Vascular disorders of kidney

Question 1

How do we call…

Thickening of renal arteioles and small arteries

Answer 1

Nephrosclerosis

Question 2

2 most common cause of nephrosclerosis

Answer 2

1.Hypertension
2.Diabetus mellitus

Question 3

Pathophysiology of nephrosclerosis

Answer 3

Damaged arterial walls–>
1.Leaky proteins–>Hyaline deposition
2.Activation of platlets (incr PDGF) promoting intimal thickening –>decr lumen size–>atrophy of organ and loss of function.

Question 4

Diagnosis relating kidney.
-2 most comm associations?

Answer 4

-Nephrosclerosis
-Hypertension and Diabetus

Question 5

Description and diagnosis

Answer 5

-Fine Granular Cortical surface
-Nephrosclerosis

Question 6

Diagnosis
Pathophysiology

Answer 6

-Hyperplastic arteriolosclerosis=Malignant Hypertension.
-SBP>200 or DBP >120–> Endothelial damage –>massive intimal proliferation due to ECM deposition.

Question 7

Diagnosis
Describe

Answer 7

-Malignant Nephrosclerosis=Hyperplastic nephrosclerosis
-Groos:Flea Bitten kidney ( BV rupture–>petechia in kidney in cortical surface)
-Hyperplastic arteriolosclerosis+Fibrinoid necrosis

Question 8

-Hematuria, protenuria, RBC cast…SBP>200
Diagnosis and describe

Answer 8

-Malignant nephritis
-Cerebral edema (Nawored sulci and Wide Gyri)

Question 9

Diabetic Retinopathy Pathophysiology

Answer 9

-Ass with chronic Hyperglycemia.
1.Proliferative-Neovascularization due to Chronic Hypoxia–> traction retinal detachment.
2.Non-Proliferative (most comm)-obstruction BV–>micro-aneurysm, Cotton wool spots, macular edema (vision loss).

Question 10

Hypertensive Retinopathy Pathophysiology

Answer 10

-Cotton woot spots, Exudate Edema.
-Papilledema presence is indicative of Hypertensive emergency–>imediate lowering od BP.

Question 11

-Bi-lateral renal artery stenosis
-Uni-lateral renal artery stenosis + absence od other kidney.

Answer 11

Volume overload

Question 12

2 most commonest causes of Renal Artery Stenosis?

Answer 12

-**Atherosclerosis (85%), Fibromuscular-dysplasia. **(strings of beads)

Question 13

Diagnosis:
-Female (20’s) with Hypertension but otherwise is normal.

Answer 13

-String of Beads(Fibromuscular Dysplasia).
-Could also be PAN.

Question 14

Renovascular Hypertension association

Answer 14

1.Refractory Hypertension
2.Sudden onset of azotemia after administration od ACE inhb and ARB
3.Abd. bruit in setting of increased BP
4.Sudden Hypertension after 30 yrs or 50 yrs.

Question 15

TTP pathogenesis

Answer 15

ADAM13 defciency–>excessive vWF activation–>platlet consumption–>small thrombies to form.

Question 16

Presentation in TTP

Answer 16

-Fever,Purpura (petechial–>small bleeding),CNS thrombi (mental status change, seizures),Kidney injury (azotemia),Micro-angiopathic Hemolytic Anemia (schistocytes).

Question 17

Treat of TTP

Answer 17

-Plasmapherisis (add ADAM13)

Question 18

Differential diagnosis

-Evidence of clot formation but NORMAL PT and PTT and Fibrinogen.

Answer 18

-TTP and HUS

Question 19

-Typical HUS

Answer 19

-O:157H:7 E.Coli–>Shiga Toxin damaging endothelial BV–>excessive coagulation–>kidney damage.
-Damages intestinal + BV linning–>Bloody diarrhea.
-Transmitted Undercooked meat (Hamburgers)

Question 20

Where is E.Coli present when it causes HUS?

Answer 20

-Bacteremia (blood)
-Normaly affects GI tract causing bloody diarrhea.

Question 21

What does HUS trigger?

Answer 21

->Thrombocytopenia

Question 22

HUS association

Answer 22

-Thrompocytopenia, kidney ischemia(uremia),Microangiopathic Hemolytic anemia (schitocyte), +Bloody diarrhea.

Question 23

Diff between DIC and TTP/HUS?

Answer 23

-DIC:consumptive coagulopathy
-TTP/HUS:NO consumption

Question 24

Diagnosis

Answer 24

-**Rhomboid cleft **(consequence of atheromatous plaque ruptures from abd aorta or renal artery–> releases cholesterol crystals)
-Embolous effect of atherosclerosis of renal artery.

Question 25

3 most comm cause of Kidney infarcts?

Answer 25

-Atheromatous plaque
-A.Fib
-Mural thrombi

Question 26

Commonest area to be affected on Kidney infarcts?

Answer 26

-PCT, most active area in nephron (uses most ATP)

Question 27

Renal Papillary necrosis ass…

Answer 27

Sickle cell or trait.

Question 28

Pathophysiology of Renal Papillary necrosis

Answer 28

-Hypoxia triggers sickling, necrosis of medulla and papillae–>sloughing of cells –>post-renal obtsr–>renal faliure.

Question 29

Do you see change in urine osmolality and urine volume in Renal Papillary necrosis?

Answer 29

-NO, because cells slought off (NO V2 recep present)
-HYPOSTHENURIA (inability of kidney to concentrate urine)

Question 30

Renal Papillary Necrosis signs

Answer 30

-Most ass with GROSS Hematuria,painless

Question 31

What is located in renal cortex?

Answer 31

Glomerulus (filtration occurs)

Question 32

Diffuse Cortical Necrosis ass?

Answer 32

-Sepsis (massive hypoperfusion)
-Placental abruption –>DIC.

Question 33

Diagnosis

Severe oliguria–>anueria, after placental abruption.
Limited to cortex

Answer 33

Diffuse Cortical Necrosis.

Question 34

Diagnosis and description
-Ass with massive anuria

Answer 34

-Diffuse cortical necrosis
-Yellow and soft.

Question 35

Where do you see “string of beads” app in angiography(2)?

Answer 35

-Fibromuscular dysplasia
-**PAN **(transmural granulomatosis)

Question 36

2 most common causes of Renal Papillary necrosis?

Answer 36

-Sickle cell and NSAIDS (chronic)

Question 37

• This presents similarly to kidney stones (flank pain, GROSS hematuria), but the CT scan is negative for the presence of stones.

Answer 37

renal papillary necrosis.

Question 38

• Why do you see clots in urine in Renal Papillary nercrosis?

Answer 38

-sloughing of the papilla, producing “clots”** in the urine along with hematuria