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Pathology Pre-Midterm > Module 1 -Path > Flashcards

Module 1 -Path Flashcards

1
Q

Renal Artery Stenosis leads to what?

A

Atrophy

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2
Q

What is atrophy?

A

Reduction in the size and/or number of cells

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3
Q

What is the etiology of atrophy?

A
  • *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)
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4
Q

What is the pathogenesis of Atrophy?

A

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

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5
Q

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

A

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

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6
Q

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

A

Asymptomatic

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7
Q

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

A

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

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8
Q

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

A

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

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9
Q

what are some investigations for renal artery stenosis ?

A

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

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10
Q

what are some complications of renal artery stenosis?

A

Renal Failure
Hypertensive changes to the heart
Brain
Retina

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11
Q

What are some additional examples of atrophy?

A

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

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12
Q

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

A

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

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13
Q

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

A

Hypertension (most common)
Aortic Stenosis
Valvar Insufficiencies

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14
Q

What are examples of etiology of physiological hypertrophy?

A

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

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15
Q

Would the prostate under go hyperplasia, hypertrophy or both?

A

Hyperplasia

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16
Q

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

A

Hemociderin laden macrophages

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17
Q

What is the pathogenesis for left ventricular hypertrophy?

A

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

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18
Q

How does left ventricular hypertrophy present?

A

Asymptomatic until end organ damage (TIA, stroke)

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19
Q

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

A

transudate

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20
Q

What investigation can you do for LVH?

A

Echocardiogram

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21
Q

What are some possible complication of LVH?

A

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

22
Q

Most common cause of right heart failure is what?

A

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

23
Q

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

A

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

24
Q

What cells can only undergo hypertrophy and not hyperplasia?

A

Permanent cells (heart and CNS)

25
Q

What is the pathogenesis for metaplasia?

A

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

26
Q

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

A

Respiratory epithelium to simple squamous?

27
Q

Second metaplasia is 2) Chronic Smoker (respiratory)

A

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
Q

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

A

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
Q

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

A

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
Q

At what point does cervical metaplasia become physiological?

A

if patient is exposed to the HPV virus.

this can lead to adenocarcinoma (endocervix) and squamous cell carcinoma (ectocervix)

31
Q

In HPV what are the first inflammatory cells to arrive?

A 
CD8 lymphocytes (Because this is a virus)!
ANY VIRUS THIS IS THE CASE
32
Q

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

A

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

33
Q

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

A

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

34
Q

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

A

Squamous metaplasia of the urinary bladder

35
Q

Are metaplasia and dysplasia reversible?

A

yep

36
Q

Is carcinoma reversible?

A

no (Basement membrane is broken)

37
Q

What are common cause of Barrett’s Esophagus?

A

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

38
Q

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

A

Metaplasia

39
Q

what is another name for transitional epithelium?

A

Urothelium

40
Q

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

A

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
Q

List all the components for Reversible cell Injury

A

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
Q

What are the microscopic findings of reversible cell injury?

A 
cellular swelling (hydrophic change)
Nuclei are still visible (DNA/RNA/ribosomes stain blue)
43
Q

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

A

Hydropic change

44
Q

Why do the proteins denature during hypoxia?

A

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

45
Q

Irreversible cell injury is when what occurs?

A

Inability of mitochondria to recover

46
Q

What are the signs of irreversible cell injury?

A 
Mitochondrial permeability an vacuolization
Plasma membrane damage 
Lysosomal Swelling and Rupture 
Nuclear Condensation (pyknosis) 
Nuclear Fragmentation (Karyorrhexis)
Nuclear Dissolution (Karyolysis)
47
Q

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

A

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

48
Q

Irreversible damage looks eosinophillic on H and E why?

A

due to denatured cytoplasmic proteins and

loss of RNA

49
Q

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

A

EM –> mitochondrial damage

Light –> nuclei are no longer visible

50
Q

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

A

Coagulative necrosis

kidney for example

51
Q

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

A

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

Pathology Pre-Midterm (35 decks)

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