Chronic Kidney Disease Flashcards
What is the aetiology of CKD?
- Diabetes (diabetic nephropathy)
- Hypertension (Hypertensive nephropathy)
- Infections
- Renal disease (RPGN/GN/PCKD)
- Obesity/Dyslipidemia/Hypertriglyceridemia/Metabolic Syndrome
- Obstruction
- Drugs/Toxins
What is prevalence?
Number of affected persons present in the population at a specific time divided by the population at the time
What is incidence?
Number of individuals developing a specific disease/illness over a particular time period
List the potential ways of treatment in chronic kidney failure and the ethical implications of each.
1) Guidelines for RRT and Organ Donation/Transplantation
• Systematic
• Fair
• Efficient
• Expensive (RRT is £17,500 peritoneal dialysis cf £35,000 hemodialysis): £20,000 QALY
2) Live donations
• Willing volunteers (autonomy)
- Ethics: Informed consent
- Safety
3) Peri-mortem donations
• Willing volunteers (autonomy)
- Ethics
- Sensitivity to situation/Dignity
What is a QALY?
cost-utility health-economics measurement used to compare an intervention/treatment against another or against none in order to decide if it is cost-effective and viable both for the patient and hospital/healthcare sector.
Define a QALY in simple terms.
- Years of perfect/full health equivalent to greater number of years in a worse state cf full health
- 10 years x 0.5 full health = 5 QALYs
- 30 years x 0.66 full health = 20 QALYs
- Measured regarding ADL, freedom of pain and mental disturbance
Outline the public health approach in the context of kidney disease.
Public Health Approach • Surveillance: ID Problem • RF ID: Aetiology • Intervention: Management approaches • Implementation: Management plan (How to do it)
What makes a finding interpreted from data ‘apparent’ or ‘real’?
Apparent: Data collection or analysis generates the finding - More investigation required to confirm
Real: Finding is due to genuine factors - Prevalence of condition - Accessibility - Co-morbidities - Different clinical practice
What approach works for donated blood?
- Systematic
- Ethics
- Donor safety: screening, safe environment
- Recipient safety: Not infected/contaminated; correct blood group
Define Hypertension and its values for all the main categories of readings.
High blood pressure (> 140/90mmHg) taken by sphygmomanometry or HBPM +/- confirmed with ABPM (if between 140/90 and 180/120mmHg)
Outline the classification of HTN.
- 1º HTN (idiopathic/essential): Unknown cause (90%)
* 2º HTN: Known cause (10%)
State 3 causes of 2º HTN.
• 2º HTN: Known cause (10%)
- Renal disease: RVD/PKD/GN
- Vascular: RAS/CoA
- Endocrine: Cushing’s/Pheochromocytoma/Thyrotoxicosis/Hyperaldosteronism (Conn Syndrome)
- Other: OSA/ Drug-induced
What is the kidney?
Bilateral bean-shaped organ which is reddish-brown in colour, is retroperitoneal and located in the posterior abdomen at T12-L3 which is responsible for filtration, excretion and blood pressure control.
What are the physiological functions of the kidney? List 5
- Regulation of body fluid volume and osmolality
- Maintenance of ion balance
- Acid-base balance
- Waste excretion
- Vitamin D hydroxylation (25-hydroxycholecalficerol + 1a hydroxylase 1,25 a hydroxycholecalciferol (calcitriol))
- EPO
- Renin production
What is blood pressure? What is the equation for blood pressure?
= pressure exerted by ventricles (circulatory system) against arterial walls
BP = CO x TPR
What is cardiac output? What is the equation for cardiac output?
= rate of blood pumped out of LV into systemic circulation (L/min)
CO = HR x SV
What factors contribute towards cardiac output?
• Heart Rate:
- PSNS (Brake)
- SNS (Accelerator)
- Adrenaline
- Drugs
• Stroke Volume:
- SNS (increased)
- EDV (SNS veins/ BV/ skeletal muscle pump/ respiratory pump ≈ venous pressure ≈ venous return)
Give 3 factors contributing to EDV.
Vasomotor tone of veins (SNS)
Skeletal muscle pump
Respiratory pump
Outline the process by which the RAAS rectifies a reduction in blood pressure.
