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BCS Lectures > Mark Nelligan BCS > Flashcards

Mark Nelligan BCS Flashcards

1
Q

Classification of CKD

A

see slide 5 of 2- progressive kidney disease lecture

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2
Q

Define rapid deterioration of renal function

A

Rapid deterioration defined as a fall in GFR of

> 5mLs/min/1.73m2 in 1 year

or
> 10mLs/min/1.73m2 in 5 years

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3
Q

Cause of deterioration of kidneys

A
  1. Lose adaptability
  2. Fail to excrete fluid load promptly
3.Fail to reduce urine volume in hypovolaemia promptly = DEHYDRATION Haemorrhage
Hypotension
Surgery
Reduced Cardiac Output
Sepsis
  1. Nephrotoxicity (NSAID’s, IV Contrast, etc)
    - Worse in Diseased Kidneys
    - Reduced Ability to Recover
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4
Q

Ist line Mx of HTN to prevent renal failure

A
  1. Angiotensin blockade (unless CI) eg. hyperkalaemia

2. Then move to ACE or CCB

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5
Q

1st line Mx of diabetic neuropathy (CHECK THIS WITH GREY BOOK AND NICE)

A
  1. Control HTN (130/80)
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6
Q

Tx of acidosis and justification

A

Sodium biocarbonate

Reduces Hyperkalaemia

Reduces Calcium Loss from Bone

Improves Catabolic State

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7
Q

Tx of hyperphosphatemia and justification

A
  1. Deranged Calcium, VitD, PTH

Normal Serum Phosphate

Reduces Renal Osteodystrophy

Reduces Calcium Loss from Bone

Improves Catabolic State

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8
Q

Dietary modifications in renal failure

A
  1. Protein Restriction 0.8 g/kg/day
  2. Avoid Ultra-Low Protein
  3. Calorie Supplements

No-Added Salt
- Sodium 60-90 mmol/day, Sodium Chloride 3.5-5 g/day

Reduced Protein

  • Chronic Renal Failure 0.8 g/day
  • Haemodialysis/CAPD 1.2 g/day

Reduced Phosphate
- <1000 mg/day

Low-Potassium Diet
- Potassium 40 mmol/day

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9
Q

Options or end stage renal failure

A
  1. End of life care
  2. Transplanatation
  3. Haemodialysis
  4. Peritoneal dialysis
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10
Q

What does dialysis `achieve

A
  1. Removes nitrogenous wastes/toxins
  2. Corrects electrolytes
  3. Removes water
  4. Corrects acid base abnormalities
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11
Q

Difference between dialysis and haemofiltration

A

Haemofiltration Blood is filtered across
a highly permeable membrane, allowing
movement of large and small solutes by
convection at almost the same rate. The
ultrafi ltrate is replaced with an equal volume
of fl uid, so there is less haemodynamic
instability. It is used in critically ill patients
for this reason, but is impractical as longterm
RRT, as it takes much longer than HD to
achieve the same clearance.

Haemodialysis removes solutes by diffusion. As such, it is relatively inefficient for solutes of high molecular weight as clearance by diffusion is inversely related to the molecular weight of the solute.

Haemofiltration removes solutes by convection. As such, efficiency remains more constant for all solutes able to cross the semi-permeable membrane.

The choice between haemodialysis and haemofiltration can be difficult. Points in favour of haemofiltration include:

better control of blood pressure
less risk of hyperlipidaemia
Those in favour of haemodialysis:

less expensive
technically easier
toxicity of molecules of high molecular weight has yet to be demonstrated
haemofiltration can only reduce, not normalise, the concentration of larger solutes

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12
Q

Advantages of haemodialysis

A

Good Clearance of small molecules

Very Efficient and Adjustable

Patient Freedom between Sessions

Does not cause Domestic Strain (Centre HD)

Acceptable to Patients

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13
Q

Disadvantage of haemodialysis

A

Expensive, Labour-Intensive, Capital-Intensive

Vascular Access

Intermittent Fluid Overload

Haemodynamic Instability during Dialysis
Restricted Fluid Intake

Poor Clearance of Phosphate

Poor Clearance of Middle Molecules

Malnutrition

Restrictive Diet

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14
Q

Types of peritoneal dialysis

A
  1. Diffusion of Chemicals – ‘Dialysis’
- Concentration Gradient
In Both Directions
- Osmotic Gradient (hypertonic glucose)
- Endothelial Membrane with larger pores
- ‘Middle Molecules’
  1. Convection of Chemicals – ‘Ultrafiltration’
  • Transmembrane Hydrostatic Pressure does not exist
  • Convection - Solvent Drag
  • Endothelial Membrane with larger pores
  • Middle Molecules’
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15
Q

Advantages of peritoneal dialysis

A

Preserves Residual Renal Function (8 ml/min virtual GFR)

Haemodynamically Stable, less challenging

Better Clearance of Middle Molecules

No Potassium Restriction

Liberal Diet

Lesser/No Fluid Restriction

Home-Based, No Travelling, More ‘Own’ time

Bloodless, Painless

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16
Q

Disadvantages of peritoneal dialysis

A

Self-Administered or Dependent on Trained Helper

Peritonitis and its Complications

Sclerosing Peritonitis

Often Chronic Fluid Overload

Poor Clearance of Phosphate

Obesity

Technique Failure after a few years

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17
Q

How is kidney function measured

A

MDRD equations gives eGFR

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18
Q

Causes of end stage renal failure

A

Diabetic Nephropathy

Glomerulonephritis

Idiopathic

Systemic (SLE, Vasculitis, Blood Dyscrasia, other)

Hypertension

Adult Polycystic Kidney Disease

Reno-Vascular Disease

Vesico-Ureteric Reflux Nephropathy and Congenital Renal
Malformations CAKUT (‘Chronic Pyelonephritis’)

Other Hereditary Renal Diseases

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19
Q

Uremia related CV risk factors

A
  1. increased ECF
  2. Calcification
  3. PTH
  4. Anaemia
  5. ROS
  6. Malnutrition
  7. Pulse pressure
  8. TG’s and LP remnants
  9. Thrombogenic factors
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20
Q

Haemostatic Fx of the kidney

A

Fluid Balance & Euvolaemia

Excretion of Metabolic ByProducts

Degradation of Metabolic ByProducts, Peptides

Regulation of Chemical Composition of Plasma/ECF

Maintenance of Normal Osmolality

Acid-Base Balance

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21
Q

Hormonal Fx of the kidney

A

HORMONAL

  1. Endocrine
    - Renin secretion
    - Erythropoietin (HIF, Peritubular Cells)
    - 1-α Hydroxylation of 25(OH)VitD3
  2. Paracrine
    - Angiotensin II production
    - Prostaglandin (PGI2, PGE2)
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22
Q

Haemostatic pathogenesis in renal failure

A

Accumulation of ‘Middle Molecules’ – ‘Uraemia’

Accumulation of Metabolic ByProducts (potassium,
phosphate, urate, oxalate, urea, creatinine)

Electrolyte Abnormalities

Acidosis

Oedema (Peripheral/Pulmonary) or Dehydration

Hyperlipidaemia

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23
Q

Compications of chronic renal failure

A

CKD1
No complications
CKD2
Increased CVD

CKD3
Increased CVD; Bone disease - raised PTH

CKD4
CVD, Anaemia, Bone disease - low Ca, high PO4

CKD5
CVD, Anaemia, Bone disease, Pruritus, Bleeding, Malnutrition

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24
Q

Symptoms of chronic renal failure

A
  1. Uraemic Muddy Colour:‘Urochrome’
  2. Severe Hypertension: Cardiac Failure, Headache, cerebrovascular Events,
  3. Fluid Overload : Peripheral Oedema, Ascites
  4. Pulmonary Oedema: Dyspnoea, Orthopnoea
  5. Hyperkalaemia: Cardiac Arrest, Diarrhoea,Peripheral Paralysis
  6. Diarrhoea, Vomiting: Gastritis, Hypermotility
  7. Peripheral Neuropathy :‘Middle Molecules’
  8. Encephalopathy, Coma: ‘Middle Molecules’, Urea
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25
Q

Cause of failure of hormonal control in CRF

A
  1. Hypertension
    Renin-Driven
  2. Anaemia
    Erythropoietin deficiency

3.Proximal Myopathy
↓ 1,25(OH)2VitaminD3, ↑ PTH

  1. Pruritus
    ↑ PTH, ↑ PO4, Iron deficiency
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26
Q

Importance of potassium in CRF

A

Hyperkalaemia in CRF

  • Reduced GFR
  • Acidosis (competition with H cations at Collecting Duct)
  • Acidosis (competition with H cations as ICF cation)
  • Fluid Overload Suppresses Aldosterone Release
  • ANP Digitalis-like Effect on the Na/K CounterTransporter

Iatrogenic Hyperkalaemia

  • ACE Inhibitors
  • Angiotensin II Receptor Blockers
  • Aldosterone Antagonists
  • β-Blockers
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27
Q

Causes of acidosis in CRF

A

Reduced GFR
►►Retained Acids (Phosphate)

Low Serum Bicarbonate
- Reduced Renal Mass – Tubular Cells
►►Reduced HCO3 Regeneration in Proximal Tubule
►►Reduced H Cation Secretion in Proximal Tubule
►►Reduced Hydrogen Secretion in Collecting Duct
►►Reduced Ammonia Production

Reduced Buffering

  • Reduced Haemoglobin
  • `High Phosphate
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28
Q

Consequences of acidosis

A

Hyperkalaemia

Hydrogen Cations Replace and Expel Calcium from Bone

Protein Catabolic Effect

Dyspnoea

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29
Q

What does the presence of casts in the urine indicate?

A

Haematuria/pyuria is of glomerular or renal tubular origin

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30
Q

Would bladder cancer or kidney stones have casts?

