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
A patient presents with pain/tenderness in the abdomen. He says it is present in his tummy and feels worse when he has the urge to go to the bathroom. O/E you notice abdominal distension in RH and talipes equinovarus. He has no other medical history other than oligohydramnios in utero and pulmonary hypoplasia at birth. He has no family history other than polycystic kidney disease on both maternal and paternal sides of the family.
What investigations would you order? What might you expect to see regarding the context of this patient.
His urinalysis shows proteinuria and haematuria. As well as this, the US shows enlarged kidneys bilaterally.
Give a DDx.
Outline the management for his queried diagnosis.
- US: Enlarged kidneys bilaterally – increased echogenicity + anechoic masses (liquid-filled cysts)
- CT
- IV Pyelogram (IVP): Obstructions in renal pelvis + urinary tract
- Liver biopsy
- Genetic testing: PKD1 or PKD2
DDx: Polycystic Kidney Disease
- Recessive
- Dominant
- -> Determine via genetic test
Management: • Supportive (delay progression): Monitoring/Avoid nephrotoxic substances/Treat arterial hypertension/Treat UTIs • Treat liver failure • Genetic counselling • RRT: Dialysis/Kidney transplantation
What is Rapidly Progressive Glomerulonephritis?
syndrome of kidney disease characterised by deposition of antibodies (IgG/IgM) at the basement membrane (anti-GBM antibodies) which results in a decline in GFR within 3 months with glomerular crescent formation seen. Can be caused by a variety of diseases such as Goodpasture Syndrome, Systemic Lupus Erythematosus or Granulomatosis with Polyangiitis.
Outline the pathophysiology of Rapidly Progressive Glomerulonephritis.
List the pathological manifestations due to the disease.
complex deposition (type III hypersensitivity) with collagen antigens in plasma depsited in fixed tissues (glomerular BM) –> activate complement system generating by-products –> attract leukocytes + monocytes and C3a + C5a increase vascular permeability and MAC ≈ disruption in BM –> Plasma leak into urinary space (Bowman’s Capsule)
• Sieve effect: Gross leaks due to numerous sites of BM damaged
• Fibrin leakage
• RBC leakage (haematuria)
• Glomerular crescents: Cell proliferation in confined space ≈ reduced capillary and glomerulus
• Urine output reduced
• Necrosis (perfusion –> ischaemia)
Which is true for Glomerulonephritis?
A. It is a nephrotic syndrome which can progress to Nephritic Signs later
B. It is a nephritic syndrome which may progress to Nephrotic signs later
C. It is a nephrotic syndrome only
D. It is a nephritic syndrome only
B. It is a nephritic syndrome which may progress to Nephrotic signs later
List the signs and symptoms of Rapidly Progressive Glomerulonephritis.
- Fatigue
- Fever
- Nausea + Vomiting
- Pain (flank/abdominal
- Haematuria
- Oliguria (≤ 0.4L/24 hours)/ Anuria (≤ 0.1L/24 hours)
- Proteinuria
- Casts in urine
- Hypertension
- Oedema
A patient presents with sudden fatigue, fever and acute, severe pain. He describes the pain as severe and ‘on his sides’, radiating towards his groin. He has also mentioned coughing up blood which is fresh and red, in small quantities. He mentions no changes to his bowel movements however he has been urinating less. He has no other morbidities. He mentions his father’s side of the family have a few members with autoimmune diseases but he cannot remember which.
O/E you notice hypertension and oedema. Additionally you notice crackles on lung examination.
What investigations would you order? What might you expect to see.
You get a positive result for anti-GBM antibodies. What is your DDx?
Outline a management plan for the patient.
- Urinalysis: Proteinuria/Leukocytes/Haematuria/pH (acidic)/RBC or WBC casts
- Metabolic Profile: Creatinine (elevated)/Urea (raised)/Bicarbonate
- Inflammatory markers: CRP
- Biopsy: Crescenteric glomerular deposits
- Serology (antibodies):
- Anti-GBM (type IV collagen)
- ANCA – Granulomatosis with polyangiitis; Churg-Strauss Syndrome; Microscopic polyangiitis
- Anti-dsDNA = Systemic Lupus Erythematosus
Anti-GBM (type IV collagen) antibodies suggest an autoimmune disease against the basement membrane in alveoli (lung involvement) and glomerulus (renal involvement). Additionally, haematuria is observed with proteinuria due to nephritic syndrome progressing to nephrotic signs. Biopsy showed crescentic glomerular deposits.
