Please enable JavaScript.
Coggle requires JavaScript to display documents.
UROLOGY / NEPHROLOGY (Heminephrectomy and
Renal Transplantation…
UROLOGY / NEPHROLOGY
-
GFR
GFR and renal perfusion
Notes:
- recall the equations for both renal perfusion and for GFR
- Renal perfusion = RP = MAP / TPR
--> make sense as renal perfusion is the average pressure going into the kidney = MAP
--> the MAP is then divided by the TPR as in the electricity equation V = IR (I = V / R)
--> TPR = the sum of both afferent and efferent resistance
--> so if both go in the opposite direction, this affects the GFR, but the TPR cancels out and the Renal perfusion stays constant
- GFR = (Δ hydrostatic pressure) - (Δ oncotic pressure)
--> between GC = glomerular capillaries and Bowman's capsule = BC
-
-
-
-
*Ren Arcuatus = horseshoe kidney
- note the isthmus = connection lies anterior to the aorta
- gets caught by the IMA
--> so sits lower than the normal kidney
--> thus doesn't have the SMA nut cracker
--> but the IMA nutcracker is over the isthmus
- ren is usually pretty benign
--> but has an increased risk for UTI
-
*Urinary Incontinence
- "SUM Bladders just OVERFLOW/OBSTRUCT"
--> stree
--> urinary
--> Mixed
--> Obstructed Overflow
*Obstructed Oveerflow Bladder
- from BPH mostly in men
- kidney stones in women
-
*Urge Incontinence
- related to detrusor suddenly contracting
- Tx = antimuscarinics
-
*CKD = Chronic Kidney Disease
- casues secondary hyper PTH
*Hyperphosphate in CKD
- this is common since you lose many functions of the kidney
--> including lowered re-absorption of phosphate
- tx = sevelamine
-
Notes:
- horseshoe kidney = ren arcuis
--> kidney ascend in embryology
--> gets stuck under the IMA
--> lower in the abdomen
- renal AGENESIS
- unilateral
--> not a huge problem early in lfe
--> hypertrophy of the kidney
--> risk of renal failure later in life from high GFR
- Bilateral kidney agenesis
--> leads to oligohydramnios = no amniotic fluid
--> baby face, legs and arms and ears pushed against mom
--> otter sequence and death
--> note that the lungs don't develop since they normally grow by the fluid strectching them
--> pulmonary hypoplasis = cause of death
- POTTER
--> pulmonaary, oligohydramnios, twisted leg + arm EXtremities, renal agenesis
- Diplastic kidney
--> NOT INHERITED
--> where you get DISPLASIA and cysts in the kidney
--> the displasia is from CARTILAGE
--> think of kidney displasia as incorrectly trying to lay bone in the kindey which starts with laying of cartilage
-
-
Congenital CYSTS in the kidney
- check whether bilateral or unilateral
- check the location of the kindey where the cysts are
--> if medulla + cortex + bilateral = PCKD
- if bilateral check if there is CARTILAGE present from aplasia
--> then it is displasia NOT PCKD
Displasia in the kidney
- NON inheritied
- get cysts
- get displasis of kidney replaced with cartilage
- usually UNILATER, BUT can be bilateral
- if you have cysts that are BILATERAL in the kidney, even though they are usually PCKD,
--> you MUST rule out NON INHERITED bilateral cystic cartilage first
- DONT ASSUM if it is bilateral that it is always PCKD
-
PCKD
- bilateral cysts
- medulla and cortex
- NO CARTILAGE
- bilateral kidneys are ENLARGED
-
PCKD is either
- autosomal recessive
--> have HEPATIC cysts too
- autodominant
--> PKD 1 on C16
--> PKD 2 on C4
autosomal recessive PCKD
- have HEPATIC cysts too
--> any small kid who present with PORTAL HTN
--> you have to RULE OUT auto recessive PCKD
--> since both their kidney and liver are invvolved
- POTTER can happen
-
-
autodominant PCKD
- gene mutations
--> PKD 1 on C16
--> PKD 2 on C4
- BERRY aneurisms
--> these are the cause of death in auto DOM PCKD
- present with high renin and HTN, hematuria, and AKI
- CYSTS in the KIDNEY = slow growing PCKD
- CYSTS in the LIVER = HEPATIC cysts
- CYSTS in the BRAIN = BERRY aneurisms
- CYSTS pushing the MV open = MV prolapse
CLASSIC FAMILY presentation with Autosomal DOMINANT PCKD
- family dads and grandpas who die from BERRY aneurism brain hemorrahe
- kidney disease runs in the family also
- think of AD PCKD
*Medullary Cystic kidney disease
- needs to be ruled out from PCKD since it is also bilateral
- DIFFERENCE = it does the opposite to PCKD
- the CYSTS are in the MEDULLA of the DUCTS
- you get SHRUNKEN kidneys
--> whereas in PCKD you have enlarged kidneys
-
*Incontinence
- stress incontinence = seen in women
- urge incontinence
- overflow incontinence
--> often seen in diabetic detruser neuropathy
*Overflow Incontinence
- can happen often in T1 DM
- overflow incontinence is from loss of autonomic function
--> can't sense a full bladder
--> thus it continually fills up and spills out
-