A

No cast but would have haematuria

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31
Q

Would acute cystitis have casts?

A

No casts, but would have pyuria

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32
Q

What do RBC casts indicate?

A
  1. Glomerulonephritis

2. Malignant HTN

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33
Q

What do Fatty casts (oval fat bodies) indicate?

A

Nephrotic syndrome (assoc. with maltese cross sign)

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34
Q

What do WBC casts indicate?

A
  1. Tubulointerstitial inflammation
  2. Acute pyelonephritis
  3. Transplant rejection
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35
Q

What do brown muddle casts indicate?

A

Acute tubular necrosis

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36
Q

What do waxy casts indicate?

A

1.ESRD/CRF

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37
Q

Normal and nephrotic range for 24 hour urinary protein

A

Normal <150 mg

(pregnancy <300 mg)

Nephrotic range >3g

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38
Q

Treatment of hyperkalemia?

A

Treatment in non-urgent cases
• Treat the underlying cause; review medications.
• Polystyrene sulfonate resin (eg Calcium Resonium® 15g/8h PO) binds K+ in the gut,
preventing absorption and bringing K+ levels down over a few days. If vomiting
prevents PO administration, give a 30g enema, followed at 9h by colonic irrigation.
If there is evidence of myocardial hyperexcitability, or K+ is >6.5mmol/L, get senior
assistance, and treat as an emergency (see p849).

Treatment for urgent hyperkalaemia:
1 Stabilize cardiac membrane with 10mL 10% calcium gluconate
2 Drive K+ into cells with 10units actrapid in 50mL 20% glucose

  • Stop all potassium-retaining/containing drugs where possible and arrange dietary
    review of potassium in diet where appropriate.
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39
Q

Treatment for anaemia

A

EPO and Iron

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40
Q

What are the causes and features of uremic syndrome

A

Cause:
Accumulated products of protein catabolism, Urea usually excreted from the kidney - in renal failure it is not so builds up in the blood

Features:

  1. Pruritus
  2. Peripheral Neuropathy
  3. Encephalopathy
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41
Q

Cause of platlelet dysfunction and haemorrhage in CRF

A

Uremia interrupts the binding of platlets resulting in haemorrhagic state

Platelet dysfunction and haemorrhage

Inhibition of platelet adhesion

Defective vWF receptor ligand

Bleeding time is useful

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42
Q

Cause of prothrombotic tendency in CRF

A

Protein C/S functional deficiency

Increased homocysteine

Inadequate tPA

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43
Q

wHAT TYPE OF CONDITION EFFECTING pth DOES crf LEAD TO?

A

Secondary hyperparathyroidism

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44
Q

Consequences of calcium dysregulation

A

Periarticular calcification

Blood vessel wall calcification

Proximal Myopathy

Calciphylaxis

Calcification of the heart

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45
Q

Symptoms of bone changes due to calcium dysregulation

A

Proximal Myopathy

Bone pain – backs, hips, legs

Joint pain

Fractures

Poor mobility

Growth retardation, deformities, child

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46
Q

Features of osteodystrophy

A

Osteitis Fibrosa Cystica: increased PTH

Osteomalacia: defective Mineralisation

Adynamic Bone Disease: low bone Turnover (low PTH)

Osteoporosis: defective bone Formation

Aluminium-Induced Calcification Failure (Newcastle
Disease – Pathological Fractures)

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47
Q

Mx of bone disease in CKD 3/4

A
  1. High PTH: Start 1a caldiol then repeat Ca2+, phospahte and PTH
  2. If still high Calcium and Low PTH stop 1a calcidiol
  3. If High PO4: PO4 restriction or calcium based PO4 binders
  4. If low Vit D: Start Vit D
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48
Q

What is the vertebral level of the kidneys?

A

T12 - L3 - they are protected by the thoracic ribs but or not in thoracic cavity as they are below the level of the diaphragm

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49
Q

How many lobes per kidney?

A

5-11

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50
Q

What are the origins of the renal pelvis?

A

Superior part of the ureter. Branches to firn two or three major calices - each of which divide again to form minor calices which collect urine from papillae of kidneys

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51
Q

Innervation of the kidney

A

Vagus (PNS) through coeliac plexus - allows RA and RV dilation

T10-L1 (SNS) - constricts RA and RV

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52
Q

Location of nephrons in the kidney

A

See slide 12 of renal anatomy lecture

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53
Q

Significance of septum between adrenal gland and kidneys?

A

Prevents damage to adrenal gland in renal transplantation

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54
Q

Site for transplanting a kidney?

A

Iliac fossa of the greater renal pelvis

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55
Q

Which structure joins the ext. iliac a.

A

RA

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56
Q

Which structure joins the ext. iliac vein

A

RV

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57
Q

What does the ureter pass over anteriorly?

A
  1. Psoas major

2. Genitofemoral nerve

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58
Q

Which structures is the left ureter related to?