DDx: Rapidly Progressing Glomerulonephritis as part of Goodpasture’s Syndrome ?
Management: • Corticosteroids: Prednisolone 40mg \+ Bisphosphonates + Calcium/Vitamin D3 • Cyclophosphamide • Plasmapheresis • RRT: Dialysis/Transplant
Describe membranoproliferative glomerulonephritis.
What type of hypersensitivity reaction is it?
Glomerular disease caused by immune complex (type III hypersensitivity) deposits in the kidney glomerular mesangium and basement membrane which results in both basement membrane and mesangium thickening
Type III hypersensitivity reaction.
State the key features of membranoproliferative glomerulonephritis.
Is this a nephritic or nephrotic syndrome?
Features: Nephrotic Syndrome
- Slow
- Haematuria
- Proteinuria
- No pain
What is Berger’s Disease?
Is this a nephritic or nephrotic syndrome?
Glomerulonephritis caused by IgA deposition in the mesangium of the glomerulus which results in mesangial proliferation
Features: Nephritic Syndrome
• Pain
• Haematuria
• Oliguria/Anuria
What is Proliferative Glomerulonephritis?
Outline the key features.
glomerular disease involving immune complex deposition (antibody against tissue antigen in type III hypersensitivity) resulting in complement fixation and pro-inflammatory reactions which mediates proliferation of endothelial cells and mesangial cells resulting in damage to the basement membrane and nephritic syndrome.
Nephritic Syndrome
• Haematuria
• Pain
• Oliguria/Anuria
Describe Goodpasture Syndrome.
autoimmune disease with anti-GBM antibodies attacking glomerulus in kidney and alveoli in lungs which cause haemoptysis and haematuria with a relatively rapid onset classed as a type II hypersensitivity reaction.
Outline the pathophysiology of Goodpasture Syndrome.
• Anti-GBM antibody-mediated (type II hypersensitivity) with a3-type IV collagen antigens in plasma and IgM/IgG deposited in glomerular membrane + alveolar membrane complement generating cytokines and C3a/C5a complement fixing with MAC creating disruption in BM ≈ leakage of plasma proteins + passage of inflammatory cells into Bowman space ≈ formation of fibbing clot + proliferation of cells (macrophages, fibroblasts, neutrophils, epithelial cells) ≈ crescent moon formation ≈ compression of glomerulus ≈ renal dysfunction
List the symptoms and signs of Goodpasture Syndrome.
Is this a Nephrotic or Nephritic Syndrome?
Nephritic Syndrome (pain, haematuria, oliguria, little/no proteinuria)
Signs and Symptoms: • Haemoptysis • Pain • Fatigue • Fever • Nausea
- Anuria/Oliguria
- Haematuria
- Crackles on lung examination
- Proteinuria
- Oedema
- Hypertension
Outline 3 investigations you would want to conduct in a queried Goodpasture Syndrome patient.
For each of the investigations, suggest what may be seen.
- Renal function: Creatinine (high)/Urea (high)/ GFR (low)
- Renal biopsy: anti-GBM immunofluorescence – crescentic glomerulonephritis
- Serology: Anti-GBM/anti-ANCA/Serum complement C3
- Hepatitis screen: exclude HBV/HCV
- Anti-streptolysin O titre: Rule out post-streptococcal glomerulonephritis
- Clotting screen: Rule out coagulopathy prior to biopsy
For a patient known to have Goodpasture Syndrome, outline the management.
