Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
62 Cards in this Set
- Front
- Back
What changes happen in the kidney with age?
|
*Thickening of the arterial walls results in decreased renal blood flow.
*There is increased thickness of the glomerular basement membrane and an increase in mesangial cells; increased mesangial matrix. *There is increased incidence of atherosclerotic changes in renal vessels with age. *Some glomeruli become nonfunctional due to sclerosis; one expects to find sclerotic glomeruli in the kidney of any elderly person. About one-half of the glomeruli have been lost by age 90 years. *There is a decrease in mass of the JGA and a corresponding decreased renin release. This is modest and doesn't account for much harm. |
|
ID and discuss.
|
*Atherosclerotic Kidney.
*Kidneys are small and scarred as result of slowly progressive ischemia. *Note circular depressions along with other scars; these also represent ischemic change. *Similar gross appearance might be seen in chronic pyelonephritis. |
|
Discuss Hypertension and the Kidney:
|
*Can result from renal disease.
*Exacerbates or causes renal disease through changes in vasculature. *A classic example is renal artery stenosis. |
|
ID and discuss.
|
*Renal Artery Stenosis.
*An uncommon cause of hypertension. *Atherosclerosis is usually at the origin of the renal artery. *More common in elderly or diabetic men. *Leads to a small kidney with atrophy due to ischemia. |
|
|
*"Goldblatt" kidney. Shrunken, atherosclerotic change.
|
|
|
JUXTAGLOMERULAR CELL HYPERPLASIA in a kidney with a narrowed renal artery.
Left: Hypertrophied JGA cells are on top of and around the black, upside down "V" looking streak. Right: EM of the JGA cells. Black dots are secretory granules that are sites of renin storage. |
|
What are the changes in Renal Artery Stenosis and Hypertension?
|
*Decreased renal blood flow.
*Increased renin production. Increased angiotensin II. Increased aldosterone. *Vasoconstriction, Na retention, increased blood volume. *This combination results in hypertension. |
|
ID and discuss:
|
Fibromuscular Dysplasia:
*Unilateral or bilateral. *A heterogeneous group of conditions. *More common in young women. *Thickening of one or all three layers by fibrous or muscular tissue. The media is most often involved. |
|
|
*Medial Fibroplasia, AKA Fibromuscular Dysplasia. Renal artery. Aorta on the right.
|
|
|
FIBROMUSCULAR DYSPLASIA WITH MEDIAL HYPERPLASIA.
*Dark pink shows hypertrophied medial muscle fibers. |
|
|
FIBROMUSCULAR DYSPLASIA OF RENAL ARTERY WITH MEDIAL HYPERPLASIA (Elastic tissue stain). The media between the two elastic lamina is tremendously thickened. This is the most common type of fibromuscular dysplasia.
|
|
|
FIBROMUSCULAR DYSPLASIA WITH INTIMAL FIBROPLASIA.
|
|
Discuss HTN:
What are the 2 kinds? How is it acquired? |
*Essential (primary): 95%.
*Secondary: renal, vascular, endocrine, neurogenic. *Hypertension is the result of altered relationship between blood volume and vascular resistance. |
|
What causes essential HTN?
Possible gene defects? Environmental? |
*Interaction of genome and environment affecting cardiac output and SVR.
*Possible gene defects: 1) Aldosterone metabolism. 2) Na reabsorption. 3) Transport of Na and Ca across SM membrane. *Environmental: stress, obesity, smoking, heavy Na intake, physical inactivity. |
|
What are 2 hypotheses for causes of essential HTN?
|
1) Cause: defects in renal Na homeostasis. Reduced renal excretion of Na in setting of previous normotension. Result: > blood volume and > cardiac output, vasoconstriction, hypertension. The “Na homeostat” has been reset at a higher level.
