Flashcards in Module 1 -Path Deck (51):
Renal Artery Stenosis leads to what?
What is atrophy?
Reduction in the size and/or number of cells
What is the etiology of atrophy?
**decreased blood supply (stenosis/atherosclerosis)
**Loss of endocrine Stimulation (ex. post menopausal ovaries)
**Increased exogenous hormones (factitious thyrotoxicosis, steroid use)
**Occlusion of secretory ducts (cystic fibrosis or calculus/stone)
What is the pathogenesis of Atrophy?
Decreased Protein Synthesis
Increased protein degradation
(decrease in organ size due to decrease in cell size)
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)
What is the most common presentation of unilateral renal artery stenosis?
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
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
what are some investigations for renal artery stenosis ?
Urinalysis, doppler ultrasound for blood flow , BUN, epigastric/bruit (sounds upon auscultation due to turbulent flow)
what are some complications of renal artery stenosis?
Hypertensive changes to the heart
What are some additional examples of atrophy?
Cut ulnar nerve (hand atrophies)
Fracture and have a cast- arm shrinks
Necrosis of pituitary and dont make TSH --> thyroid gland atrophies
What is a possible differential diagnosis for renal artery stenosis --> renal atrophy?
Hypoplasia -- >decrease in cell number and organ size due to incomplete development
What is the most common pathological etiology of left ventricular hypertrophy?
Hypertension (most common)
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)
Would the prostate under go hyperplasia, hypertrophy or both?
After 2 weeks of left ventricular hypertrophy you get heart failure cells also called?
Hemociderin laden macrophages
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
How does left ventricular hypertrophy present?
Asymptomatic until end organ damage (TIA, stroke)
Before 2 weeks of left ventricular hypertrophy what do you see?
What investigation can you do for LVH?
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
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
What are signs of Right heart failure (RHF) and/or CHF?
CHF leads to distended jugular veins, peripheral edema, hepatomegly, and ascites
What cells can only undergo hypertrophy and not hyperplasia?
Permanent cells (heart and CNS)
What is the pathogenesis for metaplasia?
Genetic reprogramming of stem cells (Always reversible because the basement membrane is intact)!!
There are five scenarios for metaplasia each card will go through one. 1) Retina
Respiratory epithelium to simple squamous?
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
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)
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
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)
In HPV what are the first inflammatory cells to arrive?
CD8 lymphocytes (Because this is a virus)!
ANY VIRUS THIS IS THE CASE
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
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)
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
Are metaplasia and dysplasia reversible?
Is carcinoma reversible?
no (Basement membrane is broken)
What are common cause of Barrett's Esophagus?
GERD (chronic) #1 cause of GERD is obesity
If patient has myositis ossificans (bone formation in the injured muscle), is this metaplasia or hyperplasia?
what is another name for transitional epithelium?
Ischemia leads to hypoxia which leads to cell injury, what is the mechanism?
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)
List all the components for Reversible cell Injury
Cellular/Mitochondrial Swelling (decrease ATP --> decrease activity of Na/K pump)
Nuclear chromatin pumping
Ribosomal/polysomal detachment (decreased protein synthesis)
What are the microscopic findings of reversible cell injury?
cellular swelling (hydrophic change)
Nuclei are still visible (DNA/RNA/ribosomes stain blue)
When water goes into the cell due to accumulation of Na+ inside the cell, what is this called?
Why do the proteins denature during hypoxia?
Anaerobic --> lactic acid buildup --> decreased pH which denatures proteins
Irreversible cell injury is when what occurs?
Inability of mitochondria to recover
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)
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)
Irreversible damage looks eosinophillic on H and E why?
due to denatured cytoplasmic proteins and
loss of RNA
Under EM and light microscopy how does irreversible cell death look?
EM --> mitochondrial damage
Light --> nuclei are no longer visible
If you have irreversible injury what necrosis does this lead to?
(kidney for example)