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URI 2 > Congenital And Neonatal Abnormalities > Flashcards

Congenital And Neonatal Abnormalities Flashcards

1
Q

What is the normal embryolical development of the adult kidney? How can this lead to incontience?

A

Embryology we have a primitive bladder. Mesonephric duct – dont worry!

Just remember; as embryo develops there are three stages and the mesonephros is the 2nd stage.

Long term stages - Kidneys form and meet with the bladder from the ureteric bud

Mesonephric is form primitive mesonephors – most important for males! Some of these retain and form their sex organs.

Anything that goes wrong here e.g. trigone or ureter = presentation in the neonate!

If the ureteric buds don’t form in the right place can cause problems.

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2
Q

Where are congenital abnormalities usually seen?

A

Small animals

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3
Q

Why might we not see congenital problems until adults?

A

•some diseases are progressive and clinical signs are not seen until the animals is an adult

–Dysfunction which builds up over life

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4
Q

What shoudl you do if you suspect a congenital abnormality?

A

•Check breed related information and advise breeder accordingly

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5
Q

What are the 2 types of congenital abnormalities?

A
  1. Structural anomalies (something physically changed) e.g.

–Absence of kidney

–Glomerulopathy due to abnormal collagen in basement membrane

  1. Functional anomalies (going wrong in urogenesis leading to other problems to occur) e.g.

–Impaired tubular reabsorption in Basenjis

–Hyperuricuria in Dalmations

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6
Q

What are structural abnormalities?

A

•Related to problems during embryonic development

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7
Q

What are the 4 classifications of structural abormalites?

A

•Agenesis (don’t happen), hypoplasia (form at an impaired rate), dysplasia (don’t form as they should) and aplasia can affect any part of the urinary tract

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8
Q

What are clinical signs of structural abnormalities related to?

A

Structure affected

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9
Q

What is this?

A

Renal dyplasia

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10
Q

Name examples of structural abnormalities? (4)

A

•glomerulopathies, nephropathies, polycystic renal disease, amyloidosis

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11
Q

Which structural abnormality happens later in life and why is this?

A

–Some conditions are progressive -> late onset signs (e.g. 1-6 years for amyloidosis)

•Need enough time for the condition to occur and start affecting the animal

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12
Q

What is this? What is the problem with it?

A

Polycystic – cat;

Impair most of the kidney – animal
will be affected

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13
Q

What is this and where is it seen?

A

Pig - cyst - often seen at PM

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14
Q

What is this?

A

Dog cysts

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15
Q

What is this? What else can we use U/S for?

A

Renal Cysts
Could also look for structural changes, and then also biopsies.

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16
Q

What is a main structural abnormaility and what causes the main clinical signs?

A

•Glomerulopathy (mainly glomerulus affected). Primary problem with filtration! Things which should remain in the animal plasma will start to appear in the urine.

–Main clinical sign ->proteinuria

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17
Q

How can you definitively diagnose glomerulopathy?

A

Biopsy

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18
Q

What breeds are affected by glomerulopathy?

A

–Bernese Mountain Dogs, Cocker Spaniels, Samoyeds, Dobermanns and Rottweilers

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19
Q

What is the difference between the genetics of samoyeds and cocker spaniels with glomerulopathy?

A
  • Samoyeds – genetic disorder inherited as X-linked dominant gene
  • English Cocker Spaniels – autosomal recessive trait
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20
Q

What is this and what can happen?

A
  • Disseminated changes in the kidney
  • Biopsy: Generalised wide spread changes, dilated tubules, protein in the tubules pathologist can tell you it is an immature glomerulus!
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21
Q

What functional abnormalities are there? (3)

A

–Fanconi’s syndrome (impaired tubular resorption)

•Things like iron channels aren’t effective

–Primary renal glucosuria (resorption defect)

–Cysteinuria, hyperuricosuria and xanthinuria (all predispose to urolithiasis)

•Related to metabolism of protein and minerals

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22
Q

How common are ectopic urters?

A

•Common congenital abnormality in dogs

–Second most common cause of incontinence in the bitch

•Less common in cats, seen occasionally in large animals

–Sub clinical- may or may not notice

–Large animals may not live long enough for it to be seen as a problem

•More common in females vs. males

–Due to uteric buds coming out of the embryonic bladder (normal ureter at trigone)

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23
Q

What is an exctopic ureter?

A
  • Normal ureters terminate at trigone
  • Ectopic ureters bypass trigone and terminate distal to this, usually in urethra

–Females: urethra, vagina, cervix

–Males: urethra, vas deferens, seminal vesicles

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24
Q

Define intramural ectopic ureters and where is it most common?

A

–nter bladder wall normally but tunnel distally along wall to urethra or vagina

•Discharge is distal to sphincter, not discharging urine into bladeder!