• Hypovolemia ± low osmotic pressure -> reduced BP + increased Na+ -> macula densa detects elevated salts -> reduced baroreceptor firing = reduced SNS drive (= NA) -> renin release (kidney) = angiotensinogen (liver) -> angiotensin I + ACE (lungs) -> angiotensin II…
List the changes AGT II brings about in the body regarding blood pressure regulation. Give a mnemonic for this.
- Arteriolar vasoconstriction (TPR increases)
- Efferent glomerular arteriole vasoconstriction (increase GFR and salt reabsorption)
- ADH secretion (AGT II binds posterior pituitary)
- Salt + water reabsorption via aldosterone release (AGT II binds zona glomerulosa of adrenal cortex = aldosterone release)
Mnemonic: ‘Pressure to get 4As’ Aldosterone release (zona glomerulosa) Arteriolar vasoconstriction Arteriole (glomerular efferent) vasoconstriction ADH release (posterior pituitary)
Outline the process by which the RAAS rectifies a reduction in blood pressure.
• Low osmotic pressure (increased osmolarity) ± reduced blood volume -> reduced BP -> hypothalamic osmoreceptors detect ∆ -> neuronal afferents to posterior pituitary gland = ADH/AVP released:
- Increased water permeability (renal collecting ducts) = increased blood volume + reduced urinary output
- Vasoconstriction = increased TPR
- Dipsogenic: Hypothalamic thirst center
List the 3 main effects of ADH on the body regarding blood pressure regulation. Give a mnemonic for this.
- Increased water permeability (renal collecting ducts) = increased blood volume + reduced urinary output
- Vasoconstriction = increased TPR
- Dipsogenic: Hypothalamic thirst center
Mnemonic: People Value Dipsogenesis
Permeability
Vasoconstriction
Dipsogenic
Outline how ANP rectifies an aberrant change in blood pressure.
• Increased osmotic pressure/increased blood volume -> increased BP -> detected by atrial cardiopulmonary baroreceptors in atrial cardia = increased baroreceptor firing -> ANP release -> afferent arteriole vasodilation + increased flow through vasa recta (reduce osmolarity of medullary interstitium) + increase collecting duct Na+ excretion -> reduce blood volume = reduce BP
List the effects ANP has on the body regarding blood pressure regulation. Give a mnemonic for this.
- Natriuresis:
- Arteriole (afferent) vasodilation
- Aldosterone reduced (zona glomerulosa)
- Vasodilation (vascular)
- Fibrosis (anti-fibrotic)
Mnemonic: FAVourite NA
Fibrosis reduced
Arteriole (afferent) vasodilation
Vasodilation
Natriuresis
Aldosterone reduced
Outline the effects PGs have on renal regulation of blood pressure.
• Reduced blood volume (hypovolemia) -> reduced O2 availability ≈ Hypoxia -> HIF-2 -> EPO enhancer -> EPO production (liver) -> increased erythropoiesis ≈ increased Hematocrit (increased MCV; reduced MCHC?) = increased BP
What is Mean Cell Volume? Give the equation. State the 3 categories and give an example of a disease for each.
MCV = Hct/ RBC
• Average volume of RBCs
- Microcytic (60-80fl): iron deficiency, thalassemia
- Normocytic (80-100fl): blood loss, chronic disease anaemia, renal impairment
- Macrocytic (100-120fl): megaloblastic anaemia, B12/folate deficiency, myelodysplasia
What is Mean Cell Haemoglobin? Give the equation.
MCH = Hb/RBC
• Average mass of Hemoglobin per red blood cell
What is Mean Cell Haemoglobin Concentration? Give the equation. State the two scenarios/categories.
MCHC = Hb/Hct
• Average concentration of Hemoglobin per volume of red blood cells
- Normochromic: Cells with normal [Hb]
- Hypochromic: Cells with low [Hb]
What are the effects of Angiotensin II and where do these occur (sites)?
Renal retention of salt and water + vasoconstriction ≈ increased arterial pressure
1) Resistance vessels: vasoconstriction≈ increase total peripheral resistance
2) Kidneys: constricts renal arteries ≈ reduce blood flow ≈ reduce glomerular filtration rate
3) Adrenal gland: Aldosterone release from adrenal cortex ≈ increase sodium and water reabsorption
4) Pituitary: ADH release
List 3 main examples which lead to renin secretion.
