Pathoma Chapter 1A Flashcards Preview

Exit Notecards > Pathoma Chapter 1A > Flashcards

Flashcards in Pathoma Chapter 1A Deck (57)
Loading flashcards...
1
Q

What are the basic principles of growth adapdations?

A

An organ is in homeostasis with the physiologic stress placed on it. An increase, decrease, or change in stress on an organ can result in growth adaptations.

2
Q

What leads to an increase in organ size?

A

An increase in stress

3
Q

Hypertrophy occurs via what?

A

an increase in the size

4
Q

Hyperplasia occurs via what?

A

an increase in the number of cells

5
Q

What does hypertrophy involve?

A

gene activation, protein synthesis, and production of organelles.

6
Q

What does Hyperplasia involve?

A

the production of new cells from stem cells.

7
Q

Permanent tissues are… Do they undergo hypertrophy or hyperplasia?

A

cardiac muscle, skeletal muscle, and nerve, cannot make new cells and undergo hypertrophy only.

8
Q

Pathologic hyperplasia leads to what?

A

(e.g., endometrial hyperplasia) can progress to dysplasia and,eventually cancer.

9
Q

What is an exception to pathologic hyperplasia leading to cancer?

A

benign prostatic hyperplasia (BPH), which does notincrease the risk for prostate cancer,

10
Q

What leads to a decrease in organ size?

A

A decrease in stress (e.g., decreased hormonal stimulation, disuse, or decreased nutrients/blood supply) (atrophy).

11
Q

Atrophy occurs via?

A

a decrease in the size and number of cells

12
Q

How does a decrease in cell number occur?

A

via apoptosis.

13
Q

Decrease in cell size occurs via what?

A

ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components.

14
Q

What happens in ubiquitin-proteosome degradation?

A

intermediate filaments of the cytoskeleton are tagged with ubiquitin and destroyed by proteosomes.

15
Q

What does autophagy of cellular components involve?

A

generation of autophagic vacuoles that fuse with lysosomes whose hydrolytic enzymes breakdown cellular components.

16
Q

What happens in METAPLASIA?

A

change in stress on an organ leads to a change in cell type

17
Q

Metaplasia most commonly involves?

A

change of one type of surface epithelium (squamous, columnar, or urothelial) to another

18
Q

How do metaplastic cells handle the new stress?

A

they are better able to handle the new stress.

19
Q

Esophagus is normally lined by what?

A

nonkeratinizing squamous epithelium (suited to handle friction of a food bolus)

20
Q

Barrett esophagus

A

Acid reflux from the stomach causes metaplasia to nonciliated mucin-producing columnar cells (better able to handle the stress of acid

21
Q

Metaplasia occurs via what?

A

programming of stem cells, which then produce the new cell type.

22
Q

Is Metaplasia reversible?

A

with removal of the driving stressor.

23
Q

Can metaplasia progress to cancer?

A

Under persistent stress, can progress to dysplasia and eventually result in cancer.

24
Q

What is an exception to metaplasia leading to cancer?

A

apocrine metaplasia of breast, which carries no increased risk for cancer.

25
Q

Vitamin A deficiency can result in what?

A

metaplasia,

26
Q

Vitamin A is necessary for what?

A

differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye.

27
Q

Keratomalacia

A

In vitamin A deficiency, the thin squamous lining of the conjunctiva undergoes metaplasia into stratified keratinizing squamous epithelium.

28
Q

Myositis Ossificans

A

Mesenchymal (connective) tissues can undergo metaplasia. A classic example is myositis ossificans in which muscle tissue changes to bone during healing after trauma

29
Q

DYSPLASIA is?

A

Disordered cellular growth

30
Q

Dysplasia most often refers to?

A

proliferation of precancerous cells

31
Q

Cervical intraepithelial neoplasia (CIN)

A

represents dysplasia and is a precursor to cervical cancer

32
Q

Dysplasia often arises from?

A

longstanding pathologic hyperplasia (e.g., endometrial hyperplasia) or metaplasia (e.g., Barrett esophagus)

33
Q

Is dysplasia is reversible?

A

yes, with alleviation of inciting stress.

34
Q

In dysplasia what happens if stress persists?

A

dysplasia progresses to carcinoma irreversible)

35
Q

What is aplasia?

A

it is failure of cell production during embryogenesis (e.g., unilateral renal agenesis)

36
Q

What is hypoplasia?

A

it is a decrease in cell production during embryogenesis, resulting in a relatively small organ (e.g., streak ovary in Turner syndrome)

37
Q

When does cellular injury occur?

A

when a stress exceeds the cells ability to adapt

38
Q

The likelihood of injury depends on what?

A

the type of stress, its severity, and the type of cell affected.

39
Q

What are highly susceptible to ischemic injury? As opposed to?

A

neurons whereas, skeletal muscle is relatively more resistant.

40
Q

Slowly developing ischemia

A

eg: renal artery atherosclerosis, results in ATROPHY

41
Q

acute ischemia

A

eg: renal artery embolus, results in INJURY

42
Q

What are common causes of cellular injury?

A

inflammation, nutritional deficiency or excess, hypoxia, trauma, and genetic mutations.

43
Q

What is HYPOXIA?

A

Low oxygen delivery to tissue; important cause of cellular injury

44
Q

What is the final electron acceptor in the electron transport chain of oxidative phosphorylation?

A

Oxygen

45
Q

Decreased oxygen results in what?

A

impairs oxidative phosphorylation, resulting in decreased ATP production

46
Q

What does a lack of ATP leads to?

A

cellular injury

47
Q

What are some causes of hypoxia?

A

include ischemia, hypoxemia, and decreased 02 - carrying capacity of blood.

48
Q

Ischemia is?

A

decreased blood flow through an organ

49
Q

Ischemia arises with?

A
  1. Decreased arterial perfusion (eg atherosclerosis) 2. Decreased venous drainage (eg Budd-Chiari syndrome) 3. Shock?generalized hypotension resulting in poor tissue perfusion
50
Q

Hypoxemia is?

A

a low partial pressure of oxygen in the blood (Pao2< 60 mm Hg, SaO2<90%).

51
Q

Hypoxemia arises with

A
  1. High altitude 2. Hypoventilation 3. Diffusion defect 4. V/Q mismatch
52
Q

High altitude to hypoxemia, how?

A

Decreased barometric pressure results in decreased PaO2

53
Q

Hypoventilation to hypoxemia, how?

A

Increased Paco, results in decreased PaO2

54
Q

Diffusion defect to hypoxemia, how?

A

PAO2 not able to push as much O2 into the blood due to a thicker diffusion barrier (e.g., interstitial pulmonary fibrosis)

55
Q

V/Q mismatch to hypoxemia, how?

A

Blood bypasses oxygenated lung (circulation problem, eg: right-to-left shunt), or oxygenated air cannot reach blood (ventilation problem, eg: atelectasis)

56
Q

Decreased O2-carrying capacity arises with what?

A

hemoglobin (Hb) loss or dysfunction

57
Q

What are some examples of Decreased O2-carrying capacity?

A
  1. Anemia 2. Carbon monoxide poisoning 3. Methemoglobinemia