- Oral corticosteroid
- Plasmapheresis
- Cyclophosphamide
• Supportive care (irreversible renal disease)
Describe membranous nephropathy.
slow progressive glomerular disease which is primary (idiopathic) or secondary (autoimmune, infections, drugs, inorganic salts, tumours) whereby immune complexes (antibodies bound to antigens in type III hypersensitivity) in glomerular basement membrane resulting in thickened glomerular basement membrane (hyperplasia).
Outline the pathophysiology of membranous nephropathy.
• Primary (idiopathic) or Secondary (autoimmune/infection/drugs/inorganic salts/tumours) result in immune complexes (type III hypersensitivity) adhere to glomerular basement membrane resulting in glomerular basement membrane hyperplasia
Give 3 risk factors for a patient to develop Membranous Nephropathy.
- M
- > 40 Years
- FHx of autoimmune
- Hepatitis B/C
- Syphilis
- Medications: NSAIDs/Penicillamine/Lithium/Captopril
List the signs and symptoms of Membranous Nephropathy.
Signs and Symptoms: Nephrotic Syndrome
• Oedema: Peri-orbital + Lower extremities
• Slow onset
- Hypertension
- Proteinuria
- Xanthelasma
- Foamy urine
Mrs Smith, a 44 year old Waitress presents with peri-orbital oedema and oedema at the lower extremities. She has Hepatitis B and previously had Syphilis which has been treated with penicillin. Her family have a history of cardiovascular disease and autoimmune diseases such as Goodpasture Syndrome on her mother’s side and Vasculitis/SLE on her father’s side.
O/E you notice she has a blood pressure of 155/94, peripheral oedema and peri-orbital oedema. Additionally xanthelasma is present as well as xanthomas on the elbows and knees.
What stage of Hypertension does Mrs Smith have? What is the difference between xanthelasma and xanthomas?
What investigations would you order. For each investigation, what might you expect to see?
Give a DDx and outline a management plan.
Stage of Hypertension 1 (140-159/90-99 mmHg)
Xanthelasma is present on the eyelids whereas Xanthoma is present anywhere on the body.
- Urinalysis: Proteinuria/Lipiduria/Bland sediment
- UACR: > 3.5 = nephrotic syndrome
- Serum urea: Normal/Elevated
- Serum creatinine: Normal/ Elevated
- eGFR: Normal/Decreased
- Serum albumin: Hypoalbuminemia (<3g/dL)
- Lipid profile: Hyperlipidemia/Normal
DDx: Membranous Nephropathy
- Lifestyle change: Low salt + Protein diet (if HTN)
- ACEi/ARB: Ramipril/Losartan (if Hyperlipidemia)
- Statin: Atorvastatin/Simvastatin (if Oedema)
- Loop diuretic: Furosemide
- Corticosteroid: Prednisolone
Describe minimal change disease. What type of hypersensitivity reaction is it?
glomerular disease which results in nephrotic syndrome due to idiopathic T-cell mediated damage (type IV hypersensitivity) of altering the glomerular basement membrane, particularly podocytes, altering permeability so increased serum proteins and albumin enter Bowman’s space, resulting in Nephrotic syndrome.
Outline the pathophysiology of Minimal Change Disease.
• Primary (kidney) or Secondary (HBV, HCV, Lymphoma, Measles) causing T-cell mediated (type IV hypersensitivity) damage of glomerular basement membrane causing effacement of podocytes with increased permeability allowing protein extrusion into Bowman’s Space
List 3 risk factors for Minimal Change Disease.
- Age < 18 years
- Viral infection
- Cancer (lymphoma)
Is Minimal Change Disease a nephritic or nephrotic syndrome?
State the features of a nephrotic syndrome.
Signs and Symptoms: Nephrotic Syndrome • History of recent viral illness • Oedema • Normal BP • Absence of haematuria
A 16 year old boy presents with oedema in the peripheries and around his eyes. He recently visited his local GP with viral infection symptoms which is being managed supportively. He also adds that there have been no changes to his bowel function but he has noticed his urine is foamy and ‘thicker’. You take a comprehensive sexual history and elucidate that he is a heterosexual man who has one sexual partner, has not travelled to any high-risk places, exhibits low-risk behaviours and is not an IVDU with no tattoos.
