Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathoma > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

hypertrophy

A

increase cell size

gene activation, protein synth, organelle production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hyperplasia

A

increase cell #

stimulate stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

permanent tissues

A

cardiac muscle, skeletal muscle, nerve, blood

only undergo hypertrophy (cardiac myocytes hypertrophy in response to HTN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pathologic hyperplasia

A

progress to dysplasia and eventually cancer

*except benign prostate hyperplasia (BPH) - pathologic but not cancerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

atrophy

A

decrease stress - decrease cell size and #;
decrease # via apoptosis;
decrease size via ubiquitin-proteosome degradation and autophagy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ubiquitin

A

tags intermediate filaments of cytoskeleton for degradation by proteosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

autophagy

A

autophagic vacuoles combine with lysosomes, enzymes break down cell components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

metaplasia

A

change in stress leads to change in cell type better able to handle new stress;
usually of the surface epithelium;
reprogramming of stem cells;
reversible if stress removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Barrett esophagus

A

change from squamous to columnar epithelium to handle acid reflux (metaplasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

persistent metaplasia

A

progress to dysplasia and cancer

*except apocrine metaplasia of breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Vitamin A deficiency

A

leads to metaplasia;

Vit. A needed for cell differentiation of specialized epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

keratomalacia

A

Vit. A deficiency (metaplasia);
change from goblet/columnar cells of conjunctiva to keratinized squamous cells;
causes dry eyes, cornea destruction, blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

myositis ossificans

A

metaplasia of connective tissue (muscle changes to bone following trauma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

dysplasia

A

disordered cell growth;
usually after prolonged hyperplasia or metaplasia;
reversible with removal of stress;
progress to carcinoma (irreversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

cervical intraepithelial neoplasia (CIN)

A

dysplasia and precursor to cervical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

aplasia

A

failed cell production during embryogenesis;

unilateral renal agenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hypoplasia

A

decreased cell production during embryogenesis;

streak ovary in Turner syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cell injury

A

stress exceeds cell’s ability to adapt;

depends on type of stress, severity, and type of affected cell;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

common causes of cell injury

A 
inflammation;
nutritional deficiency or excess;
hypoxia;
trauma;
gene mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hypoxia

A

low oxygen delivery to tissue;
oxygen is final electron acceptor in oxidative phosphorylation;
leads to decreased ATP;
lack of ATP causes cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

causes of hypoxia

A

ischemia;
hypoxemia;
decreased carrying capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ischemia

A

decreased blood flow through organ;
decreased arterial perfusion (atherosclerosis);
decreased venous drainage ( Budd-Chiari syndrome)
shock (generalized hypotension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hypoxemia

A

low partial pressure of oxygen in blood (PaO2 < 60mmHg, SaO2 < 90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

causes of hypoxemia

A

high altitude - decreased PAO2;
hypoventilation - increased PACO2, decreased PAO2 (COPD);
diffusion defect - thicker diffusion barrier prevents O2 to pass into blood (interstitial pulmonary fibrosis);
V/Q mismatch - blood bypasses oxygenated lungs (right-to-left shunt: cyanotic) or ventilation problem (atelectasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

decreased O2 carrying capacity

A

hemoglobin loss or dysfunction

26
Q

causes of decreased O2 carrying capacity

A

anemia - PaO2, SaO2 normal
CO poisoning - PaO2 normal, SaO2 decreased
methemoglobinemia - PaO2 normal, SaO2 decreased

27
Q

CO poisoning

A

causes decreased O2 carrying capacity;
classic finding is cherry-red skin;
early sign is headache

28
Q

methemoglobinemia

A

causes decreased O2 carrying capacity;
iron oxidized to Fe3+, unable to bind O2;
oxidant stress (sulfa and nitrate drugs) or in newborns;
cyanosis with chocolate colored blood;
tx with IV methylene blue (reduces Fe3+ to Fe2+)

29
Q

low ATP effects on cell

A

disrupt sodium/potassium pump - sodium and water build up in cell;
disrupt calcium pump - calcium buildup in cytosol;
switch to anaerobic glycolysis - lactic acid buildup, low pH denatures proteins/precipitates DNA

30
Q

reversible cell injury

A

cellular swelling - causes loss of microvilli, membrane blebbing;
RER swelling - ribosome dissociation, decreased protein synth

31
Q

irreversible cell injury

A

membrane damage:
plasma membrane - enzymes leak into serum (cardiac troponins), calcium buildup in cell;
mitochondrial membrane - loss of ETC (inner membrane), cytochrome c leak activates apoptosis;
lysosome membrane - hydrolytic enzymes activated by high calcium

32
Q

cell death

A

loss of nucleus via condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis);
necrosis and apoptosis

33
Q

necrosis

A

large groups of cell death followed by acute inflammation;

pathological process, never physiologic

34
Q

coagulative necrosis

A

necrotic tissues remain firm, shape and structure preserved;
ischemic infarction in all organs except brain;
often wedge-shaped and pale;
red infarction if blood reenters tissue