1) SNS nerve activation due to baroreceptor feedback
2) Renal artery hypotension via JGM
3) Decreased sodium in kidney distal tubules detected by osmoreceptors
What two main renal mechanisms influencing blood pressure control? List the factors that influence each of these and indicate whether they increase of decrease these factors).
ECF Volume: - Fall in GFR (+) - Salt reabsorption (+) - SNS (≈ salt reabsorption ≈ +) - RAAS (≈ salt-reabsorption ≈ +)
Vasoconstriction:
- SNS (+)
- RAAS (+)
- Endothelin (+)
- Renal PGs (e.g. other vasodilators) (-)
What is hypertension? State the classification and types.
High blood pressure (> 140/90mmHg) taken by sphygmomanometry or HBPM +/- confirmed with ABPM (if between 140/90 and 180/120mmHg) Classification: Aetiology
1) 1º Hypertension (Idiopathic):
- Unknown origin
- 90% cases
2) 2º Hypertension
- Known cause
- 10% cases
What are the risk factors for hypertension? How may they be stratified?
Risk factors: Modifiable and Non-modifiable • Smoking • Salt intake • Physical inactivity • Obesity • Metabolic Syndrome • Diabetes Mellitus • OSA • High cholesterol • Alcohol intake • Dietary fibre • Iatrogenic (COC, Steroids, NSAIDs, Adrenaline, Salbutamol)
- Age (> 65 years)
- Ethnicity: Black ancestry
- Family History of HTN or CAD
What is the pathophysiology of hypertension?
Salt retention: abnormal salt retention + reabsorption of sodium≈ water into intravascular compartment by osmosis ≈ increase intravascular volume ≈ baroreceptors ≈ ANP release ≈ acts on SMCs ≈ vasoconstriction ≈ increase TPR
What is the diagnosis of HTN according to NICE when considering different categories?
Clinical:
1) < 140/90 mmHg: Check every 5 years
2) 140/90 – 179/119 mmHg: ABPM/HBPM; Investigate for target organ damage + assess CVD %
3) > 180/120 mmHg: % Target organ damage, drug treatment, refer for review
ABPM/HBPM:
1) < 135/85 mmHg: Check every 5 years
2) 135/85 – 149/94 mmHg: Drug treatment/Consideration/Lifestyle factors
3) > 150/95mmHg: Lifestyle + Drug treatment
List the main investigations for blood pressure.
- Sphygmomanometry: Clinical/HBPM/ABPM
- Urinalysis: Albumin/Creatinine/Blood/Leukocytes
- Blood tests: HbA1c/U+E/GFR/Cholesterol/Thyroid/Aldosterone/Cortisol
Context dependent: • ECG • Ophthalmoscopy • Ultrasound • Biopsy
List 5 examples of complications from hypertension.
a) CV
- Congestive heart failure
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Coronary artery disease and myocardial infarction
- Atrial fibrillation
- Aortic aneurysm
- Aortic dissection
- Carotid Artery Stenosis
- Peripheral Artery Disease
- Atherosclerosis
b) Brain
- Stroke, TIA
- Cognitive changes e.g. Memory Loss
c) Kidneys
- Hypertensive nephrosclerosis
d) Eyes
- Hypertensive retinopathy
- Papilledema
What are the key lifestyle changes in the prevention and management of hypertension?
- Weight loss: BMI 25-35 (5-10%); BMI 35 < (15-20%)
- Physical activity increased: 150 CME + x2 resistance exercise
- Improve dietary intake: DASH diet = fruit + veg, low fat dairy, wholegrain, fish, nuts and poultry
- Reduce alcohol intake: < 14 units per week + education
- Stress: Advise mindfulness or social prescribing
What approach should be taken to encourage behavioural change in patients?
5As of Ask, Assess, Advise, Agree, Assist
What tool can be used to help set goals with patients? Which stage of the 5As would this fit under best?
SMART Goals which can be used in the Agree stage of the 5As
Specific Measurable Achievable Rewarding Timely
List some drugs which may cause hypertension. What is this called?
Drug-induced Hypertension (iatrogenic)
- NSAIDs (afferent arteriole vasoconstriction≈ reduced GFR ≈ reduced natriuresis + diuresis ≈ increase intravascular volume and osmolality ≈ increase pressure)
- Oral Steroids
- Venlafaxine (increase norepinephrine and potentiation of noradrenergic neurotransmission)
- Oral sympathomimetic decongestants (Pseudoephedrine - Sudafed)
- Soluble or dispersible drugs (contain Salt)
- Illicit Drug Use (cocaine, amphetamines)
List tools which may be used to assess a patient’s CV risk.
What is estimation of cardiovascular (CV) risk based on?
Assessing CV risk: ASSIGN / Q-Risk • Blood pressure • Age • Weight/height • Gender • Smoking • Cholesterol • Ethnicity • Social class • FHx • Diabetes/RA/Renal function
List some clinical features of hypertension.
• Incidental find***
–> Require regular screening
- Headache
- Dizziness
- Tinnitus
- Flushed appearance
- Epistaxis
- Chest discomfort
- Palpitations
- Nervousness
- Fatigue/sleep disturbances
- Raised JVP
- Vision disturbances
- Ankle oedema
- Ascites
State the stages of hypertension.
Stage 1: 140-159/90-99
Stage 2: 160-179/99-109
Stage 3: 180-209/109-119
Stage 4: ≥210/≥120
A patient presents with a blood pressure of 153/95. She is aged 64 years old, has no other morbidities and is Caucasian. Give the stage of her hypertension, the advice you would give and the drug choice you may Rx.
What is her blood pressure target you would encourage her to aim for?
Stage 1 HTN
Find reason: ABPM/HBPM; Investigate for target organ damage + assess CVD % (ASSIGN/Q-Risk)
CCB as over 55 and no T2DM
- Amlodipine
- Diltiazem
- Verapamil
Aim for 140/90mmHg or 135/85mmHg
A patient presents with a blood pressure of 165/103. She is aged 54 years old, has no other morbidities other than Type 2 Diabetes Mellitus and is Caucasian. Give the stage of her hypertension, the advice you would give and the drug choice you may Rx.
What is her blood pressure target you would encourage her to aim for?
Stage 2 HTN
Find reason: ABPM/HBPM; Investigate for target organ damage + assess CVD % (ASSIGN/Q-Risk)
ACEi/ARB (54 < 55 + T2DM)
- Lisinopril/Ramipril/Captopril
- Losartan/Candesartan
Aim for 140/90mmHg or 135/85mmHg
A patient presents with a blood pressure of 180/119. He is aged 54 years old, has no other morbidities other than atrial fibrillation and is Caucasian. Give the stage of his hypertension, the advice you would give and the drug choice you may Rx.
What is his blood pressure target you would encourage her to aim for?
Stage 3 HTN
Treat straight away as ≥ 180mmHg systolic blood pressure
CCB (no T2DM): Choose a rate-limiting CCB that affects heart + vasculature
- Diltiazem
- Verapamil
Aim for 140/90mmHg or 135/85mmHg
A patient presents with a blood pressure of 214/125. He is aged 84 years old, has no other morbidities other than atrial fibrillation and is from the West Indies.. Give the stage of his hypertension, the advice you would give and the drug choice you may Rx.
What is his blood pressure target you would encourage her to aim for?
Stage 4 HTN
Treat straight away as ≥ 180mmHg systolic blood pressure
CCB (Caribbean + Age > 55): Rate-limiting for his AF
- Diltiazem
- Verapamil
150/90mmHg or 145/85mmHg as over 80 years old
Outline the MOA of ACEi.
Give an example of an ACEi.
List 3 side effects.
List 3 contraindications.
Inhibit ACE enzyme to reduce AGT II production
- Ramipril
- Lisinopril
- Captopril
SEs: • Dry cough • Dizziness • Tiredness • Headaches • Angiooedema (AfroCab) • Hyperkalemia • Renal impairment
Contraindications:
• Allergy/Hypersensitivity
•
Angioneurotic oedema PMHx
Bilateral renal artery stenosis or renal artery stenosis
• Pregnancy
Outline the MOA of ARBs.
Give an example of an ARB.
List 3 side effects.
List 3 contraindications.
Antagonist to AT II-R which reduced AGT II mediating effects of vascular growth, vasoconstriction and salt-retention
- Losartan
- Candesartan
- Irbesartan
SEs: • Dizziness • Headaches • Back/Leg Pain • Hyperkalemia • Renal impairment
Contraindications:
• Allergy/Hypersensitivity
• Angioneurotic oedema PMHx
Bilateral renal artery stenosis or renal artery stenosis
• Pregnancy
Outline the MOA of CCBs.
Give an example of an CCBs.
List 3 side effects.
List 3 contraindications.
Block L-type CaVg channels to reduce vasomotor tone (PR) +(chronotropy) + power (inotropy)
- Amlodipine
- Felodipine
- Lercanidipine
- Verapamil
- Diltiazem
SEs: • Headaches • Ankle oedema • Dizziness • Flushes (increased vasodilation) --> Bradycardia if rate-limiting
Contraindications: • Uncontrolled heart failure • Cardiogenic shock (MI) • Significant aortic stenosis • Unstable angina • Pregnancy
Outline the MOA of thiazide diuretics.
Give an example of an thiazide diuretics.
List 3 side effects.
List 3 contraindications.
Relax vascular smooth muscle + Block apical NCC transporter (DCT) to reduce movement causing increased luminal ion concentration with osmosis and diuresis, reducing intravascular volume and blood pressure
- Indapamide
- Bendroflumethiazide
SEs: • Electrolyte imbalance: Low K+, Na+, Mg++ • Calcium retention/hypocalciuria • Metabolic alkalosis • Gout • Erectile dysfunction • Hyperglycaemia Hyperlipidemia
Contraindications: • Hypercalcaemia • Hyponatraemia • Hypokalaemia • Symptomatic hyperuricaemia Addison’s Disease • Diabetes
Outline the MOA of loop diuretics.
Give an example of an loop diuretics.
List 3 side effects.
List 3 contraindications.
Bind apical NKCC2 to reduce activity and absorption, elevating tubular luminal ion concentration resulting in water movement by osmosis and diuresis, reducing intravascular volume and blood pressure
• Furosemide
SEs: • Electrolyte imbalance: Low K+, Na+, Mg++ • Calcium retention/hypocalciuria • Dizziness • Fatigue • Metabolic alkalosis • Muscle spasms • Nausea
Contraindications: • Hypercalcaemia • Hyponatraemia • Hypokalaemia • Symptomatic hyperuricaemia Urinary retention (may cause prostatic hyperplasia) • Hypovolemia • Gout • Hypotension
Outline the MOA of aldosterone (mineralocorticoid receptor) antagonists..
Give an example of an MR antagonists.
List 3 side effects.
List 3 contraindications.
Bind aldosterone-specific Na,K-ATPase to reduce electrochemical gradient then less Na+ absorbed, increased osmolarity of tubular filtrate causing water in by osmosis and diuresis to reduce sodium reabsorption and potassium excretion
- Spironolactone
- Eplerenone
SEs: • Hypotension • Renal impairment • Electrolyte imbalance: Hyperkalemia and Hyponatremia • GI Upset • Metabolic acidosis • Gynaecomastia (Spironolactone)
Contraindications:
• Addison’s Disease
• Anuria/Renal failure
•
Hyperkalemia
Outline the MOA of NCB (sodium channel blockers).
Give an example of an NCB.
List 3 side effects.
List 3 contraindications.
Block apical epithelial sodium channel in collecting tubule causing reduced sodium absorption, increased osmolarity then water out by osmosis and increase natriuresis and diuresis to reduce intravascular volume and blood pressure
• Amiloride
SEs: • Hypotension • Renal impairment • Electrolyte imbalance: Hyperkalemia and Hyponatremia • GI Upset • Metabolic acidosis
Contraindications:
• Addison’s Disease
• Anuria/Renal failure
•
Hyperkalemia
Outline the MOA of ß-blockers.
Give an example of an ß-blockers.
List 3 side effects.
List 3 contraindications.
