chronic kidney disease, COPD, Interstitial Lung Disease

1. Chronic Obstructive Airway
Disease
Interstitial Lung Disease
Chronic Kidney Disease

2. PCP 702 presentation

3. What is COPD?
 Condition characterized by irreversible airflow obstruction
resulting from thickening, narrowing and destruction of
the small airways and structural damage to the lung
parenchyma.
 It encompasses 2 conditions: Chronic bronchitis (chronic
productive cough for 3 months for 2 consecutive years) and
Emphysema (abnormal permanent enlargement of the air
spaces distal to the terminal bronchioles, accompanied by
destruction of their walls)
 COPD is treatable and preventable and also has some
significant extra-pulmonary effects.

4. Epidemiology
 According to the latest WHO estimates (2004),
currently 64 million people have COPD and 3 million
people died of COPD (5% of all deaths globally).
 It is known that almost 90% of COPD deaths occur in
low- and middle-income countries.
 COPD used to be more common in men, but now
affects men and women almost equally.
 WHO predicts that COPD will become the third
leading cause of death worldwide by 2030.

5. Etiologies
 Cigarette smoking
 Environmental factors
 Airway Hyper responsiveness
 Alpha1-antitrypsin deficiency
 Intravenous drug use
 Immunodeficiency syndromes
 Vasculitis syndrome
 Connective tissue disorders
 Salla disease

6. Pathophysiology

7. Clinical Manifestations
Symptoms
 Chronic productive cough- worse in the morning with small amount of colorless sputum
 Breathlessness
 Wheezing- especially during exertion & exacerbations
 Recurrent RTI
Signs
 Increased RR
 Use of accessory respiratory muscles
 Cyanosis & elevated JVP- in advanced disease
 Barrel chest
 Wheezing
 Symmetrically reduced breath sounds
 Hyper resonant chest on percussion
 Prolonged expiration
Systemic Effects- muscle weakness, edema, weight loss, osteoporosis, inc. circulating
inflammatory mediators.

8. To distinguish between the 2 types of COPD:
Chronic Bronchitis Emphysema
Productive cough with
gradual progression to
intermittent dyspnoea,
frequent and recurrent
pulmonary infections and
progressive
cardiac/respiratory failure
with oedema and weight
gain
Long history of progressive
dyspnoea with late onset of
non productive cough,
occasional mucopurulent
relapses and eventual
cachexia and respiratory
failure
• Obese
• Freq. cough &
expectoration
• Use of accessory resp.
muscles
• Coarse rhonchi and
wheezing on auscultation
• Signs of heart failure-
oedema & cyanosis
• Thin & barrel chested
• Little or no cough
• Pursed lips and use of
accessory resp. muscles
• Chest is hyper resonant
• Wheezing on
auscultation
• Distant heart sounds on
auscultation

9. Investigations
 FBC, UECr- PCV
 ABG- PaO2 +/- hypercapnia
 PEFR- reduced
 Lung Function Tests- reduced FEV1 and FEV1/FVC
ratio

10.  CXR- usually normal in early disease, but later
demonstrates hyper expansion with a low lying flat
hemi-diaphragm, long cardiac silhouette and increased
retrosternal airspace

11. Management
Aim: to improve a patient’s functional status and quality of life by
preserving optimal lung function, improving symptoms, and
preventing the recurrence of exacerbations.
 Educate the patient about the disease and to encourage his or her
active participation in therapy.
 STOP smoking
 Nutritional support
 Bronchodilators-
i)Short- acting administered prn or bd either :
Beta-agonist eg. Salbutamol 1-2 puffs inhaled OR
Anticholinergic eg. Ipatropium bromide 1-2 puffs inhaled
ii)Long acting bronchodilators(salmetrol or tiatropium bromide)
are not on the EDL in Fiji

12. Management (cont.)
 Corticosteroids
Inhaled eg. Beclomethasone or oral eg. Prednisolone
 Methyxanthines eg. Theophylline
 Immunizations for influenza & pneumococcal
 Pulmonary Rehabilitation Programs
 Home O2
 Surgery

13. Management (cont.)
Acute Exacerbations
1. Investigate and treat for precipitant
2. Determine need for admission
 Mild: treat as an OP with inc freq of salbutamol and short course oral
prednisolone
 More severe:
- admit and administer O2 maintaining a Sao2 ≥90% (watch for signs of
hypercapnia)
- administer salbutamol nebs 1-6 hrly ± ipratropium bromide nebs 4-6
hrly
-Prednisolone oral 25-50mg daily for 7-14 days OR IV hydrocortisone
100mg 6hrly
-Amoxicillin 500mg tds for 5 days if evidence of infection
-Physiotherapy to aid sputum expectoration

15. Anatomy
the lungs are ingeniously constructed to carry out their cardinal function: the
exchange of gases between inspired air and blood.