35
Q

liquefactive necrosis

A

enzymatic lysis of cells and proteins causes liquefaction;
brain infarction - proteolytic enzymes of microglial cells
abcess - proteolytic enzymes of neutrophils
pancreatitis - proteolytic enzymes of pancreas

36
Q

gangrenous necrosis

A

coagulative necrosis resembles mummified tissues;
ischemia of lower limb or GI tract;
superimposed infection leads to liquefactive necrosis (wet gangrene)

37
Q

caseous necrosis

A

soft and friable necrosis (cheese-like);
combination of coagulative and liquefactive necrosis;
granulomatous inflammation of tuberculosis or fungal infections

38
Q

fat necrosis

A

adipose tissue with chalky white appearance due to calcium deposits;
giant cells, fat, and calcium histologically;
trauma to fat (breast) and pancreatitis to peripancreatic fat;
fat + calcium = saponification

39
Q

dystrophic calcification

A

calcium deposits on dead tissue;

normal serum calcium and phosphate levels

40
Q

metastatic calcification

A

calcium deposits in normal tissue;
high serum calcium and phosphate levels;
not always from cancer

41
Q

fibrinoid necrosis

A

necrosis of blood vessel walls;
proteins (fibrin) leak causing pink histological staining;
malignant hypertension and vasculitis

42
Q

apoptosis

A

ATP dependent cell death of single cells;
not followed by inflammation;
mediated by caspaces - activate proteases (cytoskeleton) and endonucleases (DNA)

43
Q

caspace activation pathways

A

intrinsic mitochondrial - inactivation of Bcl2 (mitoch. membrane stabilizer) causes cytochrome c leakage;
extrinsic receptor-ligand - FAS ligand binding FAS (CD95) or TNF binding TNF receptor;
CD8+ T cell mediated - perforins from CD8+ T cells create pores, allowing granzymes to enter cells

44
Q

physiologic free radicals

A

oxidative phosphorylation - cytochrome c oxidase transfers electrons to oxygen, yields superoxide, hydrogen peroxide, and hydroxyl radical

45
Q

pathologic free radicals

A

ionizing radiation - water to hydroxyl radical (most damaging);
inflammation - NADPH oxidase makes superoxide from killing neutrophils;
metals (copper, iron) - Fe2+ makes hydroxyl (Fenton rxn);
drugs/chemicals - P450 system in liver metabolizes drugs, making free radicals

46
Q

how do free radicals cause damage?

A

peroxidation of lipids;

oxidation of DNA and proteins

47
Q

free radical elimination

A

antioxidants;
metal carrier proteins (transferrin);
enzymes:
superoxide dismutase (mitochondria) - superoxide to peroxide
glutathione peroxidase (mitochondria) - free radicals to water
catalase (peroxisomes) - peroxide to O2 and water

48
Q

carbon tetrachloride (CCl4)

A

P450 (liver) converts to CCl3;
RER swelling, ribosome dissociation, decreased protein synth;
decreased apolipoproteins - fatty change in liver

49
Q

reperfusion injury

A

blood return to ischemic tissues causes O2 derived free radicals leading to more damage;
rise in cardiac enzymes (troponin) after reperfusion of infarcted myocardial tissue

50
Q

amyloidosis

A

misfolded protein deposits either systemically or locally;
many proteins can deposit as amyloid;
beta-pleated sheet configuration, congo red staining, green birefringence under polarized light

51
Q

systemic amyloidosis

A

either primary or secondary;
almost any tissue can be involved;
kidney most commonly involved (nephrotic syndrome);
restrictive cardiomyopathy or arrhythmia;
tongue enlargement, malabsorption, hepatosplenomegaly;
biopsy required to diagnose;
organ transplant, amyloid cannot be removed

52
Q

primary amyloidosis

A

systemic deposits of AL amyloid, derived from immunoglobin light chain

53
Q

secondary amyloidosis

A

systemic deposits of AA amyloid, derived from serum amyloid-associated protien (SAA);
acute reactant that increases in chronic inflammatory states, malignancy, and Familial Mediterranean fever (FMF);
FMF - dysfuntion of neutrophils, episodes of fever and acute serosal inflammation (mimics appendicitis, arthritis, or MI)

54
Q

localized amyloidosis

A

localized to single organ

55
Q

senile cardiac amyloidosis

A

non-mutated serum transthyretin in heart;

usually asymptomatic

56
Q

familial amyloid cardiomyopathy

A

mutated serum transthyretin in heart cause restrictive cardiomyopathy

57
Q

amyloidosis with type II DM

A

amylin from insulin deposits on islets of pancreas

58
Q

amyloidosis with Alzheimer disease

A

A-beta amyloid in brain causes amyloid plaques;

gene on chromosome 21 - most trisomy 21 have early onset Alzheimer disease

59
Q

amyloidosis with dialysis

A

beta2-microglobulin deposits in joints

60
Q

amyloidosis with medullary thyroid carcinoma

A

calcitonin deposits in tumor - tumor cells in amyloid background

Pathoma (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions