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Flashcards in Module 1 -Path Deck (51):
1

Renal Artery Stenosis leads to what?

Atrophy

2

What is atrophy?

Reduction in the size and/or number of cells

3

What is the etiology of atrophy?

**Decreased workload
**decreased blood supply (stenosis/atherosclerosis)
**Decreased innervation
**Loss of endocrine Stimulation (ex. post menopausal ovaries)
**Aging
**Increased exogenous hormones (factitious thyrotoxicosis, steroid use)
**Occlusion of secretory ducts (cystic fibrosis or calculus/stone)

4

What is the pathogenesis of Atrophy?

Decreased Protein Synthesis
Increased protein degradation
(decrease in organ size due to decrease in cell size)

5

What is the most common etiology of unilateral renal artery stenosis ?

atherosclerosis (however this is a chronic thing and takes a lifetime to build up)

6

What is the most common presentation of unilateral renal artery stenosis?

Asymptomatic

7

What is the most common cause of death in regards to renal atrophy (renal artery stenosis)?

JG cells can sense hypoperfusion to the kidney and therefore release renin --> hypertensive ---> stroke or MI

8

If the patient has bilateral atrophy of the renal arteries then what is the common end result?

Back up of filtrates --> decreased urine output (oliguria) --> decreased GRF and then GENERALIZED EDEMA

9

what are some investigations for renal artery stenosis ?

Urinalysis, doppler ultrasound for blood flow , BUN, epigastric/bruit (sounds upon auscultation due to turbulent flow)

10

what are some complications of renal artery stenosis?

Renal Failure
Hypertensive changes to the heart
Brain
Retina

11

What are some additional examples of atrophy?

Cut ulnar nerve (hand atrophies)
Fracture and have a cast- arm shrinks
Alzheimers disease
Necrosis of pituitary and dont make TSH --> thyroid gland atrophies

12

What is a possible differential diagnosis for renal artery stenosis --> renal atrophy?

Hypoplasia -- >decrease in cell number and organ size due to incomplete development
(DiGeorges Syndrome)

13

What is the most common pathological etiology of left ventricular hypertrophy?

Hypertension (most common)
Aortic Stenosis
Valvar Insufficiencies

14

What are examples of etiology of physiological hypertrophy?

Uterus size during pregnancy (endometrium is hyperplasia and myometrium is hypertrophy)
Breasts getting larger (hypertrophy and hyperplasia, under the influence of estrogen)

15

Would the prostate under go hyperplasia, hypertrophy or both?

Hyperplasia

16

After 2 weeks of left ventricular hypertrophy you get heart failure cells also called?

Hemociderin laden macrophages

17

What is the pathogenesis for left ventricular hypertrophy?

Increased protein synthesis and decreased protein degradation
Increase in organ size due to increase in cell size

18

How does left ventricular hypertrophy present?

Asymptomatic until end organ damage (TIA, stroke)

19

Before 2 weeks of left ventricular hypertrophy what do you see?

transudate

20

What investigation can you do for LVH?

Echocardiogram

21

What are some possible complication of LVH?

Left ventricular failure --> blood backs up in the lungs and patient unable to breathe = orthopnea
Arrhythmias (damage to purkinje fibers) + thrombus = stroke

22

Most common cause of right heart failure is what?

Left heart failure to continous back up of blood --> when both left and right heart are failing you have CHF

23

What are signs of Right heart failure (RHF) and/or CHF?

CHF leads to distended jugular veins, peripheral edema, hepatomegly, and ascites

24

What cells can only undergo hypertrophy and not hyperplasia?

Permanent cells (heart and CNS)

25

What is the pathogenesis for metaplasia?

Genetic reprogramming of stem cells (Always reversible because the basement membrane is intact)!!

26

There are five scenarios for metaplasia each card will go through one. 1) Retina

Respiratory epithelium to simple squamous?