16. Alveolar epithelium (type 1 & 2 pneumocytes) >> Alveolar basement
membrane >> surrounding interstitial fluid >> Capillary Basement membrane
>> Capillary endothelium

17. Restrictive lung diseases may be divided into the following
groups:
 Intrinsic lung diseases (diseases of the lung parenchyma)
 Extrinsic disorders (extra-parenchymal diseases)

18. Intrinsic Lung Diseases
These diseases cause either:
 Inflammation and/or scarring of lung tissue (interstitial lung
disease)
or
 Fill the air spaces with exudate and debris (pneumonitis).
 These diseases are classified further according to the
etiological factor.

19. What are interstitial lung dxs?
 ILD’s are a heterogenous group of disorders characterized
predominantly by inflammation and fibrosis of pulmonary
connective tissue, principally the most peripheral and delicate
interstitium in the alveolar walls
 Diffuse parenchymal lung disease (DPLD)
 Presentation and natural history of these disorders may differ
widely but they are frequently considered collectively as they
share similar symptoms, physical signs, pulmonary function
abnormalities and radiological changes
- these disorders account for about 15% of non-infectious
diseases seen by pulmonary physicians.(USA)

20. Pathophysiology
Intrinsic lung diseases:
 Diffuse parenchymal disorders cause reduction in all lung
volumes.
 This is produced by excessive elastic recoil of the lungs.
 Expiratory flows are reduced in proportion to lung volumes.
 Arterial hypoxemia is caused by ventilation/perfusion
mismatch.
 Impaired diffusion of oxygen will cause exercise-induced
desaturation.
 Hyperventilation at rest secondary to reflex stimulation.

22. Aetiology
Inhaled substances
• inorganic
-Silica
-asbestosis
-Berylliosis
•organic
-Hypersensitivity
pneumonitis
Drug induced
Antibiotics
Chemotherapeutic
drugs
Anti-arrhythmic drugs
Connective tissue dx
Systemic sclerosis
Polymyositis
Dermatomyositis
Systemic lupus
erythematosus
Rheumatoid arthritis
Infection
Atypical pneumonia
Pneumocystis
pneumonia (PCD)
TB
Chlamydia
Trachomatis
Respiratory synctial
Virus
Idiopathic
Sarcoidosis
Idiopathic pulmonary
fibrosis
Hamman – Rich
syndrome
Antisynthetase
syndrome
Malignancy
Lymphatic
carcinomatosis

28. Criteria Of Diagnosis
Major criteria Minor criteria
•Exclusion of known causes of ILD
•Abnormal lung function
(restriction & impaired gas
exchange)
•Hypoxia (rest or exercise)
•Bi-basilar reticular abnormalities
with minimal ground glass
opacities on HRCT
•Transbronchial lung biopsy or
bronchoalveolar lavage showing no
fts to support an alternative
diagnosis
• 50 >Age
•Insidious onset of otherwise
unexplained dyspnea on exertion
•Duration of illness >3 months
•Bibasal inspiratory crackles.

29. Pathophysiology
 Allergen sensitivity/ infection inflammation
of distal air spaces release of chemical
mediators (IL- 1, TGF- beta) & inflammatory cells
activate fibroblasts production and function
proliferation and excess elaboration of matrix
(collagen) , production of proteases and proteases
inhibitors Fibrotic remodelling of distal
airways

30. Investigations
 Chest x-ray
 Pulmonary function test (Spirometry, lung volumes and
diffusing capacity of carbon monoxide [DLCO])
 Pulse oximetry
 High resolution CT
 Complete blood count and differentials
 LFT’s, RFT’s
 Antinuclear antibody
 Rheumatoid factor
 Erythrocyte Sedimentation rate
 Transbronchial/ surgical lung biopsy

