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Regulation of Body Function > Renal Problems (Clinical Problems) (Zoysa) > Flashcards

Renal Problems (Clinical Problems) (Zoysa) Flashcards

1
Q

How do you approach AKI?

A
  • Identify patient at high risk and optimise care (old, comorbidities, medications)
  • Stop all nephrotoxic agents (e.g. NSAIDs)
  • Assess and optimise volume status
  1. Check for pulse (normal/decreased volume, e.g. tachycardia indicates volume depletion)
  2. Check blood pressure
  3. Tissue turgor (helpful in kids and elderly), mucous membranes
  4. Check for peripheral edema
  5. Listen to lungs
  6. JVP (venous pulse is compressible (fills from top) with two waves/pulse; arterial pulse is palpable with single pulsation)
    • If low JVP, then give fluids
    • If euvolaemic, maintain fluid status
  • Monitor creatinine and urine output (daily assessment)
  • Non-invasive diagnostic workup
    • Mid-stream urine (MSU), which includes proteins (creatinine, albumin), microscopy (white cells, red cells, epithelial cells, bacterial, mucus, yeast), culture (not routine in absence of pyuria)
      • Presence of blood and protein suggests glomerulonephritis
      • High proteinuria suggests inflammation or infection (e.g. interstitial nephritis is caused by NSAIDs)
    • Streptococcal serology
    • Antibodies (ANA-autoimmune antibodies, ANCA, C3, C4, anti-GBM)
    • Coagulation studies
    • Ultrasound (number of kidneys, and kidney flow via Doppler)
  • Invasive diagnostic workup (renal biopsy)
    • Shows inflammation of tubular interstitial nephritis
  • Revise drugs; diet
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2
Q

What is AIN?

A

Acute interstitial nephritis

Immune-mediated form of AKI

Characterised by an inflamatory infiltrate in ther enal interstitium and tubules

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3
Q

Describe the relationship between AKI and NSAIDs

A

NASIDs reduces pain, but block prostaglandin production via cyclooxygenase pathway (PGs important for renal blood flow)

  • NSAIDS decreases PGE2 ® renal vasoconstriction (PGE2 is vasodilatory) ® decreased renal blood flow ® âGFR
  • NSAIDs decreases PG ® inhibit renin secretion ® hyperkalaemia (unable to secret K+)

NASIDs can cause:

  • Direct toxicity to tubules, thus AKI (albuminuria)
  • Minimal change disease (renal disease in which large amounts of protein is lost in urine, one of the most common causes of nephrotic syndrome)
  • Acute interstitial nephritis (increased WBCs)
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4
Q

Describe the staging of CKD

A

CKD is classified based on cause, GFR category, and albuminuria category (CGA).

  • CKD G1 GFR > 90 ml/min
  • CKD G2 GFR 60- 90 ml/min
  • CKD G3 GFR 30- 60 ml/min
  • CKD G4 GFR 15- 30 ml/min
  • CKD G5 GFR < 15 ml/min
  • A1 < 30 mg/mmol
  • A2 30-300 mg/mmol
  • A3 >300mg/mmol
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5
Q
  • Lab results:
    • increased K, urea, Cr
    • decreased eGFR (can only be measured in more stable condition)
    • Protein/Cr ratio decreased

What is the diagnosis?

A
  • Diagnosis: CKD
    • Over 7 years, his GFR has deteriorated progressively
    • CKD G5 A2 secondary to membranous nephropathy
      • Declined for deceased donor renal transplantation in 2011
      • Planning for peritoneal dialysis
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6
Q

Define CKD

A

CKD is defined as abnormalities of kidney structure or function, present for > 3 months, with implications for health.

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7
Q

How do you manage CKD?