A
  1. sigmoid colon,
    gonadal vessels
  2. left colic branches of inferior
    mesenteric artery.
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59
Q

What structures is the right ureter related to?

A
  1. descending (2nd
    part) duodenum,
  2. terminal ileum,
  3. root of the
    mesentery,
  4. gonadal vessels,
  5. right colic and
    ileocolic branches
  6. terminal part of the
    superior mesenteric artery.
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60
Q

At which landmark does the ureter cross medially

into the pelvis?

A

Ext. iliac or common iliac vessels

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61
Q

Blood supply of the ureters

A

Proximal (near renal pelvis): Ureteric
branches from renal artery.
• Middle (most of abdomen) Ureteric
branches from gonadal arteries.
• Distal (near urinary bladder) ureteric
branches off inferior vesical artery (which
is a branch of the internal iliac artery).

62
Q

Ureteric anatomical constriction sites and their clinical significance

A
  1. ureteropelvic junction (UPJ)
  2. crossing of the common iliac/external iliac
    vessels at pelvic brim
  3. where the ureters enter the wall
  • Ureteric calculi may cause complete or
    intermittent obstruction of urinary flow at these
    sites.
63
Q

Layers of the ureters

A 
MUCOSA
– Transitional epithelium (for
expansion)
– Lamina propria (has elastic
tissue to recoil)
• MUSCULAR LAYER (smooth
muscle)
– Inner longitudinal
– Outer circular
• ADVENTITIA
– Provides protection, strength for
organs, and attaches ureters to
surrounding structures
64
Q

Features of ureteric calculus pain

A

severe rhythmic pain (ureteric colic) as it
is gradually forced down the ureter by waves of contraction.
• Depending on the level of obstruction, the pain may be referred to
the: lumbar region, hypogastric region, external genitalia or testis.
• The pain is referred to the cutaneous areas innervated by spinal
cord segments and sensory ganglia, which also supply the ureter
(mainly T11-L2).

65
Q

Difference in histology in ureter and bladder

A

Same except ureter has rugae in its mucosal layer to allow for expansion

66
Q

What is the trigone composed of and what is its fx?

A

the triangular region formed by the two ureteral orifices and the
internal urethral orifice. It is very sensitive to expansion (is always smooth to
limit expansion) and once stretched to a certain degree, the urinary bladder
signals the brain of its need to empty.

67
Q

Describe the anti-reflux mechanism of the bladder

A

The ureters pass obliquely through the bladder wall in an inferomedial direction.
An increase in bladder pressure presses the walls of the ureters together,
preventing the pressure in the bladder from forcing urine up the ureters.

68
Q

Blood supply of the bladder?

A

The bladder primarily receives its vasculature from the internal iliac vessels.

Arterial supply is delivered by the superior vesical branch of the internal iliac artery. In males, this is supplemented by the inferior vesical artery, and in females by the vaginal arteries. In both sexes, the obturator and inferior gluteal arteries also contribute small branches.

Venous drainage is achieved by the vesical venous plexus, which empty into the internal iliac vein (also known as the hypogastric vein).

69
Q

Nerve supply of the bladder

A

• Parasympathetic (S2-S4) are motor to detrusor muscle and
inhibitory to the internal sphincter.
• Sympathetic (T11-12, L1-2) cause constriction of internal
sphincter and inhibit the detrusor muscle.

70
Q

Histology and dx of urethra between men and women

A

Smooth muscle with inner mucosa
– Changes from transitional through stages to stratified squamous
near end
– Drains urine out of the bladder and body
• Male: about 20 cm (8”) long
• Female: 3-4 cm (1.5”) long
– Short length is why females have more urinary tract infections
than males - ascending bacteria from stool contamination

• Urethral sphincters
– Internal: involuntary sphincter of smooth muscle
– External: skeletal muscle inhibits urination voluntarily until proper
time (levator anni muscle also helps voluntary constriction)

71
Q

Go through case studies of Renal anatomy lectures - stavros

A

Go through case studies of Renal anatomy lectures - stavros

72
Q

Describe Paroxysmal Nocturnal Haemoglobinuria

A

Acquired life threatening disease where C’ attacks RBC’S. It may develop on its own (“primary PNH”) or in the context of other bone marrow disorders such as aplastic anemia (“secondary PNH”). Presents as blood in the urine in the morning in 26% of pts. (hence the name)

73
Q

What is located in the renal cortex?

A

Renal corpuscle (glomerulus and bowmans capsule) and tubules apart from the LOH. Also contain cortical collecting ducts

74
Q

What are the renal columns and what are their fx

A

The renal column (or Bertin column, or column of Bertin) is a medullary extension of the renal cortex in between the renal pyramids. It allows the cortex to be better anchored.
Each column consists of lines of blood vessels and urinary tubes and a fibrous material.

75
Q

Why do the pyramids have a striped appearance

A

The pyramids appear striped because they are formed by straight parallel segments of nephrons and collecting ducts.

76
Q

What is formed by the apex of a renal pyramid? What does this structure empty into?