31. Manifestation of ILD’s

34. Treatment
 Pharmocological
o IV monthly cyclophosphamide with low dose oral glucocorticoids
(equivalent of prednisone < 10mg/day)
o Liberal fluid intake is encouraged during therapy
o Alternative regimen: Azatioprine + glucocorticoids
o Montoring for renal crisis
o Supplemental oxygen therapy: via nasal cannula to prevent
hypoxemia
o Drugs:
o N-acetylcystein: slows the decline of lung function
is inhaled or delivered through a tube to the throat
o Anti-inflammatory drugs: prednisone & methylprednisolone (given as
adjuncts)
o Antibiotics: Azithromycin & Levofloxacin
o Immunosuppressants: Azathioprine, Methotrexate, Cyclosporine,
Mycophenolate mofetil

35. Treatment
 Non pharmacological tx
• Smoking cessation
• Pulmonary rehabilitaion & Exercise therapy
- build aerobic fitness and maintain physical fitness
• Avoidance of inhaled agents
• Tube thoracostomy
• Whole lung lavage
• Lung transplantation: indicated to pts. With end- stage,
particularly fibrotic ILD and it shows to prolong life
 Patient Education
 Vaccination and infection avoidance since pt. is on
immunosupressants
 Maintain hygiene

36. Specific measures
 There is ongoing controversy over the
role of specific treatments in subgroups
of ILD due to a lack of good quality
evidence for many of the specific
treatments proposed.
Idiopathic pulmonary fibrosis
-possible trial of azathioprine,
prednisolone and N-actyl
cysteine
Lung transplantation is considered
for suitable candidates
Connective tissue diseases
Tx is based on disease severity
(symptoms and LFTs) and
longitudinal dx behaviour.
Prednisolone (0.5 mg/kg/day),
tapering to a maintenance dose of
10 mg/ day.
This is often combined
immunosuppressive agents(usually
oral or IV cyclophosphamide)

37. Specific measures cont..
Sarcoidosis
- Tx is in only indicated if there is a
progressive disease on radiology
and lung function, or if there are
significant symptoms or
extrapulmonary disease.
Prednisolne (0.5 mg/kg/day) is
usually first line treatment for 1
month, weaning to a
maintenance dose that control
symptoms and then continuing
for up to 6 – 24 months
Hypersensitivity pnemonitis
-Avoidance of the antigen is
essential
- prednisolone therapy may be
required if there is severe or
progressive disease.

38. Complications
 Superinfection in patients receiving
immunosuppressants.
 Drug toxicity morbidity associated with ILD thus
prevention and monitoring is crucial
 Hemoptysis which is suggestive of vasculitis/
venooclussive dx
 Respiratory failure/ Cor pulmonale / Right Heart
failure
 Death

39. Prognosis
 Mortality rates as high as 90% have been reported in children
who develop ILD when younger than 1 year (predominantly DIP);
other studies have reported much better survival with conservative
management.
 Fan and Kozinetz reviewed the outcomes of 99 children with ILD over
15 years.[5]Survival rates at 24, 48, and 60 months after the
appearance of initial symptoms were 83%, 72%, and 64%,
respectively.
 ILD and/or Idiopathic pulmonary fibrosis has a poor prognosis
in older adults
 Sarcoidosis which is more common in young adults, generally has
a benign prognosis.

40. Primary Health Care Setting
Detailed history, medication and social history (smoking/occupation)
Physical examination
Investigations : CXR, Pulmonary function tests, Oximetry
Manage: O2, stop smoking, pulmonary rehab
Refer to divisional hosp.

41. Conclusion
 Interstitial lung disease is a term encompassing a diverse range of lung
conditions that primarily affect the lung interstitium.
 ILD should be considered in any person presenting with breathelessness or
cough along with abnormal chest radiography or lung function testing.
 High resolution computed tomography is the best imaging modality.
 Lung biopsy is often for diagnosis
 Referral to a respiratory specialist and involvement of multidisciplinary teams
are the mainstays of management.
 Specific management varies according to the underlying diagnosis.
 General management strategies: pulmonary rehabilitation, smoking cessation,
oxygen therapy as required, and treatment of commonly associated diseases.

42. MANAGEMENT OF
CHRONIC RENAL FAILURE

43. Definition
 Presence of kidney damage (albuminuria ≥ 30mg/day)
 Decreased kidney function (eGFR <60ml/min/1.73m2 )
for 3 or more months.

44. Chronic renal failure
 Chronic and irreversible loss of nephrons
 Symptoms occur only after substantial loss of functioning
kidney (>50%) and reflect the failure of its 3 major roles:
1. Regulation of fluid, electrolyte and acid-base
balance (generally manifesting as fluid overload,
hyperkalaemia and metabolic acidosis)
2. Excretion of nitrogenous waste products of protein
catabolism (the accumulation of which leads to the many
manifestations of ‘uraemia’)
3. Hormonal regulation, through production of
erythropoietin (deficiency contributing to anaemia) and
calcium homeostasis (disturbance leading to renal bone
disease).

