliary ductal obstruction outside the liver
66
Hyperbilirubinemia and a di Ritis of over 1.5 indicates
biliary ductal obstruction inside the liver
67
Alcohol causes which di Ritis ratio?
2-9 (but can be other diseases)
68
Gamm-glutamyltransferase (GGT) has the function of? Which organ has the most GGT?
GGT transports amino acids into the cell. All cells have GGT, the liver has the most.
69
Serum GGT will increase when
Acute viral hepatitis
Tylenol overdose
Alcohol
Extrahepatic biliary obstruction
70
When are GGT levels higher than AST/ALT? (2)
Cholestasis (back up of bile) extrahepatic biliary obstruction
Alcoholic liver disease
71
Alkaline Phosphatase serum is from primarily the
bone and liver
72
Increased Alk Phos is primarily indicative of
Biliary Obstruction (especially extra- b/c hepatocytes produce more Alk Phos)
73
Malignant tumors in the liver cause production of more Alk Phos or GGT?
ALP
74
What is a primary cause of lactic buildup?
Ischemia and hypoxia (anaerobic metabolism)
75
LDH builds up in
everything basically
76
What is the difference between autolysis and necrosis?
Autolysis is the gradual fading of cells (die of old age)
Necrosis recruits acute inflammatory response while autolysis doesn't.
77
What are the 4 factors that determine ischemia is reversible or not?
1: Vulnerability of tissue
2: Rate of development
3: alternative blood supply
4: blood oxygenation
78
Cerebral infarctions are which kind of necrosis?
Liquefactive
79
During an M.I., what is elevated?
CPK MB, Troponin, AST, LDH
80
Compare and contrast CPK MB and Troponin serum levels associated with M.I.?
Both start around 3 hours and peak at 24 hrs. But Troponin normalizes at 10 days while CPK MB levels out at 3 days.
81
Treatment for Gangrene?
Cut it off.
82
Treatment for Caseous Necrosis?
Looks like cheese, but caused by fungi and bacteria. Antifungals and anti-TB drugs
83
Treatment for Liquefactive Necrosis?
Abscess: drain it.
84
What is hypertrophy? Where's it occur?
Increase in the size of cells.
| Typically found in places in low capacity to proliferate (uterus-hormone, heart, muscle-mechanical)
85
What is hyperplasia?
Increase in the amount of cells.
| Prostate. Liver. Boobs.
86
What is atrophy?
Decrease in size. Move it or lose it.
87
Describe a kidney undergoing atrophy?
Ischemic. Decreases function. (denervation, decreased endocrine, aging, lower perfusion)
88
What is metaplasia?
Cells change type.
89
Is metaplasia reversible?
Always.
90
Is metaplasia ever physiologic?
Never. Always pathological
91
What is the progression of metaplasia?
Metaplasia becomes dysplasia which becomes neoplastic.
92
What is Barrots esophagus?
Metaplasia from columnar to squamous.
93
Smoking changes the epithelium in the respiratory tract from what to what?
Pseudo columnar to squamous
94
HPV changes the uterus epithelium. What to what?
Columnar to squamous.
95
Where does metaplasia start?
At the basement membrane.
96
Is dysplasia pre-neoplastic?
Basically always.
97
There are three brown pigments. Go.
Iron compounds
Lipfuschin
Melanin.
98
What are the iron compounds that stain brown?
Ferritin
| Hemosidderin.
99
Prussian blue stain is to detect which pigment?
Iron.
100
What is the wear and tear figment?
Lipofuchsin.
101
Melanin is used to do what?
Absorb uv rays and acts as a free radical reservoir.
102
What are the black pigments?
Typically are carbon.
103
How are we exposed to black pigment and what happens if it spreads?
Pulmonary is the main way to get carbon.
| "anthracosis" is the term for spreading to lung nodes and distant tissue. It's ok if nothing reacts with it.
104
Calcification is typically dystrophic or metaplastic?
Dystrophic
105
Dystrophic calcification. Describe
Localized and related to some tissue injury
106
What types of lipids can accumulate?
Triglycerides
| Cholesterol.
107
What is steatosis?
Deposits of fat (liver perhaps)
108
Kwashiorkor malnutrition is what kind of diet? Why steatosis?
High carb, low protein diet
| Can't export the fats from the liver.