A

1) Decrease BP
2) Give EPO so Hb 105-120

Summary

  • Decided on peritoneal dialysis, continue close monitoring
  • Transplantation with 5 year deceased donor score >80, requested DSE, live donation preferred but no obvious donor
  • So we want him to get a transplant but may take many years

Continue w/ regular labs, F/U few months’ time

  • Medications:
    • Warfarin as per INR
    • Doxazosin 1mg mane, 2mg nocte
    • Metoprolol 47.5mg bd
    • Candesartan 12mg bd
    • Omeprazole 20g od
    • Allopurinol 100mg od
    • Calcium carbonate (try to â phosphate) 1.25gm one tab bd
    • Felodipine 5mg nocte
    • Cholecalciferol halted
    • Folic acid halted
    • Clinicians renal vitamin one tab od
    • Erythropoietin 3000units weekly
    • Prednisolone (scleroderma) 7.5mg od
    • Frusemide 40mg od
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8
Q

Describe Anaemia and CKD

A

Prevelanet as renal function declines

Exclude other causes

Maintain Hb levels 100-120g/L (i.e. not to normalise the haemoglobin level)

When Hb falls below 100-100g/L treatment with oral iron, intravenous iron +/- erythropoiesis stsimulating agents may be considered

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9
Q

In CKD, expect _____ ______ anaemia

A

In CKD, expect normochromic normocytic anaemia

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10
Q

Describe CKD-Mineral Bone Disorder

+The key drivers of CKD-MBD

+ treatment

A

CKD–Mineral and Bone Disorder (CKD–MBD)

Disturbances of calcium and phosphate metabolism arise in moderate to severe CKD.

The key drivers of CKD-MBD are:

  • phosphate retention (due to reduced renal clearance),
  • disordered Vitamin D metabolism
  • and the consequent secondary hyperparathyroidism

Treatment:

1) Dietary phosphate restriction
2) Phosphate binders (to minise dietray phospahte absorption)

  • Calcium carbonate
  • Aluminium hydroxide

3) 1-a (OH)Vit D
4) Goal varies with stages of renal function

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11
Q

Describe Potassium and CKD/

What would you manage this?

A

Restrict dietary potassium

Review medications that mayh be contributing (ACE-I or ARB)

Correct metabolic acidosis

Consider ion exhcange resins

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12
Q

What is End stage renal disease?

A

End stage renal failure referes to patents who have insufficient kidney function to keep them feeling well.

Symptomms may include

1 ) Anorexia

2) fatigue
3) Itchiness

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13
Q

What is the optimal treatment for end stage renal failure?

A

Transplantation

  • Involves a surgical procudere to provide a healthy functioning kidney
  • Transplantation is encouraged for medically suitable patients
  • Can be from a decreased, but ideally from a medical suitable and willing live donor.
  • The waiting time is 3-5 years and depends on blood type, tissue type and the time waiting.
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14
Q

Describe Haemodialysis

A

Blood is removed from the body and passed through an artificial kidney

This is done at least 3 times a week, for 4-5 hours each time

This can be done at home or in a diaylsis clinic.

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15
Q

Decribe Peritoneal dialysis

A

Tube is placed into the abdo through which specialised PD fluid is darined

A cleansing fluid (dialysate) flows through a tube (catheter) into part of your abdomen and filters waste products from your blood. After a prescribed period of time, the fluid with filtered waste products flows out of your abdomen and is discarded.

_______

Peritoneal dialysis (PD) is a type of dialysis which uses the peritoneum in a person’s abdomen as the membrane through which fluid and dissolved substances are exchanged with the blood. It is used to remove excess fluid, correct electrolyte problems, and remove toxins in those with kidney failure.

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16
Q

What are the treatment options for CKD?

A

1) Transplataion (live vs decreased)
2) Haemodialysis
3) Peritoneal diaylsis
4) Supportive therapy

17
Q

WHat is the difference between Haemodialysis and Peritoneal dialysis?

A

In hemodialysis, blood is pumped out of your body to an artificial kidney machine, and returned to your body by tubes that connect you to the machine. (needs to be in the hospital)

In peritoneal dialysis, the inside lining of your own belly acts as a natural filter. Wastes are taken out by means of a cleansing fluid called dialysate, which is washed in and out of your belly in cycles. (can be done at home)

A cleansing fluid (dialysate) flows through a tube (catheter) into part of your abdomen and filters waste products from your blood. After a prescribed period of time, the fluid with filtered waste products flows out of your abdomen and is discarded.

18
Q

What is Glomerulonephritis?