–Most common presentation in dog

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25
Q

Define extramural ectopic ureters

Where is it most common?

A

–Bypass bladder to enter more distally (doesn’t even enter bladder, around the bladder and enters the urethra or other structure at a distal point)

–Most common presentation in cat

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26
Q

Where are ectopic ureters usually unilateral?

A

Females

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27
Q

What can be seen here?

A

Cut open bladder

Yellow – normal bladder boundary

Then wires have been used to catheterise.

Can see the opening is not in the normal boundary

Discharge urine beyond boundary = urinary incontinence and not contained in the bladder

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28
Q

What is the presenation of ectopic ureters in:

Large animals?

Dogs?

Cats?

A
  • Large animals: rare congenital defect, reported horses, cattle and sheep
  • Dogs: mainly mixed breed, some breed disposition identified
  • Cats: no breed / familial predisposition
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29
Q

What are the clinical signs of ectopic ureters?

A

•Clinical signs are urinary incontinence

–Ureter not discharging where it should for the animal to voluntary expel

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30
Q

If you find an ectopic ureter how can we diagnose?

A

•Check for other developmental or acquired abnormalities of urogenital system (as lots of other things can go wrong and be associated)

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31
Q

How can we diagnose ectopic ureters? (4)

A

•contrast radiography, urethroscopy, vaginoscopy and cystoscopy in large animals

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32
Q

What is this image showing?

A

Ectopic ureter
Depending on ureter termination can get secondary changes so should evaluate other structures
Bottom kidney – terminating in abnormal position and urine able to leak out (kidney perfectly functional)
If there Is an obstruction = back up! Hydro ureter. Pressure build and back into kidney which will enlarge.

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33
Q

How can we treat ectopic ureters?

A

surgery

34
Q

What is this image showing?

A

Top:

  • Ureteral obstruction:
  • hydrouretes/Hydronephrosis (CANT EXPEL PROPERLY)
  • All kidney enlarged – compression
  • of medulla and cortex (unfunctional)

Bottom:

  • No obstruction:
  • Incontinence
  • (NORMAL KIDNEY FUNCTION)
35
Q

What is this?

A

Normal IVU and retrograde urethrogram

All contrast in bladder

36
Q

What is this?

A

Ectopic ureters

Ureters abnormal termination and size

37
Q

What is the umbilicus?

A

•connection between the fetus and mother

38
Q

What is the umbilical vein and what happens to it when the animal is born?

A

–Umbilicial vein = source of oxygenated blood passing from dam to fetus (via liver)

–When animal born forms falciform ligament / round ligament of liver

39
Q

What is the umbilical artery and whay are the remnants when born?

A

–Umbilical arteries (paired) = branches of external iliac arteries carrying waste material from fetus to dam

–When regress forms round ligaments of bladder

40
Q

What is the urachus and what happens when the animal is born?

A

–Urachus = connection from fetus bladder to allantoic sac

–Forms scar on the apex of the bladder

41
Q

What can go wrong with the umbilicus and urachus? (3)

A
  1. Body wall does not close -> umbilical hernia
  2. Umbilical structures becomes infected -> umbilical abscess (if local) but can track up through the abdominal cavity. Important to evaluate the extent of the infection e.g. arteries/veins
  3. Urachus (bladder to umbilicus) does not close -> patent urachus (persistent communication between bladder apex and urachal remnant). Urinary continent (slightly different) – bladder leak down urachus and directly out the umbilicus
42
Q

What are the differentials for umbilical swellings? (3)

A

–Simple or strangulated hernia

–Umbilical abscess

–Patent urachus

43
Q

How can we differentiate the umbilcal swellings?

A

•Differentiate on history, clinical signs, clinical pathology (haematology/biochemistry) and ultrasonographic findings

44
Q

What are the different hernia sizes and the meaning of them?

A

–Small hernia – tend to regress and less likely to let abdo contents out (1 finger)

–Medium – can get intestine through (concern) (2-3 finger)

–Large – least likely to mend by conservative! But large enough to let out – means you can get it back in. (thumb)

–Anything larger – very unlikely to heal and would need surgery to cosmetically heal

45
Q

Where is Infection and persistent urachus uncommon?

A

Small animals

(common in large)

46
Q

What is seen with an umbilical hernia and what is it?

A

•Soft tissue swelling in ventral abdomen at site of umbilicus

–Usually present since birth

–Can increase or decrease in size over time

  • Simple hernias have no heat, pain or oedema on palpation, and can be reduced into abdomen
  • Contain intestine, omentum or other abdominal organs on ultrasound

–Strangulated hernias contain trapped and compromised tissue

–Strangulation – terminal unless surgery

47
Q

What can cause congenital hernias?

A

•Congenital hernias do have a hereditary component in large and small animals

48
Q

What is the effect of a simpel hernia?

