Cell injury Flashcards

0
Q

SaO2

A

Percent heme groups occupied by O2

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

PO2

A

Driving force for diffusion of O2 into tissue

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

Cyanosis

A

Decr O2 saturation (SaO2)

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

Oxygen

A

Electron acceptor in oxidative pathway

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

Hypoxia

A

Inadequate O2 leads to ATP depletion

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

Ischaemia

A

Decreased arterial (or venous) blood flow

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

Respiratory acidosis

A

Retention of CO2 always decreases PaO2

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

Ventilation defect

A

Impaired delivery of O2 to alveoli; intrapulmonary shunting of blood (e.g. RDS)

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

Perfusion defect

A

Absent blood flow to alveoli; incr alveolar dead space (e.g. PE)

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

Diffusion defect

A

O2 canot cross alveolar-capillary interface; interstitial lung disease (e.g. sarcoidosis)

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

Methemoglobin

A

decr SaO2; heme iron +3; oxidising agents (sulfur/nitro drugs)

Rx with IV methylene blue

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

Clinical findings of methemoglobinaemia

A

Cyanosis not corrected by O2, chocolate coloured blood

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

Carbon monoxide

A

Decr SaO2, left shift O2 binding curve

inhibits cytochrome oxidase

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

Causes of carbon monoxide poisoning

A

Car exhaust, space heaters, smoke inhalation

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

Signs + symptoms of CO poisoning

A

Headache, cherry red skin colour

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

Cyanide action

A

Inhibits cytochrome oxidase, systemic asphyxiant

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

CO + cyanide poisoning occurs in:

A

house fires

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

Left shifted O2 dissociation curve causes

A
Decr 2,3 BPG
CO
Alkalosis
HbF
Methemoglobin
Hypothermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Right shift O2 dissociation curve

A

Incr 2,3 BPG
high altitude
acidosis
fever

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

Mitochondrial poisons

A

Damages membrane and drains off protons

alcohol, salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Uncoupling agents in mitochondria

A

Drain off protons
Dinitrophenol
Thermogenin (brown fat)

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

Decreased ATP

A

Impaired Na+/K+ ATPase pump (cellular swelling); reversible

SIDE note: Digitalis acts on this pump to INCR activity for incr INOTROPY

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

Anaerobic glycolysis

A

ATP synthesis in hypoxia
lactate decr intracellular pH
Denatures proteins and enzymes

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

Irreversible injury hypoxia

  • what structures are damaged?
  • How?
A

Membrane or mitochondrial damage

Incr cytosolic Ca2+ activates phospholipase, proteases, endonuclease

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

Free radicals - what are they and what do they do?

Name 3x examples + antidotes

A

Unpaired electron in outer orbit
Damages cell membranes and DNA
- examples: superoxide –> superoxide dismutase
hydroxyl + drug FR –> neutrolised by glutathione (Paracetamol/acetominophen toxicity)
peroxide –> neutrolised by catalase

25
Q

Lipofuscin

A

Indigestible lipid of lipid peroxidation

Brown pigment increased in atrophy and FR damage

26
Q

Mitochonidrial injury

A

Cytochrome C in cytosol initiates apoptosis

27
Q

Smooth endoplasmic reticulum hyperplasia causes:

And complications

A

alcohol, barbiturates, phenytoin

Incr drug metabolism (e.g. oral contraceptives); decr vit D

28
Q

Chediak-Higashi syndrome

A

Membrane protein defect in transfering lysosomal enzymes to phagocytic vacuoles

AR; giant lysosomes

29
Q

I cell disease

A

absent enzyme marker in Golgi apparatus (Mannose-6-phosphate)
empty lysosomes

30
Q

Rigor Mortis

A

stiff muscles after death D/t ATP depletion

31
Q

Fatty change in liver

A
MCC alcohol (incr NADH)
DHAP --> G3P --> TG

Incr VLDL pushes nucleus to side
Causes: Incr synthesis of TG/FAs, Decr Beta-oxidation of FA
Decr synthesis of apoproteins
Decr release of VLDLs

32
Q

Fatty change in Kwashiorkor

A

Decr synthesis of apoproteins

33
Q

Ferritin (Fx + significance)

