Term
| 3 permanent tissues (can't undergo hyperplasia) |
|
Definition
| skeletal muscle, cardiac muscle, nerves |
|
|
Term
| Does BPH increase risk for prostate cancer? |
|
Definition
| NO. this is the exception to the general rule that pathological hyperplasia (e.g. endometrial) can progress to dysplasia & eventually cancer |
|
|
Term
Atrophy is caused by reduced cell # &/or size via removal of nutrients/hormonal stim/disuse.
What are the mechanisms taht cause decreased # & size? |
|
Definition
decreased # = apoptosis
decreased size = ubiquitin degradation of cytoskeleton proteins & autophagy of cellular components |
|
|
Term
Define & give example for each:
- Metaplasia
- Dysplasia
- Aplasia
- Hypoplasia |
|
Definition
- change of one cell type to another by reprogramming of stem cells (e.g. Barrett's esophagus, Vitamin A def causing keratomalacia, myositis ossificans)
- Disordered cellular growth (e.g. CIN) usually arising from longstanding hyperplasia/metaplasia (e.g. Endometrial hyperplasia, Barrett's esophagus)
- Failure to develop during embryogenesis (e.g. renal agenesis)
- decreased cell production during embryogenesis (e.g. streak ovary) |
|
|
Term
| Does apocrine metaplasia of the breast predispose to developing cancer? |
|
Definition
| NO, this is an exception to the general rule that long-standing metaplasia predisposes to cancer progression |
|
|
Term
| Are metaplasia & dysplasia reversible? |
|
Definition
| Yes. Everything but cancer is reversible |
|
|
Term
| Trauma to muscle causes it to regenerate as bone |
|
Definition
| myositis ossificans (type of metaplasia, non-cancerous) |
|
|
Term
| In regaurd to Hypoxia, which tissue is very susceptible & which one is very resistant: neurons & muscle |
|
Definition
Neurons are very susceptible (most, probably)
Skeletal muscle is very resistant to hypoxia |
|
|
Term
| Slowly developing ischemia (e.g. renal artery atherosclerosis/fibromuscular dysplasia) will result in ischemic injury or atrophy? |
|
Definition
atrophy.
In contrast quickly developing ischemia (e.g. renal artery embolus) results in injury |
|
|
Term
| 2 common causes of budd chiari |
|
Definition
| PCV (most common), lupus anticoagulant |
|
|
Term
| Differentiate hypoxemia from hypoxia |
|
Definition
| Hypoxia is the more general term. Hypoxemia is hypoxia w/ PaO2 < 60 (SaO2<90%), e.g. altitude, hypoventilation, V/Q mismatch, etc |
|
|
Term
| cyanosis w/ chocolate colored blood |
|
Definition
methemoglobinemia (Fe3+), commonly occurs with nitrate/sulfa drugs (e.g. dapsone, TMP)
Infants are particularly susceptible (have decreased number of enzymes that reduce Fe3+), especially when consuming nitrate-contaning H2O |
|
|
Term
| detection of cellular contents in plasma (e.g. troponin in MI; ALT in hepatitis) is an indication of reversible or irreversible cellular injruy? |
|
Definition
irreversible. This shows that there is membrane damage, a feature of irreversible injury (others: mitochondrial swelling, cytC leakage, lysosomal membrane damage)
Cellular swelling is a sign of REVERSIBLE injury (e.g. microvilli effacement, blebs, ER swelling w/ reduced protein synthesis) |
|
|
Term
| Hallmark of cell death is loss of nucleus. Define Pyknosis, Karyorrhexis, & Karyolysis |
|
Definition
Pyknosis: nuclear condensation
Karyorrhexis: fragmentation
Karyolysis: Dissolution |
|
|
Term
Name the thing responsible for liquifaction for each type of liquifactive necrosis:
1) Brain infarct
2) abscess
3) Pancreatitis |
|
Definition
1) microglia release proteolytic enzymes
2) Neutrophils release proteolytic enzymes
3) Pancreatic enzymes (e.g. trypsin) |
|
|
Term
| What are the two things that can cause acute inflammation? |
|
Definition
|
|
Term
| Delineate dry & wet gangrene |
|
Definition
Dry gangrene = coagulative necrosis leading to "mummification" of tissue
Wet gangrene: infection causes more liquifactive necrosis
Gangrene is NOT a distinct histologic pattern of death, it is a clinical distinction (e.g. limbs in a diabetic) |
|
|
Term