Antagonist of ß1-adrenoceptor causing reduced cAMP production, reducing sympathetic drive: reduced contractility of cardiac tissue + vasomotor tone + reduces renin release
- Atenolol
- Bisoprolol
- Carvedilol
SEs: • Fatigue • Cold peripheries • Bradycardia • Peripheral Vascular Disease • Bronchospasm GI Upset • Erectile Dysfunction • Heart failure • Sleep disorders
Contraindications: • Asthma • Cardiogenic Shock/Uncompensated HF • Hypotension • Marked Bradycardia • Severe Peripheral Arterial Dise
Outline the MOA of a-blockers.
Give an example of an a-blockers.
List 3 side effects.
List 3 contraindications.
Antagonist of a1-adrenoceptor in SMC which reduces vasoconstriction causing vasodilation and reduced TPR and blood pressure
- Doxazosin
- Prazosin
SEs: • Postural Hypotension • Dizziness • Lethargy • GI Upset • Headache • Peripheral oedema
Contraindications:
• History of micturition syncope
• Postural Hypotension
What is multi-drug treatment?
Multidrug therapy is using two or more drugs in combination
List the advantages and disadvantages of multi-drug treatment.
Advantages:
+ Reduced mortality/morbidity
+ Numerous sites/targets of action
+ Reduce dose burden of individual drugs ≈ minimise side-effects
Disadvantages:
- Concordance
- Side effects may increase
- Cost
Which aide-memoir can be used for producing a differential diagnosis in pathology such as CKD?
- Trauma: Physical (Acute, Chronic or Complex)
- Tumor: Non-neoplastic, Benign, Malignant (1º or 2º)
- Tubercle: Chronic inflammation or immune-response related
- Inflammation: Acute, Infection, Immunological
- Stone: Metabolic or Genetic
List the potential anatomical regions where pathology may occur giving rise to CKD.
CKD may affect any part of urogenital tract: kidney/ureter/bladder/prostate/urethra
Describe the cause of haematuria.
Damage to the glomerulus (or Bowman’s Capsule) results in pathologically increased permeability to blood cells passing resulting in blood present in the urine (haematuria) which is a feature of nephritic syndrome
Describe the causes of proteinuria.
Damage to the glomerulus (or Bowman’s Capsule) results in pathologically increased permeability with increased protein passing resulting in protein present in the urine (proteinuria) which is a feature of nephrotic syndrome.
Define HTN.
High blood pressure (> 140/90mmHg) taken by sphygmomanometry or HBPM +/- confirmed with ABPM (if between 140/90 and 180/120mmHg)
Classify the types of HTN.
• 1º HTN (idiopathic/essential): Unknown cause (90%)
• 2º HTN: Known cause (10%)
- Renal disease: RVD/PKD/GN
- Vascular: RAS/CoA
- Endocrine: Cushing’s/Pheochromocytoma/Thyrotoxicosis/Hyperaldosteronism (Conn Syndrome)
- Other: OSA/ Drug-induced
List 8 risk factors for Hypertension.
- Smoking
- Salt intake
- Physical inactivity
- Obesity
- Metabolic Syndrome
- Diabetes Mellitus
- OSA
- High cholesterol
- Alcohol intake
- Dietary fibre
- Iatrogenic (COC, Steroids, NSAIDs, Adrenaline, Salbutamol)
- Age (> 65 years)
- Ethnicity: Black ancestry
- Family History of HTN or CAD
- Gender
Outline the pathophysiology of Hypertension.
• Salt retention water into intravascular compartment via osmosis increase intravascular volume baroreceptors ANP release acts on SMCs ≈ vasoconstriction = increase TPR
List the signs and symptoms of Hypertension. Are they always seen?
• Incidental find***
Require regular screening
- Headache
- Dizziness
- Tinnitus
- Flushed appearance
- Epistaxis
- Chest discomfort
- Palpitations
- Nervousness
- Fatigue/sleep disturbances
- Raised JVP
- Vision disturbances
- Ankle oedema
- Ascites
Outline the diagnostic categories of hypertension.