A

Papilla. Drains into the minor calcyes then into the major calyces then to the renal pelvis then to the ureter

77
Q

What is the normal position for right and left kidneys?

A

T12-L3 - Right slightly lower than the left due to the presence of the liver

78
Q

Origin of the renal arteries

A

The kidneys are supplied with blood via the renal arteries, which arise directly from the abdominal aorta, immediately distal to the origin of the superior mesenteric artery.
Due to the anatomical position of the abdominal aorta (slightly to the left of the midline), the right renal artery is longer, and crosses the vena cava posteriorly.

Each renal artery enters the kidney via the renal hilum, dividing into segmental branches.

79
Q

Venous drainage of the kidney

A

The kidneys are drained of venous blood by the left and right renal veins. They leave the renal hilum anteriorly to the renal arteries, and empty directly into the inferior vena cava.

As the vena cava lies slightly to the right, the left renal vein is longer, and travels anteriorly to the abdominal aorta.

80
Q

Anomoly of renal pelves location in horseshoe kidney?

A

Normal posterior rotation of the kidney is prevented by the fusion resulting in the renal pelves becoming orientated anteriorly.

81
Q

What are areas do interlobar and interlobular arteries supply?

A

interlobar are between pyramids in the renal columns. Interlobular are the smaller branches in the renal cortex

82
Q

What structures are located within a renal lobe?

A

The renal lobe is a portion of a kidney consisting of a renal pyramidand the renal cortex above it

83
Q

Difference between normal and ectopic kidneys

A

Ectopic kidneys have blood vessels derived from the distal aorta and iliac artery, are smaller in size and have a short ureter. Prevalence is between 1:500 and 1:1200 cases.

84
Q

While the pelvic placement of the kidney in the above case was abnormal, the typical site for transplanting a kidney is in the iliac fossa. Why is this the case?

A

Shorter ureter and can connect transplanted kidney to iliac artery and vein

85
Q

To which parts of the skeleton are the kidneys normally related?

A

left = 11th and 12th rib

right 12th rib

86
Q

In a lumbar surgical approach to a normal kidney, which posterior abdominal muscles must the surgeon go through?

A

Psoas major
Quadratus lamborum
Transverse abdominis

87
Q

Which nerves are related posteriorly to kidneys in a normal position?

A

Subcostal
Iliohypogastric
ilioinguinal

88
Q

Significance of P wave and normal length

A
  • Atrial depolarisation
  • Waves travels inferiorly from right to left therefore lead II is positive whereas AvR is negative
  • Determines HR
  • Should not exceed 0.12 secs (3 small sq.)
89
Q

Significance of PR interval and normal length

A
  • Wave traveling from artia to ventricles via AV node and HIS-Purkinje fibres
  • Should be between 0.12-0.2 sec (3-5 small sq.)
  • If > this it suggests AV heart block
  • If < suggests extra conduction tissue
90
Q

Significance of QRS wave

A
  • Ventricular depolarisation
  • Determines axis
  • Should be 0.12 sec (3 small sq.)
  • If > suggests BBB
  • If in leads V1 and V2 (septal leads) more suggestive of RBBB
  • If in V5 and V6 (lateral left view) more suggestive of LBBB
91
Q

sIGNIFICANCE OF st SEGEMENT

A
  • Repolarisation
  • Elevation = infarction
  • Depression = ischaemia
92
Q

Significance of the T wave

A

Represents rapid phase of ventricular repolarisation

Normally positive in leads I, II, (III), aVL, aVF,V2-6 (i.e.
QRS-T concordance).

Most sensitive area for looking at ventricular disease
processes

If inverted = ischaemia.

If peaked = hyperkalaemia (potassium).

93
Q

Significance of QT interval

A

Length of interval varies with rate!

Prolongation can be:

Due to inherited conditions

Acquired e.g. due to drugs

When prolonged can cause of life-threatening arrhythmias

94
Q

Immune mechanisms underlie most forms of glomerular injury

A

 Antibody-mediated injury
 Cell-mediated immune injury
 Activation of alternate complement pathway

95
Q

Glomerular response to injury

A
  1. Cellular proliferation
     Mesangial or endothelial cells
     Leukocytic infiltration
     Formation of ‘crescents’ (accumulations of proliferating epithelial
    cells and infiltrating leukocytes)
  2. Basement membrane thickening
     Light Microscopy: Thickening of the capillary walls (PAS stain)
     Electron Microscopy:
     Deposition of amorphous electron dense material (most often
    immune complexes) on the endo- or epithelial side of the BM or
    within the glomerular BM itself.
  3. Glomerular scarring = ‘Sclerosis’
96
Q

Definition of diffuse glomerular injury

A

> 50% of glomeruli are involved

97
Q

Definition of focal glomerular injury

A

<50% of glomeruli are involved

98
Q

Definition of global glomerular injury

A

A whole glomerulus is involved

99
Q

Definition of segmental glomerular injury

A

Part of a glomerulus is involved (e.g. focal

and segmental glomerular sclerosis)