A

acute inflammation of the kidney, typically caused by an immune response.

  • Glomerulonephritis (GN), also known as glomerular nephritis, is a term used to refer to s_everal kidney diseases_ (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name,[1] but not all diseases necessarily have an inflammatory component.*
  • As it is not strictly a single disease, its presentation depends on the specific disease entity: it may present with isolated hematuria and/or proteinuria (blood or protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease.*
  • Nephrotic syndrome is triad of heavy proteinuria, hypoalbuminaemia, peripheral oedema; (and hypertension, dyslipidaemia)
    • High proteinuria -> hypoalbuminaemia -> peripheral oedema
  • Nephritic syndrome is haematuria, proteinuria, peripheral oedema, hypertension ± reduced renal function, lymphoedema
  • _Rapidly progressive GN i_s haematuria, deteriorating renal function, proteinuria crescents present on renal biopsy.
  • Asymptomatic urine abnormalities is signs of nephritic syndrome but without oedema, hypertension etc.
  • Glomerulonephritis can lead to AKI and CKD
19
Q

What is abnormal here?

haemoptysis, dyspnoea

  • 21 y/o male smoker
A
    • decreased Hb, N Plt, N WBC (neutrophil), increased ESR
      • increased Cr, K
      • Blood and protein in urine
      • U/S normal
      • Ascultation with coarse crepitations.
      • ANCA –ve, serum anti-GBM –ve
      • CXR unremarkable
      • Renal biopsy shows glomerular spaces filled, hypercellular

Diagnosis: Glomerulonephritis

20
Q

Describe Glomerula Crescents

A

Glomerular crescents is non-specific response to injury of capillary wall (immune response)

  • Physical gaps appear in filtration barrier
  • “Rents” allow circulating cells, inflammatory mediators and plasma proteins to enter into Bowman’s space
  • Contents in Bowman’s space can enter interstitial, contributing to peri-glomerular inflammation

In general, severity of glomerulonephritis (GN) is assoc. w/ degree of crescent formation. It is reversible in early stage.

21
Q

Classify RPGN

A

Classification Of RPGN (Rapidly Progressive Glomerulonephritis)

  1. Anti-glomerular BM disease
  2. Immune complex (post-infectious, lupus nephritis, membranoproliferative glomerulonephritis, Henoch-Schontein purpura, IgA nephropathy, collagen-vascular disease, mixed cryoglobulinaemia, fibrillary GN, idiopathic)
  3. Pauci-immune ANCA +ve, ANCA –ve
    • ​Pauci-immune (pauci- Latin: few, little) vasculitis is a form of vasculitis that is associated with minimal evidence of hypersensitivity upon immunofluorescent staining for IgG
    • The linear and granular patterns are examples of positive immunofluorescence and are associated with Goodpasture syndrome and post-streptococcal glomerulonephritis accordingly.[1] A negative pattern or pauci-immune pattern can be associated with systemic vasculitis such as microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (EGPA) or granulomatosis with polyangiitis (GPA).
  • Type I[edit]*
  • Accounting for approximately 20% of RPGN, type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane(GBM). It is also called anti-GBM glomerulonephritis. The antibodies are directed against a particular protein found in the GBM, type IV collagen, specifically the noncollagenous region of its α3 chain.[2] In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with antibodies directed against the basement membrane of lung alveoli, producing Goodpasture syndrome. The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic.[2]*
  • Type II[edit]*
  • RPGN caused by the deposition of immune complexes accounts for 25% of RPGN and is classified as type II. Thus any immune complex disease that involves the glomerulus may progress to RPGN if severe enough. These diseases include systemic lupus erythematosus, acute proliferative glomerulonephritis, Henoch–Schönlein purpura and IgA nephropathy.[2]*
  • Type III[edit]*
  • Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of neutrophils in response to ANCA. Type III RPGN may be isolated to the glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most cases of the latter, the systemic disease is an ANCA-associated vasculitis such as granulomatosis with polyangiitis, microscopic polyangiitis or eosinophilic granulomatosis with polyangiitis.[*
22
Q

Describe Goodpasture’s Syndrome

How can you manage these patients?