Clinical:
1) < 140/90 mmHg: Check every 5 years
2) 140/90 – 179/119 mmHg: ABPM/HBPM; Investigate for target organ damage + assess CVD %
3) > 180/120 mmHg: % Target organ damage, drug treatment, refer for review
ABPM/HBPM:
1) < 135/85 mmHg: Check every 5 years
2) 135/85 – 149/94 mmHg: Drug treatment/Consideration/Lifestyle factors
3) > 150/95mmHg: Lifestyle + Drug treatment
Outline the clinical stages of Hypertension.
Stage 1: 140-159/90-99
Stage 2: 160-179/100-109
Stage 3: 180-209/110-119
Stage 4: >210/>120
Outline the factors involved in assessing cardiovascular risk. Which two decision making tools are there.
Assessing CV risk: ASSIGN / Q-Risk • Blood pressure • Age • Weight/height • Gender • Smoking • Cholesterol • Ethnicity • Social class • FHx • Diabetes/RA/Renal function
Outline the investigations which can be used in Hypertension and its complications.
- Sphygmomanometry: Clinical/HBPM/ABPM
- Urinalysis: Albumin/Creatinine/Blood/Leukocytes
- Blood tests: HbA1c/U+E/GFR/Cholesterol/Thyroid/Aldosterone/Cortisol
Context dependent: • ECG • Ophthalmoscopy • Ultrasound • Biopsy
List 5 non-pharmacological ways to manage hypertension.
- Weight loss: BMI 25-35 (5-10%); BMI 35 < (15-20%)
- Physical activity increased: 150 CME + x2 resistance exercise
- Improve dietary intake: DASH diet = fruit + veg, low fat dairy, wholegrain, fish, nuts and poultry
- Reduce alcohol intake: < 14 units per week + education
- Stress: Advise mindfulness or social prescribing
Outline 5 pharmacological classes of treatments for Hypertension. For each class, give two examples.
- ACEi: Ramipril/Lisinopril/Captopril
- ARBs: Losartan/Candesartan
- CCBs: Amlodipine/Lercanidipine/Verapamil/Diltiazem
- Thiazide diuretics: Indapamide/Bendroflumethiazide
- Loop diuretics: Furosemide
- Aldosterone (MR) antagonists: Spironolactone/Eplerenone
- NaCB: Amiloride
- Beta blockers: Atenolol/Bisoprolol
- Alpha 1 antagonists: Doxazosin/Prazosin
What aide-memoir could be used for identifying the DDx of CKD?
- Trauma: Physical (Acute, Chronic or Complex)
- Tumor: Non-neoplastic, Benign, Malignant (1º or 2º)
- Tubercle: Chronic inflammation or immune-response related
- Inflammation: Acute, Infection, Immunological
- Stone: Metabolic or Genetic
Describe the glomerulus.
glomerular tuft surrounded by Bowman’s capsule, consists of: afferent and efferent arteriole, endothelium held by mesangium and surrounded by basement membrane, parietal epithelial cells and podocytes.
- Endothelial cells of glomerular capillaries (fenestrations + glycocalyx): filtering + negatively charges ≈ electrostatic repulsion
- Glomerular basement membrane: type IV collagen + heparin sulphate ≈ negatively charged
- Podocytes (Epithelial cells of Bowman’s Capsule): specialized epithelial cells forming visceral layer of capsule –> filtration slits + negative ≈ filtration + electrostatic repulsion
List the 3 main features of the glomerulus.
- Endothelial cells of glomerular capillaries (fenestrations + glycocalyx): filtering + negatively charges ≈ electrostatic repulsion
- Glomerular basement membrane: type IV collagen + heparin sulphate ≈ negatively charged
- Podocytes (Epithelial cells of Bowman’s Capsule): specialized epithelial cells forming visceral layer of capsule –> filtration slits + negative ≈ filtration + electrostatic repulsion
Outline the key differences between a nephritic syndrome and a nephrotic syndrome.
Nephritic: • Pain • Hematuria • Oliguria • Little proteinuria
Nephrotic: • Massive proteinuria (<3g/100mL) • Lipid proteins elevated • Oedema • Hypertension
List the 3 differentiations of CKD based on location. Give examples for each category.
i) Pre-Renal
• Atherosclerosis
• Real hypoplasia
• Bilateral renal agenesis (Potters Syndrome)
ii) Renal • Glomerulonephritis • Diabetes Mellitus • Hypertension • Polycystic Kidney Disease
iii) Post-renal
• Obstruction
Outline the pathophysiology of renal hypoplasia.