O/E you identify a blood pressure of 126/85mmHg, a heart rate of 76bpm.
What investigations would you order? Give an anticipated find for each.
Suggest a DDx and outline a management plan.
Investigations:
• Urinalysis: Hyaline casts/Oval bodies/Proteinuria/No significant haematuria
• UPCR: > 2 = 2g/24 hours
• Serum albumin levels: < 3g/dL
• Serum lipid profile: hyper-TG, Hyper-Cl
• U+E: Hyperuremia; Hyponatremia
• GFR: Normal
• US-Abdomen: Normal; May be echogenic and loss of corticomedullary differentiation if severe oedema
DDx: Minimal Change Disease
Management:
• Corticosteroids: Prednisolone 40mg for 6/52. 60mg PE on Day 1
• Low salt and protein diet
• Loop diuretic: Furosemide 1-2mg/kg IV every 6-12 hours
Outline the pathophysiology of Focal Segmental Glomerulosclerosis.
What type of hypersensitivity reaction is this?
Primary (idiopathic) or Secondary (viruses, toxins, autoimmune) cause T-cell mediated (Type IV hypersensitivity) damage podocytes = detach from glomerular basement membrane expose glomerular basement membrane + parietal epithelial cells which stimulates proliferation of endothelial, epithelial and mesangial cells and fibrosis with sclerosis in a segment of glomerulus (segmental) Podocytes and Epithelial cells die with protein leaking across membrane and cholesterol levels rise due to hepatic synthesis and loss of fat-binding proteins in serum (proteinuria depletes them).
A 45 year old male presents with weight gain over a few months. He has a family history of a kidney disease which has a slow progression but he cannot remember the name of it. He is an obese gentleman with a history of heroin abuse which lead to him having chronic viral infection - Hepatitis B Virus. He says he takes no over the counter drugs apart from Entecavir. He says he has no bowel changes but has noticed a change in his urine, it is thicker and foamy.
O/E you notice peripheral oedema, a blood pressure of 167/98mmHg, xanthelasma and Muehrcke’s Lines.
i) Why is he taking Entecavir?
ii) Why may his urine be foam? Give two reasons.
iii) What stage of hypertension does he have?
iv) What do Muehrcke’s Lines suggest?
Outline the investigations you would conduct and the anticipated findings
Give a DDx. .
Outline the management plan for this patient.
i) Antiviral drug for his HBV - Entecavir
ii)
a) Proteinuria from his Nephrotic syndrome
b) Pyuria from a UTI
iii) Stage 2 hypertension (160-179/99-109mmHg)
iv) Banding on nails suggesting hypoalbuminemia
- Serum Urea: Elevated
- Creatinine: Elevated
- eGFR (MDRD): Decreased
- Urinalysis: Proteinuria/Fatty casts/Oval fat bodies
- UPCR:
- UPCR < 1 = asymptomatic
- UPCR > 3 = symptomatic ≈ 3g/24 hours
- Serum albumin: Hypoalbuminemia (nephrotic syndrome)
- Renal biopsy: Focal segmental areas of mesangial collapse and sclerosis
DDx: Focal Segmental Glomerulosclerosis
- Corticosteroid: Prednisolone 1mg/kg PO OD ≈ 40mg
- ACEi/ARB: Lisinopril 2.5 mg PO OD
- Dietary modification: Reduce sodium + Protein intake
- Statin: Atorvastatin/Simvastatin/Risovustatin/Pravastatin
- Loop diuretics: Furosemide
Describe Vasculitis.
c-ANCA or p-ANCA antibodies bind to neutrophils adhered to endothelium of vessels restricting flow and causing inflammation of vessels
State the 3 categories of Vasculitis. Give an example for each.
Categories:
1) Large-vessel vasculitis
• Takayasu’s arteritis
• Giant cell arteritis
2) Medium-vessel vasculitis
• Polyarteritis nodosa
• Kawasaki’s disease
3) Small-vessel vasculitis
• ANCA-associated vasculitis (granulomatosis with polyangiitis; microscopic polyangiitis; eosinophilic granulomatosis
• Henoch-Schonlein Purpura
• Leukocytoclastic angiitis
Outline the pathophysiology of Vasculitis.