A

Goodpasture’s syndrome is antibody targets glomerular BM membrane. It is associated with deteriorating renal function and haematuria.

Therapy includes:

  • Prednisone
  • Cyclophosphamide
  • Plasma exchange (remove his plasma which had antibodies, and replace his plasma)
  • Hemodialysis
23
Q

How would you treat someone with Goodpastures Syndrome

A
  • Prednisone
  • Cyclophosphamide
  • Plasma exchange (remove his plasma which had antibodies, and replace his plasma)
  • Hemodialysis
24
Q

What are the 6 mmost important message about Hypertension?

A
  1. Common
    • 90% is essential hypertension (genetic and environmental influences)
    • Most common environmental risk factors are á BMI, á Na intake >100mmol/L
    • Prevalence based on age (since she is so young, need to think of other causes)
  2. Hypertension is major cause of morbidity and mortality!!
  3. Salt restriction important is vital!
  4. Long-acting diuretics are cornerstone of therapy
  5. Treat to target using complementary multi-drug therapy and lifestyle changes
  6. Always monitor BP for 24 hours before starting on BP lowering therapy (one BP measurement does not mean HT diagnosis)
25
Q

Describe the Therapy for Hypertension

A
  • Lifestyle modification
    • Weight loss
    • Low sodium diet (vital)
      • Final common pathway is disordered handling of salt.
      • If sodium intake is <50mmol/L, then hypertension or age related increases in BP do not develop.
    • Exercise
  • Monotherapy (age-dependent)
    • <55 y ACEi (younger patients have RAAS activation)
    • >55 y diuretic/CCB
  • Indications (treat other co-morbidities too):
    • IHD: beta blocker
    • CHF: thiazide/ACEi/ARB/beta blocker
    • DM: ACEi/ARB/thiazide
    • CKD: ACEi/ARB
  • Further management if not reaching target?
    • Optimise drug dose
    • Add another drug (most patients will need ³__2 drugs!)
26
Q
  • Hx:
    • Prev. relevant medications are sertraline 50mg od, AVA 30 for some years changed to AVA 20 a few days ago
    • Regular periods, no Hx of migraine, no Hx VTE
    • No renal FHx
    • FHx hypertension
  • Ix:
    • SCr 68umol/L, eGFR >90
  • Clinically obese, combined oral contraceptive pill stopped on GP consultation
  • BP 148/90
  • HR 80, regular, radial-radial delay
  • Resting tremor, anxious, sweating
  • Exam:
    • Ht 1.72m, Wt 89.8kg
    • HR 70bpm, regular
    • BP 112/70 R + L arms
    • No other significant symptoms (HS dual, no added sounds, no cardiac bruits, chest clear) (abdo exam, soft, non-tender, nil masses. nil hepatosplenomegaly, bowel sound (BS) present, no bruit heard) (no proximal myopathy, brisk but symmetrical reflex)
  • Ix:
    • Urinalysis shows no blood or protein
    • Plasma metanephrines N
    • Plasma aldosterone high
    • U/S + Doppler N (renal)

How would you treat this patient?

A

Therapy for Hypertension

  • Lifestyle modification
    • Weight loss
    • Low sodium diet (vital)
      • Final common pathway is disordered handling of salt.
      • If sodium intake is <50mmol/L, then hypertension or age related increases in BP do not develop.
    • Exercise
  • Monotherapy (age-dependent)
    • <55 y ACEi (younger patients have RAAS activation)
    • >55 y diuretic/CCB
  • Indications (treat other co-morbidities too):
    • IHD: beta blocker
    • CHF: thiazide/ACEi/ARB/beta blocker
    • DM: ACEi/ARB/thiazide
    • CKD: ACEi/ARB
  • Further management if not reaching target?
    • Optimise drug dose
    • Add another drug (most patients will need ³__2 drugs!)
27
Q

How would you treat resistant hypertension?

A

Resistant hypertension is BP not at target despite optimal dose of 3 complimentary drugs, one of which is a diuretic (must be long-act at correct dose!)