100
Q

Categories of glomerular diseases

A 
1. Primary Glomerulonephritis
 Kidney is the only or the
predominant organ involved
 Termed Glomerulopathies
when no cellular inflammatory
component is involved
  1. Secondary Glomerulonephritis
     Glomeruli are injured as a
    secondary consequence of
    another systemic disease
101
Q

Name the primary glomerular disease

A
  1. Membranous Glomerulonephritis
  2. Focal Segmental Glomerulosclerosis
  3. Membranoproliferative
    Glomerulonephritis
  4. IgA Nephropathy
  5. Chronic Glomerulonephritis
  6. Acute Diffuse Proliferative
    Glomerulonephritis
  7. Crescentic Glomerulonephritis
  8. Minimal Change Disease
  9. Alport Syndrome
  10. TBMN (thin basement membrane nephropathy
102
Q

Types of secondary glomerular diseases

A
  1. SLE
  2. DM
  3. Amyloidosis
  4. Polyarteritis nodosa
103
Q

Features of MCD

A 
Normal Light Microscopy
 Negative ImmunoFluorescence
 Fusion of Foot Processes
of Podocytes
 Commonest cause of
Nephrotic Syndrome in
Children (>95%)
 Heavy Proteinuria
 Steroid-Responsive 
Good prognosis, without
permanent injury
104
Q

Features of membranous nephropathy/glomerulonephritis

A 
 Most common cause of nephrotic
syndrome in caucasian adults
 Form of chronic Ag-Ab-mediated
disease
 Diffuse thickening of the
glomerular capillary walls
 Basement membrane projections
(“spikes”) [Silver stains]
 Immunofluorescence: Granular
and linear pattern of IgG and C3
 Electron Microscopy: Subepithelial
deposits along the BMs,
with effacement of podocyte foot
processes
105
Q

Progression of membranous glomerulonephritis

A
  1. Proteinuria
    - Spontaneous complete remission 5%-30% at 5 yrs
    - Spontaneous partial remission 25%-40% at 5yrs
    - End Stage Renal Disease (ESRD)
     14% 5 years
     35% 10 years
     41% 15 years
106
Q

Tx for membranous glomerulonephritis

A

Immunosuppression 6 to 12 months
 Cyclophosphamide
 Steroids

107
Q

Feautures of FSGS

A

This lesion is characterized by sclerosis of some (but not all)
glomeruli (focal) and in the affected glomeruli, only a portion is
involved (segmental)
FSGS occurs in the following settings:
 As idiopathic (primary) disease
 In association with other known conditions e.g. HIV, sickle cell
disease, massive obesity
 As a secondary event, reflecting glomerular scarring, in other
forms of focal glomerulonephritis e.g. IgA nephropathy
 As a component of the adaptive glomerular ablation response in
advance stages of renal disorders

-  In sclerotic segments there is:
 Collapse of the basement
membranes
 Increase in matrix
 Deposition of hyaline
masses (hyalinosis)
108
Q

IF of FSGS?

A

iGm OR c3 (THIS DIFFERS FROM FIRST AID WHICH SAYS THERE WOULD BE NO IF DEPOSITS

109
Q

EM of FSGS

A 
diffuse loss of podocytes
foot processes and focal
detachment of podocytes
from the underlying GBM
Note the capillary collapse
and mesangial sclerosis
110
Q

Naural Hx of FSGS

A
  • Proteinuria
     Nephrotic Syndrome ‘Lipoid Nephrosis’, similar to MCNS
     Low Proteinuria suggests secondary to familial abnormality
  • Prognosis
     Dependent on diagnosis and response to treatment
     High rate of recurrence in renal transplants
111
Q

Tx of FSGS

A

Immunosuppression
 Steroids Responsive 50%, sustained 25%
 Cyclophosphamide For steroid-dependent
 Cyclosporine For steroid-dependent

112
Q

Features of IgA nephropathy

A 
 Berger’s disease
 Probably the most common
glomerular disease worldwide
 Presence of prominent IgA
deposits in the mesangial regions,
detected by IF microscopy
 Genetic or acquired abnormality
of immune regulation leading to
increased mucosal IgA synthesis
 Presents invariably with
episodic haematuria +/- nephrotic
syndrome or proteinuria
113
Q

Microscopic findings of IgA nephropathy

A

 Mesangial cell proliferation
 Segmental endo-capillary proliferation
 Segmental glomerulosclerosis and adhesion
 Focal accumulation of hyaline
 Focal presence of glomerular crescents
 Tubular atrophy with interstitial fibrosis

114
Q

Natural Hx of IgA nephropathy

A

 Most patients do well without treatment

 End Stage Renal Disease: 30% at 20 years

115
Q

What indicates a poor prognosis in IgA nephropathy

A

 Elevated serum Creatinine concentration
 Hypertension (>140/90 mmHg)
 Nephrotic/Persistent protein excretion above 1000 mg/day
 Crescentic Nephritis
 Tubular Atrophy