• Idiopathic (unknown cause) with antigen exposure leading to immune response immune-complexes mediate damage of the blood vessel wall = fibrinoid necrosis of vessel wall with karyorrhexis (nuclear fragmentation and chromatin break-up) with red blood cell extravasation
State 5 signs and 3 symptoms of Vasculitis.
- Arthralgia
- Myalgia
- Malaise
• Headache (GCA)
- Amaurosis fugax (= painless vision loss) (large vessel vasculitis)
- Upper extremity/jaw claudication (large vessel)
- Asymmetric pulses (large vessel)
- Bruits (SCA and AA) (large vessel)
- Abdominal pain (medium-vessel)
- Foot/Wrist drop (medium-vessel)
- Cutaneous levers (medium-vessel)
• Vasculitic rash: Purpura/Petechial
- Haematuria (small-vessel)
- Otorrhoea (small-vessel)
- Wheeze (small-vessel; eosinophilic granulomatosis with polyangiitis)
A 51 year old caucasian female presents with headache, myalgia, malaise and fever. She mentions she has experienced some vision loss in her right eye but there is no pain. She also mentions that she has been experiencing some tightness in her jaw. She has a PMHx of diabetes mellitus, coronary artery disease and Coeliac Disease. She has a family history of autoimmune diseases which include Glomerulonephritis, SLE, Vasculitis and Ankylosing Spondylitis.
O/E you notice asymmetric pulses, bruits in her Subclavian Artery and Aortic Artery. You also identify a vasculitis rash which is approximately 15cm by 18cm present on the anterior leg that is a confluent patch with purpura. The rash is non-blanching. Additionally you notice foot drop, compensated by her gait.
i) What is a bruit?
ii) What is the term for a skin manifestation of vasculitis?
iii) What nerve is affected in foot drop? Give the three main muscles innervated by this nerve.
iv) What type of gait is compensating for the foot drop?
What Investigations would you run and what may you anticipate?
Give a DDx and outline the management plan.
i) Turbulent blood flow heard on auscultation over an artery
ii) Cutaneous vasculitis
iii) Deep peroneal/fibular nerve (L4-S1)
Anterior leg compartment: Extensor digitorum, Tibialis Anterior, Extensor Hallucis Longus
iv) High-stepping gait
Investigations:
• ESR: > 100mm/hour
• CPR: Elevated
• ANCA:
• Positive cANCA against proteinase-3 = granulomatosis with polyangiitis
• pANCA against myeloperoxidase = microscopic polyangiitis/eosinophilic granulomatosis with polyangiitis
• Serum urea + creatinine: Elevated (Small-vessel vasculitis -> GN)
• Urinalysis (small-vessel): Haematuria/Proteinuria/RBC casts
• Biopsy: Fibrinoid necrosis/Karyorrhexis/Red blood cell extravasation
DDx: Vasculitis
(Large-vessel)?
Management: • Corticosteroids \+ • Bisphosphonates: Alendronic acid 5mg PO OD \+ • Vitamin D3/Calcium
• Cyclophosphamide: 1.5-2mg/kg PO OD for 2/12-6/12
Give the alternate, eponymous name for Thrombotic Thrombocytic Purpura (TTP). Describe TTP.
(Moschcowitz Syndrome)
= Thrombotic microangiopathy whereby microthrombi comprising of platelets form in glomerular endothelium causing occlusion to microvasculature
Outline the pathophysiology of Moschcowitz Syndrome.
• ADAMTS-13 deficient/inactive = large vWF multimers in circulation interacting with platelet membranes –> platelet aggregation at sites of high intravascular shear stress –> thrombi causing TTP pentad: microangiopathic haemolytic anaemia; thrombocytopenic purpura; neurological dysfunction; renal dysfunction; fever
An overweight African, American Female patient presents with fever, fatigue and pallor. She also reports experiencing a seizure which reduced her movement. She has no other medical conditions but notes that her father had similar symptoms which went undiagnosed.
