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phase 2a mine > GU middle tier > Flashcards

GU middle tier Flashcards

1
Q

nephritic syndrome pathophysiology

A
  • 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
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2
Q

nephritic syndrome investigations/ symptoms

A

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

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3
Q

nephritic syndrome causes

A

AAV (ANCA associated vacilitis, small vessel)

goodpastures disease (acute, autoimmune)

SLE, systemic sclerosis

IE

upper resp tract infection

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

viral (hepB/C, malaria)

bacterial (MRSA)

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4
Q

Nephritic syndrome treatment

A

Treat underlying disease

Recovery happens spontaneously

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5
Q

nephrotic syndrome pathophysiology

A
  • 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)
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6
Q

nephrotic syndrome symtpoms

A

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
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7
Q

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

A

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
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8
Q

what is the most common secondary cause to nephrotic syndrome

+ others

A

diabetes

hepB/C
SLE
drugs/toxins
amyloidosis
RA
malignancy
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9
Q

nephrotic syndrome treatment

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

if membranous, immunosup

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10
Q

glomerulonephritis = aka

A

nephritic syndrome!!

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11
Q

nephrotic vs nephritic

A

nephrotic has higher proteinuria !

nephritic also has capillary damage –> blood loss!

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

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12
Q

uraemia symptoms

A

uraemia = high serum urea

anorexia
pruritus (itchy) rash
lethargy
nausea

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13
Q

what does frothy urine indicate?

A

high protein

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14
Q

dominant polycystic kidney disease

  • penetrance high/low
  • commoness
  • gender
A

high penetrance
common
m>F

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15
Q

is dominant/recessive polycystic kidney disease more common

A

dominant

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16
Q

dominant/recessive polycystic kidney disease age of presentation

A

dom - largely 20 onwards

rec - infancy

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17
Q

which genes are affected in dominant/recessive polycycstic kidney disease

A

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

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18
Q

dominant polycystic kidney disease pathophysiology

A
  • 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
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19
Q

recessive polycystic kidney disease pathophysiology

A

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.

20
Q

dominant polycystic kidney disease progression

A
  • 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
21
Q

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

A
  • Liver/pancreas - have cysts but function unaffected
  • Heart - valve disorders
  • brain/vessels - berry aneurysms → subarach haem
22
Q

recessive polycystic kidney disease symptoms

A
  • Enlarged kidneys
  • Renal cysts
  • Hepatic fibrosis– Portal hypertension
  • Kidney failure
23
Q

polycystic kidney disease investigation including diagnosis

A

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

24
Q

polycystic cysts management

A

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

25
Q

what is a testicular lump until proven otherwise?

A

testicular cancer

26
Q

epididymal cyst age

A

rare in chilren

40y

27
Q

spermatocele =

A

= epididymal cyst

milky contents - fluid and sperm filled cyst around epididymus

28
Q

hydrocele

A

collections of fluid surrounding entire testicle

29
Q

varicocele

A

dilated veins that increase with increases in abdominal pressure

30
Q

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

A

the only way is through apsiration (sperm inside)

clinically unable to

31
Q

where is an epididymal cyst (spermatocele)

A 
at the (in the) head of the epididymis 
above and behind the testis
32
Q

describe the lump of an epididymal cyst

A
  • smooth
  • well defined
  • small (often Asymptomatic. painful if large)
  • often multiple
  • often bilateral
33
Q

epididymal cyst investigations

A
  • Transilluminate the area - bright light will pass through as it is fluid
  • Scrotal ultrasound
  • Examination –Above and behind the testis
34
Q

epididymal cyst treatment

A

Treatment not usually necessary

Surgical excision if painful /symptomatic

35
Q

hydrocele causes

A
  • 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
36
Q

hydrocele presentation. describe the lump

A
  • 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
37
Q

hydrocele investigations

A
  • It transilluminates
  • Ultrasound
  • Examination- anterior and below testis
38
Q

hydrocele treatment

A
  • Resolve spontaneously, most by 2y old
  • Therapeutic aspiration (avoid rupture)
  • Surgical removal
39
Q

haematocele is a complication of which scrotal disease

A

hydrocele

40
Q

varicocele - which side is more common and why

A

L

Due to angle left testicular vein enter left renal vein

41
Q

varicocele age

A

rare under 10

increase in incidence after puberty

42
Q

varicocele pathophysiology and causes

A

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
43
Q

varicocele presentation

A
  • 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
44
Q

varicocele investigations

A

examination
Venography
Colour doppler ultrasound- see blood flow

45
Q

what is the varicocele treatment and when to use

A

Surgery

- if pain, infertility or testicular atrophy

phase 2a mine (38 decks)

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