Chronic Kidney Disease Flashcards
1
Q
Definition of CKD
A
- Progressive and Irreversible loss of renal function as a result of sustained kidney injury
- Glomerular Filtration Rate (GFR) of below 60ml/min
2
Q
Stages of CKD (+ S&S at each stage)
A
- Normal Kidney Function, GFR > 90mls/min: None/Hypertension
- Mild Kidney Function, GFR > 60-89mls/min: Subtle hypertension, Increased Urea and Creatinine
- Moderate Kidney Damage, GFR 30-59mls/min: Mild hypertension, Increased Urea and Creatinine
- Severe Kidney Damage, GFR 15-29mls/min: Moderate hypertension, Increased Urea and Creatinine, Anaemia, Hyperphosphatemia, Increased Triglycerides, Metabolic Acidosis, Hyperkalemia, Salt/Water Retention
- End-Stage Kidney Disease, GFR < 15-29mls/min: Severe hypertension, Increased Urea and Creatinine, Anaemia, Hyperphosphatemia, Increased Triglycerides, Metabolic Acidosis, Hyperkalemia, Salt/Water Retention
3
Q
Causes of CKD
A
- Associated with Systemic Diseases
- Diabetes Mellitus (Most significant risk factor)
- Hypertension
- Acute Kidney Injury
- Chronic Glomerulonephritis (Inflammation of tiny filters in the Kidney)
- Chronic Pyelonephritis (Pyogenic infection of the Kidney)
- Obstructive Uropathies (Structural or Functional hindrance of normal urine flow)
- Vascular Disorders
4
Q
Pathophysiology of CKD
A
- Nephron Adaptation:
- Surviving nephrons undergo compensatory hypertrophy to maintain excretion
- It becomes insufficient as function declines below 25%
- Gradual progressive decrease in nephrons causes decreased GFR, accumulation of wastes and toxins, leading to CKD - Progression Mechanisms
- Proteinuria: Due to glomerular hyper filtration, increases capillary permeability and loss of negative charge, contributing to tubulointestinal injury, inflammation and fibrosis
- Angiotensin II Activity: Vasoconstriction of Efferent Arterioles, causes glomerular hypertension, and increases glomerular capillary permeability, and leads to proteinuria. Increased tubulointestinal inflammation and fibrosis, causes renal scarring and leads to systemic hypertension
5
Q
(12) Clinical Features of CKD
A
- Creatinine & Urea Clearance
- Fluid & Electrolyte Balance
- Calcium, Phosphate & Bone
- Metabolism
- CVS
- Pulmonary System
- Haematological System
- Immune System
- Neurological System
- Gastrointestinal System
- Endocrine & Reproductive System
- Integumentary System
6
Q
(CF) Creatinine & Urea Clearance
A
- Decreased GFR, increases plasma creatinine as there is no regulatory adjustment (an Index for changing glomerular function)
- Decreased GFR, increases Urea, which is filtered and absorbed
7
Q
(CF) Fluid & Electrolyte Balance
A
- Sodium level:
- Normal until late-stage disease by compensatory mechanisms of increased excretion
- Retention of sodium and water with decreased GFR and activation of the RAAS
- Retention of Na, Water -> Oedema, HPT, Heart Failure - Potassium levels rise (Hyperkalemia):
- May become threatening - Metabolic Acidosis - develops when GFR decreases to 20%:
- Mainly due to decreased H+ removal, HCO3- reabsorption
8
Q
(CF) Calcium, Phosphate & Bone
A
- Hypocalcemia (Decreased calcium level)
- Due to impaired renal synthesis of Vitamin D3 with decreased reabsorption of calcium from GIT
- Stimulates the parathyroid hormones, mobilises calcium from bone - Hyperphosphatemia (Increased phosphate level)
- Binds to calcium, further contributing to hypocalcemia - Renal Osteodystrophies
- Combined effect of hyperparathyroidism & Vitamin D deficiency
- Osteoperosis, Osteomalacia, Osteofibrosa
- Bone pain, fractures
9
Q
(CF) Metabolism
A
- Proteinuria, Inflammation, Anorexia contributes to negative nitrogen balance, resulting in decreased muscle mass, and serum proteins
- Hyperlipidemia is common due to the decreased removal of Low-Density Lipoprotein (LDL) from decreased lipoprotein lipase activity, leading to risk of atherosclerosis
10
Q
(CF) Cardiovascular System
A
- CV Disease is a major cause of death
- Hypertension - From increased extracellular fluid (ECF) volume and RAAS activation resulting in Left Ventricle Hypertrophy (LVH), Congestive Cardiac Failure (CCF)
- Ischemic Heart Disease, Acute Myocardial Infarction, Peripheral Vascular Disease - From hyperlipidemia and artherosclerosis
- Pericarditis (Inflammation of the Pericardium) - From inflammatory uremic toxins
11
Q
(CF) Pulmonary System
A
- Fluid overload, Congestive Heart Failure, Dyspnoea
- Pulmonary Oedema
- Metabolic Acidosis develops-> Kussmaul Breathing
- Pulmonary Hypertension:
- Left Ventricle Dysfunction
- Uremic; Associated Vascular changes
12
Q
(CF) Haematological System
A
- Normochromic, Normocytic Anaemia
- Decreased erythropoietin (EPO), decreases RBC life span due to uremia - Impaired platelets function
- Increased bleeding tendency
- Bruises, Epistaxis, GI Bleed, Cerebrovascular haemorrhage - Alteration in Thrombin & other clotting factors
- Hypercoagulability
13
Q
(CF) Immune System
A
- Suppression of the immune system due Uraemia
- Aggravated by Malnutrition, Metabolic Acidosis, and Hyperglycaemia
- Systemic inflammation
- Increased risk of infection, Virus-associated Cancers (HPV, Hep B & C, Epstein-Barr Virus)
14
Q
(CF) Neurological System
A
- Neurologic symptoms are common and often progresses due to accumulation of toxins
- Include headache, sleep disorders, impaired concentration, and judgement, memory loss (Uremic Encephalopathy)
- Peripheral neuropathies with Uraemic toxins
- Impaired sensations with lower limbs
15
Q
(CF) GI System
A
- Bleeding ulcer due to uraemic gastritis
- Non-specific symptoms (Common)
- Nausea, Vomiting, Diarrhoea, Anorexia (Often results in Malnourishment and loss of weight) - Uremic Factor
- Type of bad breath caused by breakdown of urea by salivary enzymes