Causes include:

  • Suboptimal therapy (no diuretic, inadequate dose, non-complementary drugs)
  • Non-compliance
  • Competing drug (sodium, NSAIDs, OCP)
  • White coat HT (hypertension when patient is in a clinical setting, not in another setting)
  • Secondary HT
    • Endocrine such as phaeochromocytoma, Conn’s, hyperthyroidism
      • Hyperthyroidism presents with tremor, palpitations, intolerance to heat, weight loss, tachycardia, bruits, exophthalmous, lid lag, wrist reflex
      • Cushing’s syndrome presents with buffalo hump, obesity, moon face, abdominal striae
      • Phaeochromocytoma presents with episodic palpitations
      • Primary hyperaldosteronism is due to hyponatraemia, hypokalaemia
    • Renal such as GN, CKD, RAS
    • Obstructive sleep apnea (OSA)
28
Q

What are 4 good drug combinations

What are 3 bad drug combinations?

A
  • Good
    • Thiazide + ACE-I
    • ACE + CCB
    • b-blocker + a-blocker
    • Thiazide + CCB
  • Bad
    • ACE-I + b-blocker
    • ARB + b-blocker
    • ACE-I + ARB
29
Q
  • 59 y/o female
  • PC: fever, dysuria
  • Ix: MSU shows á WBC, growth of E. Coli (UTI)
    • Leucocytes >100 x 106/L (<40)
    • Erythrocytes <10 x 106/L (<35)
    • Epithelial Cells 4 x 106/L
    • Culture shows >108/l growth of Escherichia coli
    • Susceptibilities shows Amoxicillin S Co-amox/Clav(Augmentin) S Cefalexin S Nitrofurantoin S Trimethoprim R.
    • Amoxicillin/clavulanate (augmentin) result is for treatment of uncomplicated cystitis

How would you treat her?

A

• Cystitis – an infection of the bladder
• Pyelonephritis – an infection of the upper
urinary tract

  • Cystitis: 3 – 5 days of oral
  • Pyelonephritis: 7-10 days.

Trimethoprim (Bactrim DS, Septra DS, others)

Nitrofurantoin (Macrobid, Macrodantin)

30
Q

How long do you need to treat patients for UTIs in uncomplicated cases/

A
  • Cystitis requires 3-5 days of oral
  • Pyelonephritis requires 7-10 days
31
Q

Describe UTI in men

A

UTIs in men are usually considered ‘complicated’. Incidence is lower, more complex. Treat longer

  • Cystitis requires 7 days
  • Pyelonephritis requires 10-14 days

Also needs to consider prostatitis, urethritis.

32
Q

Describe Bacturia

A

Bacturia

Bacturia occurs 2-7% pregnancies.

  • Smooth muscle relaxation and ureteral dilation occurs
  • Increased risk preterm birth, low birth weight, perinatal mortality

Treatment reduces complications:

  • In asymptomatic non-pregnant woman, drink a lot w/o antibiotics
  • In symptomatic non-pregnant women, treat w/ antibiotics
  • In asymptomatic pregnant woman, treat w/ antibiotics to reduce complications
    • Amoxycillin and cephalexin (3-7days)
    • Fosfomycin single dose
    • Screening at 12-16 weeks (generally not repeated unless symptomatic or at high risk)

Follow-up include:

  • Repeat MSU one week after completing therapy (30% don’t clear infection)
  • If still signs of bacteria, repeat with a longer course
  • Consider suppression if >2 courses
  • Repeat MSU monthly or give prophylaxis antibiotics to someone with multiple UTIs
33
Q

What is a “recurrent infection”

A

Definition and Epidemiology

Recurrent infection is >2 infections in 6 months, or >3 infections in a year

  • If not associated with abnormal urinary tract, then it should not cause disease
  • Recurrent cystitis is not infrequent
  • Recurrent pyelonephritis is uncommon
34
Q

What are some prevention strategies for UTI

A

Prevention

  • Alter behaviour
    • Contraception
    • Post-coital void/fluid
    • Cranberry juice?
  • Antimicrobial prophylaxis (3-6 months)
    • Continuous
    • Post-coital
    • Intermittent self-treatment
  • Topical oestrogen in postmenopausal women

Regulation of Body Function (36 decks)

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