2) Cause: increased vascular resistance. This increase in resistance can be caused by either/or: *Vasoconstriction. *Hypertrophy and/or hyperplasia of SM cells, resulting in thickening of vascular walls and narrowing of lumens. |
|
What are the Renal Causes of Secondary Hypertension?
|
*Vascular disease.
*Glomerular diseases –-> volume expansion. *Chronic renal diseases such as pyelonephritis or interstitial nephritis. *Chronic renal failure by increasing blood volume through salt and water retention. *Tumors of JG apparatus --> increased renin. |
|
What are the CV Effects Of Hypertension?
|
*Functional and structural changes in small arteries and arterioles.
*Atherosclerosis affects larger elastic and muscular arteries. *HTN indirectly affects these vessels by ACCELERATING atherosclerosis. |
|
Discuss Hyaline Arteriolosclerosis:
|
*Gk. Hyalinos: made of crystal or glass.
*Kidney is small or normal size, fine nodularity on the surface, thin cortex. *Seen most commonly in hypertension. THIS IS A HALLMARK OF PEOPLE WITH ESSENTIAL HTN! *Also in diabetes and the elderly. |
|
|
L: Hypertensive renal disease.
R: Normal kidney disease. *Disregard color ∆. Note that normal kidney is smooth and glistening. On hypertensive kidney, capsule was adherent; this is why you see pocking, scarring, granularity. This is typical of uncomplicated hypertensive renal disease. |
|
|
L: Hypertensive renal disease. Cortical region is quite thin. This is due to tubular atrophy and fibrosis.
R: Normal kidney disease. |
|
|
*FOCAL CORTICAL ATROPHY (HYPERTENSION).
*Note some normal tubules in lower right. Note wedge-shaped area depressing down; this is fibrosis/scarring; this is what causes the gross granularity. |
|
|
*HYALINE ARTERIOLOSCLEROSIS.
*Note dramatically reduced lumen, due to massive thickening of arteriolar wall. THINK HTN!!! |
|
ID and discuss this image.
|
*HYALINE ARTERIOLOSCLEROSIS.
*The lesions are characterized by glassy thickening of arterial and arteriolar walls. In this section an involved arteriole (arrow) is adjacent to a sclerotic glomerulus (asterisk). Though seen in other conditions, hyaline arteriolosclerosis is most common and most severe in hypertensive patients. |
|
What is the pathogenesis of Hyaline Arteriolosclerosis?
|
*Glassy thickening is due to plasma components leaking across injured endothelium and to increased ECM production by SM.
*Consists of plasma proteins, fibrin, collagen, and basement material. *Clinically referred to as “benign nephrosclerosis.” |
|
Discuss Malignant Hypertension:
|
*Usually, this is superimposed on essential or secondary HTN. Less frequently, it will be the first manifestation of HTN.
*Associated with HYPLERPLASTIC arteriolosclerosis, AKA Malignant nephrosclerosis. |
|
|
*Gross kidney in malignant HTN.
*Note brownish red areas on kidney surface; these represent areas of hemorrhage in the renal tissue. |
|
|
*Cut surface of kidney of a 23 y/o man. Cerebral hemorrhage. Malignant hypertension. Note hemorrhages in pelvis and sinus.
|
|
|
*Malignant hypertension, gross, high magnification.
*Pinpoint hemorrhages represent glomeruli. Note hemorrhagic streaks in medulla. Histology showed fibrinoid necrosis of arteriolar walls. |
|
Discuss and describe Hyperplastic Arteriolosclerosis:
|
*Associated with malignant hypertension.
*Thick laminated walls with narrow lumen. *EM shows abundant SM cells in intima. *Fibrinoid necrosis when severe. *Sometimes mucoid changes in wall. *These lesions occur in other organs. |
|
|
Hyperplastic Arteriolosclerosis. Increased number of SM cells in a concentric arrangement.
|
|
|
Hyperplastic Arteriolosclerosis. Note laminar arrangement in vascular wall, “onion skin lesion”.
|
|
|
MALIGNANT HYPERTENSIVE NEPHROPATHY. Hyperplastic Arteriolosclerosis. Onion skinning; lumen of vessels is essentially obliterated.
|
|
Discuss Fibrinoid Necrosis:
|
*Necrosis of arteriolar walls.