27

Second metaplasia is 2) Chronic Smoker (respiratory)

Pseudostratified ciliated columnar epithelium with goblet cells --> stratified squamous
Presentation: cough and recurrent infections (unable to clear mucus b/c losing goblet cells and cilia)
Investigation: bronchoscopy and biopsy
Complication: Squamous cell carcinoma of the lung

28

Third type of metaplasia is 3) Barrett's Esophagus (or considered intestinal metaplasia or glandular metaplasia as well)

Stratified squamous non-keratinized --> tall columnar with goblet cells
Presentation: waterbrash (bad metallic taste in mouth due to the acid coming up)
Investigation: Endoscopy or biopsy
Complications: Adenocarcinoma (lower 1/3) and squamous cell carcinoma (upper 2/3)

29

Fourth type of metaplasia 4) Cervical Metaplasia and this is physiological

Simple Columnar to Simple Squamous at endocervix
Presentation: Asymptomatic (enlargement of the endocervix toward the vagina -->transforming zone and this happens at puberty so its completely normal)
Change in epithelium is due to the need for a more acid environment

30

At what point does cervical metaplasia become physiological?

if patient is exposed to the HPV virus.
this can lead to adenocarcinoma (endocervix) and squamous cell carcinoma (ectocervix)

31

In HPV what are the first inflammatory cells to arrive?

CD8 lymphocytes (Because this is a virus)!
ANY VIRUS THIS IS THE CASE

32

Fifth type of metaplasia 5) Squamous metaplasia of the urinary bladder

Transitional to Stratified Squamous
Presentation: Similar to UTI (urinary frequency, suprapubic pain)
Investigation: Cystoscopy and biopsy

33

What is the name of the parasite that is responsible for squamous metaplasia of the urinary bladder?

S. haematobium (this is found in rivers like the nile or amazon)

34

So if you are treating a patient for a UTI with abx and this patient is not getting better, what should you be thinking?

Squamous metaplasia of the urinary bladder

35

Are metaplasia and dysplasia reversible?

yep

36

Is carcinoma reversible?

no (Basement membrane is broken)

37

What are common cause of Barrett's Esophagus?

Obesity
Hital Hernia
GERD (chronic) #1 cause of GERD is obesity

38

If patient has myositis ossificans (bone formation in the injured muscle), is this metaplasia or hyperplasia?

Metaplasia

39

what is another name for transitional epithelium?

Urothelium

40

Ischemia leads to hypoxia which leads to cell injury, what is the mechanism?

Reversible!
Lack of 02 --> abnormalities of cell membrane integrity --> Na/K pump failure due to lack of ATP --> water follows Na and the cell swells and lactate enters the cell (due to decrease in oxidative phosphorylation) --> degranulation of RER --> cell surface blebs and myelin figures --> mitochondrial swelling
(if oxygen restores then cell goes back to normal)

41

List all the components for Reversible cell Injury

ATP depletion
Cellular/Mitochondrial Swelling (decrease ATP --> decrease activity of Na/K pump)
Nuclear chromatin pumping
decreased glycogen
fatty change
Ribosomal/polysomal detachment (decreased protein synthesis)
Membrane blebbing

42

What are the microscopic findings of reversible cell injury?

cellular swelling (hydrophic change)
Nuclei are still visible (DNA/RNA/ribosomes stain blue)

43

When water goes into the cell due to accumulation of Na+ inside the cell, what is this called?

Hydropic change

44

Why do the proteins denature during hypoxia?

Anaerobic --> lactic acid buildup --> decreased pH which denatures proteins

45

Irreversible cell injury is when what occurs?

Inability of mitochondria to recover

46

What are the signs of irreversible cell injury?

Mitochondrial permeability an vacuolization
Plasma membrane damage
Lysosomal Swelling and Rupture
Nuclear Condensation (pyknosis)
Nuclear Fragmentation (Karyorrhexis)
Nuclear Dissolution (Karyolysis)

47

When Ca2+ accumulates in the cell (due to the inactivation of the pump) what does this activate?

Phospholipases (membrane damage)
Proteases (cytoskeleton damage)
Endonucleases (cleave DNA)

48

Irreversible damage looks eosinophillic on H and E why?

due to denatured cytoplasmic proteins and
loss of RNA

49

Under EM and light microscopy how does irreversible cell death look?

EM --> mitochondrial damage
Light --> nuclei are no longer visible

50

If you have irreversible injury what necrosis does this lead to?

Coagulative necrosis
(kidney for example)

51

What is a classic example of ischemia --> hypoxia --> cell death?

Gun shot wound leads to bleeding --> hypovolemic shock --> ischemia/hypoxia-->reversible injury --> irreversible injury