• ∆RDGs + Environmental factors + Drugs (ACEi/ARBs) ≈ ∆ embryonic development ≈ reduced nephron number
State 3 symptoms and 5 signs of renal hypoplasia.
• Asymptomatic
- Oligohydramnios
- Prematurity
- Low birth weight
- IUGR
- Polyuria
- Enuresis (urinary incontinence)
- Urinary urgency
- Nocturia
- UTI
A newborn presents with oligohydramnios, low birth weight and IUGR. Give 3 investigations you would order.
On a voiding cystourethrogram, retrograde urine movement is seen.
Give your DDx and outline the management plan for this newborn.
- Urinalysis: Haematuria/Proteinuria/Urea/Creatinine
- Metabolic profile: Urea/eGFR/LFTs
- US: Anatomical abnormalities
- IV Pyelogram (fluoroscopy): Anatomical anomalies
Renal hypoplasia
Management:
• RRT: Dialysis/Transplantation
• IV fluids and electrolytes
• Diuretics: Thiazide diuretics (bendroflumethiazide/Indapamide); Loop diuretics (Spironolactone/Eplerenone)
Outline the pathophysiology of Bilateral Renal Agenesis (Potter’s Syndrome).
• ∆RDGs + Environment/Drugs ≈ ∆ ureteric bud development + X differentiation of metanephric blastema (both structures develop to kidney) ≈ kidney fails to develop
List 5 symptoms a child with Potters Syndrome (Bilateral Renal Agenesis).
- Proteinuria
- Hypertension
- Oligohydroamnios
- Extra-renal manifestations (Potter Sequence): oligohydroamnios + talipes equinovarus (clubbed feet), pulmonary hypoplasia, craniofacial abnormalities.
- Pulmonary hypoplasia
- Club feet (Talipes equinovarus)
- Renal insufficiency
List the symptoms in Potters Sequence.
Talipes Equinovarus
Oligohydramnios
Pulmonary hypoplasia
Craniofacial abnormalities
A neonate presents with difficulty breathing following a pregnancy which had known oligohydramnios. O/E you notice talipes equinovarus, hypertension and proteinuria.
What investigations would you order? What might you expect to see?
Give a DDx and outline the management for this child.
Why does this disease occur?
Investigations:
• Metabolic profile: Creatinine (elevated)/Urea (elevated)/eGFR (low)
• US: Absent kidney(s)
Seen:
- Hypercreatinemia
- Uremia
- eGFR low
- Absent kidneys bilateral
DDx: Bilateral renal agenesis
Cause: RDGs ∆ + Environment/Drugs ≈ ∆ ureteric bud development + X differentiation of metanephric blastema ≈kidneys fail to develop
Management:
• RRT: Dialysis/Transplantation
• IV Fluids and electrolytes
• Diuretics: Thiazide diuretics (bendroflumethiazide/Indapamide); Loop diuretics (Spironolactone/Eplerenone)
What is polycystic kidney disease?
Congenital disease which results in cysts developing in the kidneys, compromising renal function and predisposing to chronic renal disease
Outline the pathophysiology of Polycystic Kidney Disease.
• ∆PKD1 or PKD2 gene (Autosomal recessive/ dominant) ≈ ∆ cell cycle or ∆ calcium channel ≈ cysts in epithelial organs
Give the sigs and symptoms of PCKD for both types of PCKD.
ARPKD:
• Haematuria
• Proteinuria
• Abdominal distension (renal enlargement)
• Extra-renal manifestations (Potter Sequence): oligohydroamnios + talipes equinovarus (clubbed feet), pulmonary hypoplasia, craniofacial abnormalities.
• Obligate liver involvement (portal fibrosis + portal hypertension)
• Hypertension
ADPKD:
• Haematuria
• Proteinuria
• Abdominal Distension (Renal enlargement)
• Recurrent UTI
• Extra-renal manifestations: Potter’s Sequence (TE/OH/PH/CFA); HTN/ epithelial tissue cysts; colon diverticula; cerebral berry aneurysm