45. Patho-
genesis of
Progressive
Renal
Disease

46. Etiology
1. Metabolic disorders
diabetes mellitus
amyloidosis
2. Renal vascular disorders
renal artery stenosis
nephrosclerosis –hypertension
renal vein thrombosis
3.Immunological disorders
glomerulonephritis
polyarthritis nodosa
systemic lupus erytheromatosus
4.Infections
chronic pylonephritis
TB
5.Primary tubular disorders
nephrotoxins e.g.heavy
metals,tetracyclins, analgesics
6. Urinary tract obstructions
recurrent renal calculi
BPH
urethral stricture
7.Congenital disorders
polycystic diseases
congenital absences of kidney
tissues.

47. Progression of Chronic Renal Failure
 Initial pathogenetic insult
 Reduced renal reserve (loss of nephrons)
 No change in urea or creatinine or homeostasis
 Renal insufficiency
 mild elevation in urea and creatinine
 mild symptoms: eg. Nocturia & easy fatigability
 Renal failure
 Disturbance in water, electrolyte and acid-base
metabolism
 Uraemic syndrome
 Multiple dysfunctions of major organ systems
 End stage renal disease
 Inability to sustain normal body function

48. Diagnosis
1. History DM, HBP, nocturia, polyuria
2. Physical exam
3. investigations
Blood tests
 Serum Creatinine and urea ( Cr cl using kockroft and gault equation)
 Electrolytes hyperkalemia, hyperphosphatemia, hypocalcemia
 FBC anemia
 lipid profile inc. cardiovascular risk
 ANA/ds DNA antibody SLE
Urine tests
 Urinalysis – macroscopic , microscopic and dipstick – BROAD CAST : SPECIFIC FOR CRF (DILATED
SURVIVING NEPHRONS). Non-specirfic : proteinuria, RBC
 24hr urine tests – protein excretion, Cr cl
 Spot urine – ACR, UAC
Imaging
 Ultrasound hydrinephrosis, retroperitoneum fibrosis, tumor, small echogenic kidney
 Plane x-ray ureteric obstruction, calculi
 Contrast urography ureteric obstruction,
 CT renal mass, cyst, calculi
Biopsy
 For unclear dx

50. CKD Stages

51. Role of the GP
 Responsible for managing CKD patients with stages
1,2,and3.
 Principal goals of CKD management are:
-slow the rate at which nephrons are lost.
-reduce cardiovascular and renal risk
-early detection and management of CKD complicati0n
-avoidance of nephrotoxic medications and ensuring
that dosage of other prescribed drugs are appropriate for the
level of kidney function, avoiding contrast x-rays.
-and timely referral of CKD patients nephrologist.

52. Indications for referral
 eGFR<30ml/min/1,73m2[stage 4 or 5 CKD]
 Rapidly declining kidney function[>15% decr. in GFR
over 3 months.
 Significant proteinuria >1g/24hrs
 Glomerular haematuria
 Kidney impairment plus hypertension that proves
difficult to control
 Diabetes with kidney impairment or
proteinuria/albuminuria

53. How to slow rate of
progression of CKD

54.  target blood pressure of less than 130/80 mm Hg.
(KDOQI, JNC VII)
 Target bp of less than 125/75 with proteinuria
 RASI 1st choice of tx – renal protective
 Enalapril 5-15mg po bd
 Edema – loop diuretics 1st choice tx
 If serum creatinine levels increase more than 30%
from baseline after adding RAS blockers, RAS blockers
should be stopped.
 Avoid in stage 3b, bilateral renal artery stenosis, or
renal artery stenosis.
 eGFR < 40 risk of hyperkalemia
1. Aggressive blood pressure control

55. 2. Proteinuria goal
 One of the main factor for progression of ckd
 Target proteinuria of <1000mg/day.
 RASI 1st choice of tx.
 non-dihydropyridine calcium channel blockers and
aldosterone antagonist also have anti-proteinuric effect
3. Avoid further damage
• Avoidance of nephrotoxins including intravenous (IV)
radiocontrast media, nonsteroidal anti-inflammatory agents
(NSAIDs), and aminoglycosides.
• Ensuring that dosage of other prescribed drugs are
appropriate for the level of kidney function.