A

No effect on the animal, apart from cosmetic appearance

49
Q

How can an animal get an acquired hernia? (3)

A

secondary to infection, trauma or surgery

50
Q

What are umbilical infections associated with?

A

•Associated with localised or systemic infection

–acquired lesions (not present at birth)

51
Q

What are the 3 ways infections can spread along umbilical structures?

A

–Omphalophlebitis – sepsis of umbilical veins (tracks to liver)

–Omphaloarteritis – sepsis of umbilical arteries (tracks along round ligaments)

–Urachal sepsis – sepsis of urachus (tracks to bladder)

–Anywhere between 1 and 3 of the above organs can be affected.

52
Q

What is seen with umbilical infections/abscesses? How can we diagnose this?

A

–Infection = heat, pain, oedema and cellulitis

–Other systemic signs (pyrexia, joint infection)

–+/- discharge

–Ultrasonography: encapsulated soft tissue mass, with flocculent fluid (pus) or gas. Determine the structures.

–Knowing where the 3 structures go to allow us to workout where it tracks to

53
Q

How can we treat an umbilical infection?

A
  • Assess and correct underlying cause (failure of passive transfer, hygiene and management)
  • Medical treatment (systemic antibiotics) for localised infection only

–Must monitor for and identify other problems (septicaemia, joint infection, hepatic abscesses) as result of the primary in the umbilical system.

•Surgical treatment

–Where infection has spread back into the abdo structures

–Cases not responding to medical treatment, surgery is indicated

–Must excise or marsupialise entire extent of infection

•We want the infection that is inside and bring it out. Where is can effectively drain and not spread.

54
Q

When is a patent urachus seen and what signs are shown?

A
  • Present at birth (may not be noticed initially)
  • Dribbling of urine from umbilicus

–(uncommon but possible to have no drainage and uroperitoneum into the peritoneum itself). Think of this in the animal with fluid and extending abdomen.

55
Q

what might a patent urachus be associated with?

A

Umbilical infection

56
Q

What can be seen in foals with a patent urachus?

A

•frequent posturing/straining to urinate

57
Q

What can a patent urachus persist as?

A

•Some may persist as a cyst or urachal diverticulum in the bladder

58
Q

What diagnostics do we need to do for a patent urachus? (2)

A

•Ultrasound or contrast radiography (dogs and cats) to identify extent of problem and other structures involved

59
Q

How can we treat a patent urachus?

A
  • Leave to resolve (very young animals)
  • Local treatment for non-infected conditions (clamps, astringent agents which will promote an inflammatory response e.g. 7% iodine, silver nitrate applicators in large animals)
  • Medical treatment:

–Broad spectrum antimicrobial treatment/prophylaxis, ideally based on culture and sensitivity

•Surgical treatment:

–Resection back to bladder (closing over the apex scar)

–Treat any other associated problems (sepsis of other structures, uroperitoneum)

60
Q

What can cause uroperitoneum? (3)

A
  • Patent urachus
  • Damage to ureters or urethra
  • Bladder rupture or perforation
61
Q

What is the most common cause of uroperitoneum in large animals?

How and where does it happen?

A

–Most common cause in large animals = bladder rupture

  • Common site is dorsal bladder wall
  • Can be spontaneous
  • Can be result of trauma / moving animal
62
Q

What can the effect of a urachal infection be on the bladder wall?

A

–Urachal infection can compromise bladder wall (weakens it and more likely to rupture secondary to other things)

63
Q

How can a bladder rupture happen in adults? (4)

A

–Bladder rupture can occur secondary to trauma (e.g. blunt trauma such dogs failing to jump into car), RTA, sepsis or neoplasia

–Bladder rupture can occur secondary to obstruction (usually urethral e.g. urolithiasis in male sheep, goats and cats)

•Male sheep and goats – especially those having a bad diet. Ewe diets are not appropriate for the males due to minerals!

64
Q

What is this?

A

Bladder rupture

65
Q

What are the signs of a ruptured bladder? (7)

A

–Fluid distension of the abdomen

–Fluid thrill on palpation

–Unable to palpate bladder (if ruptured)

–Peritonitis (abominal pain, ileus)

–Dehydration

–Acid-base and electrolyte imbalances (cardiac arrhythmias)

•Severe secondary complications

–Decreased urination

66
Q

What additional signs of bladder rupture are seen in neonates? (4)

A

•lethargy, not suckling, collapse, sepsis

67
Q

Will an animal still pass urine with a bladder rupture?

A

•Some animals can still pass small volumes or urine, and a small bladder may be visible on imaging

68
Q

How can we diagnose a ruptured bladder? (7)

A

•Aspiration of peritoneal fluid

–Smell (normal fluid shouldn’t have an odour), presence of urea and creatinine (ratio peritoneal:serum creatinine > 2:1)

•Ultrasonography or contrast radiography to confirm peritoneal effusion and defect in bladder

–Contrast into abdo on retrograde urethrogram

•Other findings:

–Uraemia

–Dehydration

–Electrolyte abnormalities

–Hyperkalaemia – most important

–Hyponatraemia, hypochloraemia

69
Q

How is the normal cell membrane potential maintained?