*Occurs when hypertension is very severe. *Lesions contain fibrin, Gammaa Globulins, albumin, and complement. *Rarely, there are inflammatory cells; this is called "necrotizing arteriolitis." *EM shows electron-dense deposits. |
|
|
Fibrinoid Necrosis. Inflammatory cells are present, so this is necrotizing arteriolitis.
|
|
|
A. FIBRINOID NECROSIS OF AFFERENT ARTERIOLE
B. HYPERPLASTIC ARTERIOLITIS |
|
|
Maternal vessel in HTN as part of eclampsia.
|
|
Discuss Renal Arterial Embolism:
|
*Causes infarcts.
*Embolus comes from heart, aorta, or renal arteries. *Rarely, paradoxical embolism (originates in venous blood, but due to patent foramen ovale, crosses into arterial circulation). *Recent infarcts are pale and wedge-shaped; surrounded by red border. *Old infarcts pale depressed white V-shaped scars. |
|
|
*Orientation: Aorta on left. RA has been opened to show embolus.
*Pale red embolus occludes renal artery at origin. The rest is propagated thrombus. RHD with MS. |
|
|
*Renal Infarcts. A classical pale wedge-shaped renal infarct with the base of the triangle on the capsule. They may be solitary or multiple, unilateral or bilateral. They are surrounded by a congested, red border. This is coagulative necrosis.
|
|
|
Shows a repeated renal emboli. There are fibrosed remnants of old infarcts. Note depressions. The point: an isolated renal infarct won't kill you, but these things can keep on happening.
|
|
|
*ATHEROMATOUS (atherosclerotic) EMBOLUS in an artery branching off from the renal artery. This is a chunk of atherosclerotic plaque that popped off a patient during a cardiac catheterization.
|
|
|
*AORTIC ATHEROSCLEROSIS. This is just to show that catheterization can pop off these plaques, and they can embolize...including to the kidney.
|
|
Discuss ATHEROMATOUS EMBOLI to the kidney:
|
*More likely in Elderly persons.
*Occur with manipulation of aorta at surgery or catheterization or ballooning. *Embolization occurs from fragments of plaques from aorta or renal artery or aortic valve. |
|
What are some miscellaneous diseases With Renal Vascular Involvement?
|
*Lupus erythematosis.
*Polyarteritis nodosa. *Scleroderma. *Wegener’s granulomatosis. *Microscopic polyangiitis. |
|
Discuss Renal Vein Thrombosis:
What causes it? Who do you see it in? |
*A result of compression, phlebitis, renal tumors, amyloidosis, and hypercoagulation syndromes.
*Sometimes seen in fetuses of diabetic mothers. *Or in infants with severe gastroenteritis. *Hemorrhagic cortical infarction. *Nephrotic Syndrome. |
|
|
Renal vein thrombosis. Looks pretty much like any other thrombus; just need to be able to tell that this is in a vein.
|
|
Discuss Papillary Necrosis:
What causes it? Who do we see it in? |
*Characterized by impaired blood flow in vasa recta; results in necrosis of papilla.
*Acute pyelonephritis. *UT obstruction. *Diabetes mellitus. *Sickle cell nephropathy. *Analgesic nephropathy. |
|
|
Papillary necrosis in a case of diabetes. Yellow areas represent necrosis of the papillae.
|
|
What are Thrombotic Microangiopathies?
What do they have in common? Where do you see them? 3 |
*A group of diseases not easily differentiated.
*Characterized by endothelial injury and/or platelet activation/aggregation. *You see thrombi in interlobular arteries, afferent arterioles, and glomerular capillaries. |
|
What are the changes in the blood that you see in Thrombotic Microangiopathies?