| Name the 2 types of necrosis seen in pancreatitis & what is responsible for each? |
|
Definition
coagulative necrosis of pancreatic tissue (proteolytic enzymes, e.g. trypsin)
Fat necrosis of peripancreatic fat (pancreatic lipase, leading to saponification) |
|
|
Term
| Is there elevated calcium in dystrophic calcifications (e.g. psammoma bodies & saponification)? |
|
Definition
| NO. Calcification occurs b.c. there is a nidus of necrotic tissue |
|
|
Term
| Malignant hypertension leads to this type of necrosis |
|
Definition
| fibrinoid necrosis (e.g. placenta in preeclampsia) |
|
|
Term
All these things activate what?:
- FAS
- TNF
- Granzyme
- CytC |
|
Definition
caspases, which subsequently turn on proteases (shrink cell via protein destruction, including cytoskeleton) & nucleases (shrink nuclear size)
NOTE: CD8+ cells release perforins which poke holes in membranes to allow granzyme to leak in and activate caspases
NOTE: DNA damage, cell injury, or loss of hormonal stim decrease bcl2 --> leakage of CytC --> activation of caspases |
|
|
Term
| Negative selection of T-cells in thymus is an example of what type of apoptosis-mediated cell death? |
|
Definition
| FAS-FASL interactions (FAS = CD95, it is on target cell) |
|
|
Term
| Which free radical is most damaging to tissue? |
|
Definition
|
|
Term
| mechanism of tissue damage in hemochromotosis & wilson's disease? |
|
Definition
fenton reaction (free radical, OH*, production via free metal)
In normal people, metal carrier proteins prevent these molecules from causing free radical damage
OH* = hydroxyl free radical |
|
|
Term
O2--> O2* --> H2O2 --> HOCl
name enzyme responsible for each step |
|
Definition
1) NADPH oxydase
2) Superoxide dysmutase
3) Myeloperoxidase |
|
|
Term
O2* --> H2O2 --> H2O + O2
Name each enzyme
H2O2 --> O2* --> H2O
Name enzyme responsible for 2nd step (first one is spontaneous) |
|
Definition
1) superoxide dysmutase (in mitochondria)
2) Catalase (in peroxisomes)
-----------------
1)Glutathione peroxidase (in mitochondria) |
|
|
Term
Is CCl4 directly toxic to hepatocytes?
What is the morphological hallmark of CCl4 damage? What causes it? |
|
Definition
NO; CCl4 must be converted to the free-radical CCl3 via P450
Fatty change. CCl3 damage causes decreased protein synthesis --> no apolipoproteins --> lipids can't be excreted |
|
|
Term
| Person has a coronary thromboses. After recanalization, cardiac enzymes continue to rise (even at a higher rate). What happened? |
|
Definition
| reperfusion injury. O2 delivery to irreversibly damaged tissue results in O2 free radical production |
|
|
Term
Systemic amyloidosis has 2 types:
1) primary
2) secondary
name the amyloid protein in each |
|
Definition
1) AL amyloid (light chain, usually seen in plasma cell dyscrasias)
2) Serum amyloid-associated protein (SAA). Seen in inflammatory disorders, cancers, & familial mediterranean fever |
|
|
Term
What is the most common organ involved in systemic amyloidosis (i.e. AL or SAA)?
Name manifestations for the following organs:
- Heart
- Kidneys
- Tongue
- GI tract
- Liver/spleen |
|
Definition
Kidneys are most commonly involved --> cause nephrotic syndrome
Heart: restrictive cardiomyopathy & arrhythmias
Kidney: nephrotic syndrome
Tongue: Macroglossia
GI: malabsorption (bowel is "thickened")
- Hepatosplenomegaly noted |
|
|
Term
| Where do you biopsy for diagnosis of systemic amyloidosis? |
|
Definition
| abdominal fat pat or rectum |
|
|
Term
Name type of amyloid in each type of LOCALIZED amyloidosis:
1) Senile cardiac
2) Familial amyloid cardiomyopathy
3) Type 2 diabetes
4) Alzheimers
5) Dialysis-associated
6) Medullary carcinoma of thyroid |
|
Definition
1) Transthyretin (second most prevalent serum protein); this is a benign condition seen in 25% population >80
2) mutated transthyretin; causes restrictive cardiomyopathy; 5% of blacks
3) Amylin
4) Amyloid beta (Chr21 --> downs get alzheimers @40)
5) Beta2 microglobulin (on MHCI); deposits in joints; results b.c. dialysis doesn't effectively remove these
6) Calcitonin (C-cells); think MEN2 (ret) |
|
|
