GU middle tier Flashcards by David Sog

nephritic syndrome pathophysiology

inflammation of glomeruli
glomerular capillary develop large pores, allowing blood to flow into the urine (rbc and wbc (sterile pyuria))
podocytes also damaged (proteinuria)
rapid decline in function
low renal function – low urine output
fluid overload –> hypertension, oedema

How well did you know this?

Not at all

Perfectly

nephritic syndrome investigations/ symptoms

dipstick

haematuria!
proteinuria (little)
sterile pyruria
high creatinine

urinanalysis – red cell casts (microscopic haematuria- red cells clumped togeth)

cola coloured urine

oliguria

low output volume
decreased GFR

fluid overload , hypertension, oedema

uraemia

How well did you know this?

Not at all

Perfectly

nephritic syndrome causes

AAV (ANCA associated vacilitis, small vessel)

goodpastures disease (acute, autoimmune)

SLE, systemic sclerosis

upper resp tract infection

IgA nephritis (days, common, )
post streptococcal infection (weeks, often tonsilitis)

viral (hepB/C, malaria)

bacterial (MRSA)

How well did you know this?

Not at all

Perfectly

Nephritic syndrome treatment

Treat underlying disease

Recovery happens spontaneously

How well did you know this?

Not at all

Perfectly

nephrotic syndrome pathophysiology

Damage to podocyte foot processes –> gaps in podocytes
Glomerular permeability increased so protein lost as it filters through into urine
Albumin lost → hypoalbuminemia (and proteinuria) → decreased intravascular oncotic pressure → fluid moves into surrounding tissue, causing oedema
Hypoalbuminemia → liver compensation → increased lipid production → hyperlipidaemia/ Less of the protein enzymes that convert → storage or that catabolise (lipase)
Increased risk of thromboembolism due to liver compensation
Increased susceptibility to infection (Ig lost in urine)

How well did you know this?

Not at all

Perfectly

nephrotic syndrome symtpoms

triad

heavy proteinuria (frothy wee)
hypoalbuminaemia
peripheral oedema
hyperlipidaemia/ hypercholesterolaemia (due to more production due to lipid compensation /lipases and storage conversion enzymes lost in urine)
increased susceptibiltiy to infection (Ig lost in urine)
increased risk of thromboembolism (liver compensation)
potentially haematuria

How well did you know this?

Not at all

Perfectly

causes of nephrotic syndrome with detail inc pathophsy, cause, epidem, treatment

minimal change

fused podocytes –> loss of foot processes
vacuolation
microvilli appear in glomerulus
see with electron microscopy (not light)
often children
related to atopy
steroids and anti-oedema

membranous

thickened basement membrane
secondary to drugs, autoimmune, infection, malignancy
asymptomatic but investigations same
steroids and immunosup

focal segmented glomerulosclerosis (FSGS)

unknown reasoning
steroids and immunosup

How well did you know this?

Not at all

Perfectly

what is the most common secondary cause to nephrotic syndrome

+ others

diabetes

hepB/C
SLE
drugs/toxins
amyloidosis
RA
malignancy

How well did you know this?

Not at all

Perfectly

nephrotic syndrome treatment

loop diuretics for oedema
BP control - for proteinuria
statins - for hyperchol
anticoag
steroids (in children and ?)

if membranous, immunosup

How well did you know this?

Not at all

Perfectly

glomerulonephritis = aka

nephritic syndrome!!

How well did you know this?

Not at all

Perfectly

nephrotic vs nephritic

nephrotic has higher proteinuria !

nephritic also has capillary damage –> blood loss!

can be related though - eg nephritic syndrome with a nephrotic element

How well did you know this?

Not at all

Perfectly

uraemia symptoms

uraemia = high serum urea

anorexia
pruritus (itchy) rash
lethargy
nausea

How well did you know this?

Not at all

Perfectly

what does frothy urine indicate?

high protein

How well did you know this?

Not at all

Perfectly

dominant polycystic kidney disease

penetrance high/low
commoness
gender

high penetrance
common
m>F

How well did you know this?

Not at all

Perfectly

is dominant/recessive polycystic kidney disease more common

dominant

How well did you know this?

Not at all

Perfectly

dominant/recessive polycystic kidney disease age of presentation

dom - largely 20 onwards

rec - infancy

How well did you know this?

Not at all

Perfectly

which genes are affected in dominant/recessive polycycstic kidney disease

dom - PKD1 (main) and PKD2
(- PKD1 encodes polycystin 1 - involved in cell-cell and cell-matrix interactions, regulates tubular and vascular development
- PKD2 encodes polycystin 2 - = calcium channel)

rec- PKHD1

How well did you know this?

Not at all

Perfectly

dominant polycystic kidney disease pathophysiology

PKD1 encodes polycystin 1 - involved in cell-cell and cell-matrix interactions, regulates tubular and vascular development
PKD2 encodes polycystin 2 - = calcium channel
cyst formation
These increase in size with age → renal enlargement → progressive destruction of renal tissue
PKD1 mutation has a quicker course, more reach ESRF end stage renal failure than PKD2 mutation

How well did you know this?