116
Q

Tx of IgA nephropathy

A 
 Angiotensin Blockade : ACEI preferable
 Omega-3 Fish Oils, in large dose
- Immunosuppression for Acute Glomerulonephritis
 Cyclophosphamide
 Azathioprine
 Steroids
117
Q

Relationship between SLE and renal disease

A
  • Clinical evidence of renal disease seen in 50-70%
  • SLE causes a heterogeneous group of lesions and clinical
    presentations
  • Glomerular changes are classified into:
    1. Class I Minimal Mesangial Lupus Glomerulo-Nephritis (LGN)
  1. Class II Mesangial Proliferative LGN
  2. Class III Focal LGN (<50% of glomeruli)
    Class IV Diffuse LGN (>50% of glomeruli; subdivide into IV-S and IV-G)
  3. Class V Membranous LGN
  4. Class VI Advanced Sclerotic LGN (>90% sclerotic glomeruli)
118
Q

Features of Class I (Minimal Mesangial LGN):

A

Mild disease with small
amount of swelling

- Mesangial deposits of Immunoglobulins
and/or complement
(mainly in the mesangium),
without morphologic changes
identified in Light Microscopy
119
Q

Features of Class II (Mesangial Proliferative LGN):

A

Still fairly mild
disease but more swelling than Class I. Mesangial deposits of
Immunoglobulin

-  Mesangial hypercellularity or
mesangial matrix expansion
(Light Microscopy)
 Few isolated subepithelial or
subendothelial deposits (IF
or EM)
120
Q

Features of Class III focal LGN

A 
Moderate degree of swelling with less
than 50% of the glomeruli affected
 Proliferation of endothelial and mesangial cells
 Infiltration with neutrophils 
- Association with focal subendothelial
deposits (EM)
121
Q

Features of Class IV (Diffuse LGN)

A 
Severe degree of swelling with
greater than 50% filtering units affected
 Proliferation
 Necrosis and hyaline thrombi
 Subendothelial deposits (wire-loops)
- Segmental thickening of capillary
walls by wire-loop deposits
122
Q

Features of Class V (Membranous LGN):

A

Most of the swelling is
confined to the outer layer surrounding the filter unit
 Widespread thickening of the capillary wall (LM)
 Sub-epithelial IgG deposits (IF or EM)

123
Q

Features of class VI Advanced Sclerotic LGN)

A

Sclerosis of ≥90% of the filter units

show scarring

124
Q

Renal Tx of SLE

A 
Dependent on Histological Class
 Class IV Cyclophosphamide &amp; Steroids
 Class V Azathioprine &amp; Steroids
 All - Mycophenolate
 Resistant - Rituximab
125
Q

Features of Alport Syndrome

A

 X-linked Alport (80%): Mutations on COL4A5 gene; α5 chain
of collagen type IV

 Autosomal Alport (20%): Mutations on COL4A3 and
COL4A4 genes; α3 and α4 chains of collagen type IV

 Mutations interfere with the structure and function of collagen
IV and thus with the GBM ultra-structure. Mechanism is not
well understood

 Often associated with sensorineural hearing loss and ocular
abnormalities

 Initial renal manifestation of Alport syndrome is asymptomatic
persistent microscopic hematuria, which is present in early
childhood in affected patients

126
Q

Morphological features of Alport

A 
Presence of
irregular foci of
thickening and
thinning, with
pronounced splitting
and lamellation of the
GBM
127
Q

Features of CFHR5 Nephropathy (Troodos Nephropathy)

A

 Inherited (autos. dominant) kidney disease; endemic in Cyprus
 Caused by a mutation in the gene CFHR5 (duplication of exons
2 and 3 of CFHR5)
 Estimated that 1:6500 Cypriots carry the mutation
 CFHR5: Synthesized in the liver
 CFHR5-Function: Inhibits C3 Convertase activity and binds
Heparin and CRP
 Clinical picture: Persistent microscopic hematuria and episodes
of synpharyngitic macroscopic hematuria (1-2 days after upper
respiratory tract infection)
 Subendothelial and mesangial C3-deposits and occasionally
subepithelial basement membrane C3-deposits

128
Q

What is the uteropelvic junction

A

The point at which the renal pelvis narrows to form the ureter

129
Q

The ureter is in contact with which structures of the posterior abdominal wall?

A

psoas major

130
Q

How do the ureters enter the pelvic area

A

At the area of the sacroiliac joints, the ureters cross the pelvic brim, thus entering the pelvic cavity. At this point, they also cross the bifurcation of the common iliac arteries.

At the level of the ischial spines, they turn anteromedially, moving in a transverse plane towards the bladder.

131
Q

Which structures pass anterior to the ureter? Does this differ in males and females?

A

ureters run in close proximity to ovaries so need to take care when performing an ovariectomy esp. during ligation of the ovarian arteries.

Also, 2cm superior to ischial spine, ureters run underneath the uterine artery (take care during hysterectomy) In men, the uterine arteries are the vas deferens

132
Q

Which layers does the suprapubic catheter pass through?