A

Primary iron storage protein; serum level reflects marrow storage of iron

34
Q

Hemosiderin

A

Insoluble ferritin degradation product visible with Prussian blue stain

35
Q

Atrophy

A

Reduction in cell/tissue mass by either loss or cell shrinkage

36
Q

Brain atrophy

A

Ischaemia; alzheimers

37
Q

Exocrine gland atrophy in CF

A

duct obstruction by thick secretions

38
Q

Labile cells:
Stable cells:
Permanent cells:

A

Labile - stem cells (skin, marrow, GIT)
Stable: in G0 phase (smooth muscle, hepatocytes) –> can enter cell cycle with influence of growth factors or hormones
Permanent cells: cannot replicate; cardiac, striated muscle; neurons

39
Q

Hypertrophy

A

Incr in cell size (structural components, DNA)

40
Q

LVH and RVH

A

LVH - incr preload (valve regurgitation), increased afterload (HTN, aortic stenosis)

RVH - pulmonary HTN

41
Q

Bladder smooth muscle hypertrophy As/w

A

prostate hyperplasia constricting urethra

42
Q

Removal of kidney causes:

A

hypertrophy of remaining kidney

43
Q

Hyperplasia

A

Increase in number of cells

44
Q

Hyperplasia in tissues:

Endometrial; RBC; prostate; gynecomastier

A

Endometrial - dt unopposed oestrogen (obesity, taking oestrogen)
RBC - d.t increased EPO (blood loss, ectopic secretion, high altitude)
Prostate - increased dihydrotestosterone
Gynecomastia - hyperplasia in male breast tissue. Normal in newborn, adolescent, elderly

45
Q

Metaplasia

A

one adult cell type replaces another cell type

46
Q
Examples of metaplasia:
Squamous metaplasia in bronchus
Intestinal metaplasia in stomach
Squamous metaplasia in bladder
Barret's oesophagus
A
  • smoking
  • paneth cells, goblet cells; H.pylori chronic atrophic gastritis
  • schistosoma hematobium infection
  • glandular metaplasia of distal oesophagus due to GORD
47
Q

Dysplasia + examples
Squamous dysplasia in cervix
Squamous dysplasia in bronchus

A

Atypical hyperplasia or metaplasia are precursors for cancer

  • HPV
  • smoking
48
Q
Necrosis defn
Types of necrosis:
- Coagulation
- Liquefactive
- Caseous
A

Death of groups of cells

  • Coagulation - preservation of structural outline (due to incr lactic acid). Can be pale of haemorrhagic
  • Liq - brain infarct, bacterial infections, wet gangrene
  • Caseous - variant coagulation; granulomas due to TB or systemic fungi
49
Q

Granuloma

A
Activated macrophages (epithelioid cells); multinucleated giant cells
CD4T cells
  • Type 4 hypersensitivity
50
Q

Granuloma associated cells:

  • Epithelioid cells
  • Multinucleated giant cells
A
  • epithelioid - Gamma-IFN released by CD4Tcells activates macrophages
  • MNGC - fusion of epithelioid cells together
51
Q

Enzymatic fat necrosis

A

As/w pancreatitis, soap formation
soponification
Ca++ with fatty acids

52
Q

Fibrinoid necrosis

A

Necrosis of immune reactions (immune vasculitis, endocarditis)

53
Q

Post mortem necrosis

A

Autolysis - no inflammatory reaction

54
Q

Dystrophic calcification

A

Calcification of damaged tissue; normal serum calcium

pancreatitis or atherosclerotic plaque

55
Q

metastatic calcification

A

Calcification of normal tissue

Increased serum calcium or phosphorus

56
Q

Nephrocalcinosis - Definition + S/S

A

Metastatic calcification of collecting tubule basement membranes

Polyuria due to nephrogenic diabetes insipidus; renal failure

57
Q

Apoptosis + signals for apoptosis

A

Gene regulated individual cell death
Signals: Mullarian inhibitory factor, tumor necrosis factor, hormone withdrawal

Signal modulators: TP53 suppresor gene, Bcl-2 genes

58
Q

Bcl-2 genes

A

Anti-apoptosis gene - prevents cytochrome C from leaving mitochondria

59
Q

Caspases

A

Responsible for enzymatic cell death in apoptosis

proteases and endonucleases

60
Q

Markers of apoptosis

A

Eosinophilic cytoplasm, pyknotic (ink dot) nucleus.