Not at all

Perfectly

recessive polycystic kidney disease pathophysiology

Study These Flashcards

Collecting duct dilation and elongation → Result in kidney enlargement and tissue destruction.
Loss of kidney function due to mechanical compression, apoptosis of healthy tissue (Atrophy) and reactive fibrosis.

dominant polycystic kidney disease progression

Study These Flashcards

Clinically silent for many years (family screening important)
Bilateral kidney enlargement
Hypertension
Renal stones
progressive renal failure
loin/abdomen pain
Renal colic (clots)
cyst haemorrhage /infection /urinary tract stone
– Haematuria
– Acute loin pain
Nocturia
Excessive water and salt loss
Cysts may become infected

where else is affected by PKD1/2 mutation (dominant)

Study These Flashcards

Liver/pancreas - have cysts but function unaffected
Heart - valve disorders
brain/vessels - berry aneurysms → subarach haem

recessive polycystic kidney disease symptoms

Study These Flashcards

Enlarged kidneys
Renal cysts
Hepatic fibrosis– Portal hypertension
Kidney failure

polycystic kidney disease investigation including diagnosis

Study These Flashcards

Ultrasound
- Liver and pancreas cysts in dominant
- Salt and pepper appearance for recessive
- Diagnosis:
15-39 y ≥2 or 3 cysts total (uni/bilateral)
40-59y ≥ 2 cysts each kidney
60y+ ≥4 cysts each kidney
Exclude if less than 2 cysts total above 40 y . cannot exclude diagnosis if less than 30y

PKD1/2 /PKHD1 genetic testing

BP- raised

Monitor liver (rec) -

CT/MRI
- MRI- to screen for intracranial aneurysms

polycystic cysts management

Study These Flashcards

Family screening
- Ultrasound

Genetic testing
If early onset/prenatal diagnosis, atypical disease, reproductive choices, potential kidney donor available?

No treatment slows progression

Disease progression monitored with serum creatinine

Treat stones, UTIs, HTN (ACEi), pain (analgesia)

Renal replacement for end stage renal failure ESRF

Surgical

removal of cysts laparoscopically - helps with pain
Nephrectomy - removes whole kidney

Counselling, support

what is a testicular lump until proven otherwise?

testicular cancer

epididymal cyst age

rare in chilren | 40y

spermatocele =

= epididymal cyst milky contents - fluid and sperm filled cyst around epididymus

hydrocele

collections of fluid surrounding entire testicle

varicocele

dilated veins that increase with increases in abdominal pressure

how can you differentiate between hydrocele and spermatocele (epididmyal cyst) ?

the only way is through apsiration (sperm inside) clinically unable to

where is an epididymal cyst (spermatocele)

``` at the (in the) head of the epididymis above and behind the testis ```

describe the lump of an epididymal cyst

- smooth - well defined - small (often Asymptomatic. painful if large) - often multiple - often bilateral

epididymal cyst investigations

- Transilluminate the area - bright light will pass through as it is fluid - Scrotal ultrasound - Examination --Above and behind the testis

epididymal cyst treatment

Treatment not usually necessary | Surgical excision if painful /symptomatic

hydrocele causes

- by excessive production of fluid within the sac, e.g. secondary hydrocele - through defective absorption of fluid - by interference with lymphatic drainage of scrotal structures as in case of elephantiasis - by connection with a hernia of the peritoneal cavity in the congenital variety, which presents as hydrocele of the cord

hydrocele presentation. describe the lump

- no pain, unless it is infected - Scrotal enlargement - non-tender, smooth, cystic swelling - Testes normally palpable unless hydrocele v large - lump is Anterior and below testis

hydrocele investigations

- It transilluminates - Ultrasound - Examination- anterior and below testis

hydrocele treatment

- Resolve spontaneously, most by 2y old - Therapeutic aspiration (avoid rupture) - Surgical removal

haematocele is a complication of which scrotal disease

hydrocele

varicocele - which side is more common and why

L | Due to angle left testicular vein enter left renal vein

varicocele age

rare under 10 | increase in incidence after puberty

varicocele pathophysiology and causes

Abnormal dilation of testicular veins in the pampiniform venous plexus, caused by venous influx - Venous influx to pampiniform plexus (which is the venous network draining testis and epidiymis - Due to increased reflux due to compression of renal vein eg kidney tumour - Lack of effective valves between testicular and renal veins -- backlog

varicocele presentation

- Visible distended scrotum blood vessels - “bag of worms” - Scrotum hangs lower on side of the varicocele - May see dilated veins - these will be palpable too - dull ache /scrotal heaviness

varicocele investigations

examination Venography Colour doppler ultrasound- see blood flow

what is the varicocele treatment and when to use

Surgery | - if pain, infertility or testicular atrophy

GU middle tier Flashcards

(45 cards)