A

The bladder is an extraperitoneal organ, The suprapubic catheter would pass superior to the pubis through the layers of the anterior abdominal wall.
If the bladder is distended at the time of the procedure, the tube can then continue through the bladder wall into the bladder. As the bladder fills with urine, it rises into the abdomen between the peritoneum and the transversalis fascia of the anterior abdominal wall.

133
Q

Consequence of bladder rupture in males vs. females

A

in men the bladder is intra and extra peritoneal whereas in women it is extraperitoneal. So a rupture of the bladder in women is very rarely intraperitoneal, this is more common in men however
In most cases the superior surface ruptures since it is the thinnest wall and becomes increasingly thinner as distension increases.

The term ‘‘superior surface’’ actually refers to the relatively flat roof of a non-distended bladder;
however, it becomes increasingly convex with filling, developing superolateral and posterosuperior surfaces.

Rupture of the thinned-out wall also tears the peritoneum that covers it, so that the urine and blood escape into the peritoneal cavity.

134
Q

Relationship between urethra and anterior vaginal wall

A

Urethra is fused to the anterior vaginal wall

135
Q

Paraurethral gland homologue

A

prostate gland

136
Q

Why is the passage of cystoscopes or catheters easier in the female than the male?

A

Urethra is shorter and less curved in females.

137
Q

Systematic approach to a sick patient?

A

History

Examination

Differential

Investigations

Diagnosis

Treatment

138
Q

Order to assess the systems

A
  • Call for help early
  • Priority of Tx
  • Complete initial assessment and then reassess
  • Pt. responsiveness to Tx

A: airway (with C-spine protection in trauma)

B: breathing

C: circulation

D: deficits in neurological status

E: environment (exposure)

(O2, IV access and fluids ± specific treatment can be repeated as many time as possible

Should not take more than 5 minutes

139
Q

How to recognize an obstructed airway

A

Can the patient talk?

Does the patient sound distressed?

Shortness of breath

Noisy breathing

stridor, wheeze, gurgling

See-saw respiratory pattern,

140
Q

Common causes of airway problems

A

CNS depression

Blood

Vomit

Foreign body

Trauma

Infection

Inflammation

Laryngospasm

141
Q

Approach to assessment of breathing problems

A
  1. Look
    - Inspect respiratory distress, accessory muscles, cyanosis, Respiratory rate very
    important. RR>20 sign of a sick patient
  2. Listen
    - Auscultate breath sounds, noisy breathing
  3. Feel
    - palpate expansion, percussion, tracheal position
    - Pulse oxymetry: Saturation 94%: on oxygen ?
142
Q

Tx of breathing problems

A
  1. Airway
  2. Oxygen
  3. Treat underlying cause
    - e.g. drain pneumothorax
    - e.g . Nebulizers
  4. Support breathing if inadequate
    - e.g. ventilate with bag valve mask
143
Q

How to assess circulation

A
  1. Look at the patient
  2. Pulse – central pulse (carotid)
  3. peripheral pulse
  4. Peripheral perfusion
  5. capillary refill time
    ( normally <2 sec)
  6. Blood pressure
  7. Monitor
144
Q

Primary causes of circulatory problems

A
  1. Acute coronary syndromes
  2. Dysrhythmias
  3. Hypertensive heart disease
  4. Valve disease
  5. Drugs
  6. Electrolyte / acid base
    abnormalities
145
Q

Secondary cause of circulatory problems?

A
  1. Hypoxaemia
  2. Blood loss
  3. Hypothermia
  4. Septic shock
146
Q

Tx of circulatory problems

A
  1. Airway, Breathing
  2. Oxygen
  3. IV access, take blood sample and lab
    investigations
  4. Treat cause
  5. Give fluids
  6. Haemodynamic monitoring
147
Q

What is a fluid challenge?

A

A positive response is an increase in cardiac output in
response to the increased volume.

Heart rate decreases

Mean arterial pressure increases

Arterial pulse pressure increases

Urine output increases

Lactate clearance increases

Cardiac output or stroke volume increase

148
Q

Know how to do a glasgow coma score

A

see slight 33 on recognising a sick patient lecture

149
Q

What is AVPU

A

Used to measure consciousness.

Alert – a fully awake patient (not necessarily orientated)

Voice –Responds to voice or confused/agitated

Pain – Makes a response when mild pain is inflicted e.g. trapezius pinch

Unresponsive – No response to voice or pain

A fall in the AVPU score should always be considered
significant

More detailed conscious level and neurological data should
be recorded on ‘neurological observations’ chart if required

This should include a ‘Glasgow Coma Scale’ assessment

150
Q

What is the significance of urine output in a sick patient?

A

Urine output is one of the few signs of end-organ
perfusion

In a sick patient catheterisation should be considered to
allow measurement (and documentation) of hourly urine
volume The weight is essential to get an accurate urine
output.

BCS Lectures (8 decks)

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