56. 4. Aggressive glycemic control. The American Diabetes
Association (ADA) recommendations (target hemoglobin A1c
[HbA1C] < 7%)
5. Treatment of hyperlipidemia.
 Total chol < 4.0 mmol/L
 T2DM
 IHD
 Chronic renal failure
 Dietary advice and Statin therapy simvastatin 5-40mg nocte
6. Protein restriction, salt, k, phosphate restriction.
7. Smoking cessation (nephrosclerosis)
8. Exercise and weight loss may reduce proteinuria
9. SNAPSS
10. All patient with CRF should be started on ACEI

57. Treating Complications of CKD

58. Treating edema and fluid
overload
 Usually develops in stage 5
 Dec. GFR, RAS, aldosterone
 Loop diuretic is the best diuretic to use
 USE IV furosemide if severely edematous (poor absorption due to
gut edema)
 Adverse effect – diuresis related, hypersensitivity and ototoxicity.
 Dietary sodium restriction <2g/day
drug Daily oral Moderate CKD Severe CKD
Furosemide 20-80 mg 80mg 200mg

59. Hyperkalemia
 Usually does not develop until the GFR falls to less than 20-25
ml/min/1,73m2.
 Mild levels: low potassuim diet.
 Severe hyperkalemia can cause cardiac arrest!
 Avoid drugs that raise serum k eg NSAIDS, nonselective beta-
blockers
 Chronic or non-emergency control
 Resonium (binds K+ in gut) 5-10g tds
 Emergency treatment of high potassium (>7 mmol/l) with ECG
changes –REFFER PATIENT
 First: - decrease myocardial excitability due to hyperkalemia
with IV Calcium chloride(500-1000mg infusion for 2-3 mins) or
Calcium gluconate (1000mg infusion for 2-3 mins)(note:
Calcium does not reduce potassium level; it is cardioprotective
in presence of high potassium)
 Then, lower potassium level by facilitating the uptake of
potassium into cells with 50ml of 50% dextrose and 10 units IV
insulin -
 Sodium bicarbonate (if acidosis)

60. Hypertension
 Driven by volume expansion
 3+ medications
 1st line: enalapril 20mg BD
 2nd line: HCT 50mg daily
 3rd line: CCB, BB

61. Anemia in chronic renal failure
 Type of anemia
 Normocytic normochromic
 Pathogenesis of anemia
 Dec. erythropoetin, Uremia-induced platelet dysfunction,
nutritional deficiency.
 Treatment
 Observation. FBC every 6/3 monthly for stage 3 and
below
 Correct iron deficiency. Ferrous sulphate 300mg PO 6Qhr
 Severely symptomatic refer - blood transfusion (Hb<7)
 Recombinant erythropoetin ($$$$$$$)

62. Renal osteodystrophy
 Usually develops in stage 4 and 5
 Patients with renal disease often develop low serum
calcium levels and bone disease
 Pathogenesis
 The kidney is less able to produce calcitriol, and so is less
able to reabsorb calcium
 Gut reabsorption of calcium is also decreased
 Therefore serum calcium levels are low
 Low serum Ca++ levels lead to secretion of PTH
 PTH leads to resorption of calcium from the bones
 If this goes on long enough, it isn’t particularly
good for the skeleton!

63. Renal osteodystrophy
 Treatment
 Hyperphosphatemia
 Restrict dietary phosphate(milk, cheese, egg)
 Phosphate binding drugs: calcium carbonate 500mg po/d
 Hyperparathyroidism
 Calcitriol supplements: 0.125mg po/d
 Hypocalcemia
 Calcium carbonate
 Calcitiol
 Caltrate 600mg/d

64. Metabolic Acidosis
 Usually does not develop until stage 5
 Kidney is the only organ to excrete hydrogen ions.
 MA is associated with:
 protein-energy malnutrition, loss of lean body mass,
and muscle weakness.
 Contributes to development of bone osteodystrophy
bone acts as a buffer for excess acid, with resultant loss of mineral
 tx- refer
- sodium-bicarbonate: 840 mg/d

65. ESRD - Uremia
 When do you get symptoms?
 Stage 5
 Associated with high blood urea nitrogen levels
 Less associated with serum creatinine
 Distressing symptoms
 Anorexia, nausea and vomiting
 Lassitude, pruritis, twitching, platelet dysfunction
 Major complications
 Uremic encephalopathy
 Uremic neuropathy
 Pericarditis
 Bleeding tendency
 Restless leg syndrome
 Treatment
 Referral
 Renal replacement therapy

66. Vinaka