A

Think of every cell as a pumpkin… Pump K+ in

Cells are pumpkins

A normal cells pumps potassium in

Problem with this – cells die

98% of potassium is in cell, 2% in ISF and blood

Na is outside the cell… we need to maintain the balance

Inappropriate concentration of Na or K – kidney is responsible to deal

If kidney cant excrete = build of K = problems

Need Na outside and K inside for the cell membrane potential

Cl and P adds to it – but not as important

Start changing concentration – change membrane potential

Gets bad if it affects cardiac potential

70
Q

What is potassium regulation determined by?

A

•Potassium regulation is determined by renal excretion

–K+ excreted = K+ filtered - K+ reabsorbed + K+ secreted

71
Q

What is the effect of bladder rupture on potassium?

A

•Bladder rupture: animal is unable to excrete potassium

–The 2% will build up

•Potassium also reabsorbed through peritoneal membrane which can lead to hyperkalaemia

72
Q

What are the clinical effects of hyperkalaemia? (3)

A
  • Potassium is the major intracellular cation (sodium extracellular)
  • Difference between intracellular and extracellular concentration determines resting membrane potential of excitable tissues (inc. cardiac conduction)
  • Potassium uptake into cells is linked with glucose uptake as a co-transporter
73
Q

What is the normal membrane potential?

A

Where they should be!

Start putting more potassium – more positive resting membrane and changes likelihood of firing

74
Q

What are the cardiac affects of hyperkalaemia of a ruptured bladder?

A
  • Potassium important in cardiac conduction cycle
  • Increasing levels cause ECG abnormalities

–Changes in t wave – repolarisation of cardiac muscle.

–Less of a difference – cant repolarise as well

–Hyperkalaemia - ends to get change in shape – prolonged

–S hyper kalaemia progresses; P disappearance, QRS turn into smooth rather than spikey

–atrioventricular conduction disturbances ->VPDs-> ventricular fibrillation -> death

–Get bradycardia

•No exact value where the cardiac affects happens. Conc around 5.. But cant say at certain numbers things happen! We just know bad things happen if left but cant say when!

75
Q

What do we do if there is hyperkalaemia associated with uroperitoneum?

A

Treat immediately; EMERGENCY

76
Q

What do we do with an anaesthetic and bladder rupture?

A

•Hyperkalaemia must be stabilised prior to attempting any anaesthesia or surgery to correct the bladder rupture

77
Q

How do we treat ruptured bladder? (4)

A
  1. Correct hydration and electrolyte imbalance
  2. Treatment uroperitoneum (drain with care don’t want to remove really fast, flush)
  3. Surgical treatment of bladder defect
  4. Post-op fluid therapy, anti-inflammatories and antibiotics
78
Q

What fluid therapy do we give for a ruptured bladder?

A
  • Avoid fluids containing potassium
  • 0.9% saline best option
  • Lactated Ringers has potassium, but does correct acidosis (has bicarbonate so can help with this complication of acidosis)
  • Bolus administrations:

–Dogs max rate of 60-90 ml/kg/hr

–Cats max rate of 40-60 ml/kg/hr

•Maintenance rates 2-4ml/kg/hr

–Foal maintenance 5-10ml/kg/hr

79
Q

How can we treat hyperkalaemia? (2)

A

•Calcium gluconate

–Functional antagonist of potassium

–Stabilises membrane excitability by affecting K on outside of cell

–Short duration of action: 20-30 minutes

•Dextrose/glucose and insulin

–Drives K into cells as taken up with glucose

–Pushing glucose in – takes potassium with it. Uses the co-transporter.

80
Q

What must we do alongside as well as treating the hyperkalaemia?

A

Must monitor acid-base status as well as treating hyperkalaemia! The animal cannot deal with this well and develop acidosis

81
Q

What is different about the renal function of the neonate?

A

•Neonate has a limited ability to alter renal function

–Glomerular filtration rates and renal blood flow are reduced in the neonate (adult function from 10 weeks in puppies and kittens)

–Limited ability to respond to changes in ECF (dilute and concentrate urine)

–Limited ability to respond in acid-base imbalances

–Neonate has a high body water concentration, due to small amounts of body fat (80% neonate body weight = water vs 60% in adult)

82
Q

What is the effect of a neonate with fluid therapy?

A
  • All this means that they are predisposed to hypovolaemia and have a poor ability to respond to fluid, electrolyte and acid-base imbalance
  • Fluid therapy needs to be accurate and regularly monitored

URI 2 (44 decks)

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