What are the 3 types I need to know? |
*Microangiopathic hemolytic anemia, thrombocytopenia, thrombi formation, and acute renal failure are present.
*Classification: HUS and TTP: 1) Typical hemolytic-uremic syndrome 2) Atypical hemolytic-uremic syndrome 3) Thrombotic thrombocytopenic purpura. |
|
Discuss Typical HUS. What causes it? What does it look like? What can it result in?
|
*Most common in children.
*A toxin from infection by E. coli, 0157:H7 or Shigella dysentery. *GI symptoms or flu-like syndrome at onset. *Bleeding, oliguria, hematuria, neurological changes. *Microangiopathic hemolytic anemia and acute renal failure. |
|
Discuss toxin role in Typical HUS:
|
*The Shiga toxin is carried by neutrophils in the circulation.
*It acts on the endothelium of the glomerular capillaries to increase adhesion of leukocytes, increase production of endothelin, and decrease nitric oxide. DAMAGE TO ENDOTHELIUM IS KEY!!! *It can also enter the cells and cause cell death. |
|
What pathological traits do HUS and TTP have in common?
|
*Cortical necrosis, subcapsular petechiae.
*Thick glomerular capillary walls. *Mesangial matrix can become disrupted. *Platelet-fibrin clots are present in capillary lumens. THIS IS KEY! *Fibrinoid necrosis in walls of small arteries and afferent arterioles. |
|
|
HEMOLYTIC UREMIC SYNDROME (FIBRINOID NECROSIS OF HILAR ARTERIOLE). Irregular pinkish areas represent fibrinoid necrosis.
|
|
|
HEMOLYTIC UREMIC SYNDROME. Fibrinoid necrosis visible within the glomerulus.
|
|
|
TTP WITH STAIN FOR FIBRIN; the red thrombin is totally occluding the capillary lumina. NOT GOOD! REMEMBER THIS SLIDE.
|
|
DISCUSS Atypical HUS:
Who does it affect? What characterizes it? |
*Most common in adults.
*No Diarrhea, or not much. *Not related to Shiga toxin. *Can occur in a number of clinical settings. |
|
What kinds of causes are to blame for Atypical HUS? 6
|
1) Mutations in complement genes:
*Commonly factor H which normally protects cells from complement activation. 2) Pregnancy or post-pregnancy complications: *Postpartum renal failure after uncomplicated pregnancy and delivery. *After placental abruption. 3) Antiphospholipid antibodies. 4) Vascular diseases affecting the kidney: *Systemic sclerosis. *Malignant hypertension. 5) Chemotherapy or immunosuppression: Mitomycin, cyclosporine, et al. 6) Radiation of the kidney. |
|
What is Postpartum Renal Failure?
|
*It is renal failure and microangiopathic hemolytic anemia within 10 days following an uncomplicated pregnancy.
*This entity is distinct from renal failure following abruption, PP hemorrhage, AF embolism, puerperal sepsis. |
|
|
*POSTPARTUM RENAL FAILURE (Atypical HUS).
*No platelets are visible! *RBCs are small and "helmeted." |
|
Discuss Thrombotic Thrombocytopenic Purpura (TTP):
What symptoms? Who does it occur in? What's the differential? What's the pathogenesis? |
*Rare disease, most common in young women.
*Fever, neurological changes, hemolytic anemia, thrombocytopenia, and renal failure. *Differential diagnosis from adult HUS; severe neurological manifestations and less severe renal disease favor TTP. |
|
What is the pathogenesis of TTP?
|
*Different pathogenesis from HUS (which results from endothelial injury and activation).
*TTP due to acquired defect in proteolytic cleavage of von Willebrand Factor (vWF) multimers (can be autoimmune, can be due to drugs). *Rarely, hereditary. *The defect is in a vWF protease, ADAMTS 13, a disintegrin and metalloprotease. *WEIBEL-PALADE BODIES SECRETE MULTIMERS!!!!!!! |