Module 4: Renal: Blood Vessel Disorders Flashcards
(42 cards)
The first topic of blood vessel disorders is Benign Hypertension. What is the gross and histology of this?
Long Standing HTN
Gross: Granular appearance of kidneys due to tubular atrophy (Effects are bilateral)
Histology: medial and intimal thickening –affects afferent arterioles – hyaline arteriolosclerosis via leakage of plasma proteins to tunica media
What are the most common cause of chronic benign hypertension
Most common cause of hyaline arteriosclerosis
–afferent arteriole
DM (but that does both arteriole) b/c remember sugar goes everywhere
What are the symptoms for chronic benign hypertension?
Generally asymptomatic with mild proteinuria
What are the complications for chronic benign hypertension?
Few progress to chronic renal failure
–renal artery stenosis: atherosclerotic plaques, atrophy of kidneys to chronic renal failure
Kidney appears granular/leathery
–tubular atrophy
Moving onto malignant hypertension. What is the gross and histological appearance of sudden malignant ?
Gross: greater than 180/120 with papilledema (cerebral edema)
–petechial hemorrhages in the kidney are called flea bitten kidney
Top Image: Necrotizing arteriolitis (fibrinoid necrosis) and again kidney has flea bitten appearance
–sudden malignant HTN get endothelial damage of afferent arteriole and you get thrombosis of the lumen (So thats why media is undergoing necrosis because lumen supplies the media with O2 so media is undergoing coagulative necrosis)
What is the histological appearance of long standing malignant HTN?
Bottom Image: Long standing — concentric due to hyperplasia of tunica media
–onion skin appearance or hyperplastic (proliferation of SM cells and intimal thickening)
What is the presentation for benign or malignant HTN?
Hematuria Oliguria Proteinuria Edema --most common in young black males
What are the complications of benign or malignant HTN?
Acute renal failure (organ damage develops in hours or days)
Cerebral Edema
Stroke
Aortic Dissection — heart failure (HTN is an important factor for the intima tear)
–affects the small vessels so anything is resulting of the burst of these vessels
Moving on to the thrombotic microangiopathies. What is the pathogenesis?
Abnormal platelet aggregation — thrombosis (fibrin) in arterioles/capillaries — microangiopathic hemolytic anemia (Schistocytes in PB smear)
The microvascular thrombi lead to what?
Ischemic injury to the kidneys, brain and heart
Patients with thrombotic microangiopathies present with what?
Thrombocytopenia Purpuric rash Acute renal failure Neurological abnormalities Fever
There are two types of Thrombotic Microangiopathies. The first one is hemolytic uremic syndrome (HUS), what is this associated with?
HUS: seen in children 1 week after bloody diarrhea caused by enterohemorrhagic E. Coli (0157:H7)
–more severe renal failure, less CNS involvement
HUS is associated with what?
Viral Infections
Shigella
Salmonella
HUS can be drug induced, by what drugs?
Quinine (tonic water) Gemcitabine Cyclosporine Ticlopidine Oral Contraceptives
The second thrombotic microangiopathies is thrombotic Thrombocytopenia Purpura (TTP), what are some features?
CNS involvement more pronounced, less severe renal failure
–associated with SLE, HIV, hematological malignancy
Moving on to the last blood vessel disorder is renal artery stenosis, what is the pathogenesis?
Occlusion of renal artery by atheromatous plaque — diffuse ischemic atrophy —- crowded glomeruli, atrophic tubules, interstitial fibrosis
Why is there no significant arteriosclerosis in renal artery stenosis?
b/c arterioles of the affected kidney is protected from transmission of high pressure due to stenotic renal artery
However in renal artery stenosis there is hypertensive arteriosclerosis in the contralateral kidney, why?
due to increased systemic pressure
What is the most common presentation for renal artery stenosis?
Most common presentation is asymptomatic b/c other kidney compensates
What are the complications of renal artery stenosis?
Renal Failure, HTN changes to heart, brain and retina
- -note: JG cells can sense hypo-perfusion to the kidney and release renin, leading to hypertension, which can cause a stroke or MI
- -if bilateral atrophy, then there is a back up of filtrates, decreased urine output (oliguria), decreased GFR and generalized edema
What do you see on investigation for renal artery stenosis?
Epigastric/flank bruit due to turbulent flow
US: asymmetrical kidney size (smaller on side of stenosis)
Doppler: measure blood flow velocities in renal arteries compared to aorta
Renal Arteriogram: Gold Standard
What is the treatment of renal artery stenosis?
Angioplasty and Stent
-indications: uncontrolled HTN, declining renal function (increased Cr) and recurrent pulmonary edema
Moving onto to cystic diseases of the kidney. First lets start with polycystic kidney disease. There is autosomal dominant and autosomal recessive. Lets first start with autosomal dominant. What is the pathogenesis?
Genetic mutations on PKD (polycystin gene) on chromosome 16 and 4 (PKD1 and PKD2) – bilaterally enlarged kidneys with multiple cysts in both kidneys
Where are the cysts from in polycystic kidney disease?
Born with cysts and they are asymptomatic and the origin in heterogenous (aka they can come from anywhere PCT, DCT, CD)
–as the kidney gets bigger the cysts get bigger