O/E you notice conjunctival pallor, a purpuric rash on her abdomen.
i) What type of seizure could lead to reduced movement? Be specific and give the area of brain that may be affected.
Suggest the investigations you would wish to order. List the anticipated finds for each investigation.
Suggest a DDx.
Outline the Management plan for this patient.
i) Jacksonian Seizure: Motor cortex of the cerebrum
Investigations: • Platelet count: Thrombocytopenia • Haemoglobin: Low (anaemia) • Haptoglobin: Decreased • Peripheral blood smear: Schistocytes • Reticulocytes: Raised • Urinalysis: Proteinuria • Urea and creatinine: Uremia/Hypercreatinemia
DDx: Thrombotic Thrombocytic Purpura (Moschcowitz Syndrome)
• Plasma exchange
• Corticosteroids: Prednisolone 1mg/kg/day PO
• Caplacizumab: 10mg IV 1st day then 10mg SC OD for 30 days
–> Caplacizumab mAB against vWF
• Aspirin
• Folic acid: 3-5mg PO OD
List the risk factors for Thrombotic Thrombocytic Purpura.
- Female
- Obesity
- Pregnancy
- Black
- Cancer Tx
Describe Tubulointerstitial Nephritis.
Acute or Chronic condition whereby immune-mediated infiltration of kidney interstitium by inflammatory cells may progress to fibrosis
Give 3 RFs for Tubulointerstitial Nephritis.
- Older age
- Chronic inflammatory disease
- Drugs: ABX; NSAIDs; Diuretics; PPIs; H2As; Immunotherapy
Outline the pathophysiology of Tubulointerstitial Nephritis.
• ABX/PPIs/Immunotherapy agents/Diuretics/H2a/Allopurinol/ Warfarin/Infection/Systemic Diseases/Malignancies/Idiopathic –> antigen-initiated cell-mediated injury ≈ inflammatory cell infiltrate in renal interstitium and tubules ≈ reduced GFR
List the signs and symptoms of Tubulointerstitial Nephritis.
- Fever
- Arthralgia
- Flank pain
- Headache
- Oedema
- Rash
- Costovertebral Angle Tenderness
A 76 year old Male with a history of chronic inflammatory disease presents with fever, arthralgia and flank pain. The pain is localised to the Right Hypochondrium. The patient is currently on the following drugs: Warfarin, Allopurinol, Bendroflumethiazide.
O/E you notice a rash which is 20cm x 15cm on the central upper back of the patient. It is a confluent maculopapular rash with erythema and no secondary characteristics. Additionally, you notice oedema and abdominal distension (enlarged kidney).
i) What risk factors are present for your DDx?
Outline the investigations you would order for this patient. State any anticipated changes with each investigation.
Give your DDx. Outline the management.
Investigations: • Urea + Creatinine: Uremia/Hypercreatinemia • FBC: Eosinophilia • Urinalysis: Sterile pyuria/Low-grade proteinuria/WBC casts • Discontinue offending medication • US-Kidney: Large, echogenic kidneys • Serology: - ANCA (vasculitis) - ANA (SLE) - dsDNA (SLE)
DDx: Tubulointerstitial Nephritis
Management:
• Discontinue offending medication
• Supportive care: Fluids, electrolytes, urea, creatinine
• Diuretic: Furosemide 40-100mg IV 8-12 hours (maximum 600mg/day)
• Corticosteroid: Prednisolone 40-60mg PO OD for 2/52 then 2-3/§1
• Dialysis
What is renal papillary necrosis?
nephropathy involving necrosis of renal papilla (collects urine from nephron) due to ischaemia from diminished renal flow
List the causes of Renal Papillary Necrosis.
Give the aide-memoire/Mnemonic for remembering this.
Causes: POSTCARDS • Pyelonephritis • Obstruction • Sickle Cell Disease • Tuberculosis • Cirrhosis • Analgesics (NSAIDs) • Rejection (renal transplant) • Diabetes Mellitus • Systemic Vasculitis
Outline the pathophysiology of renal papillary necrosis.
• (POSTCARDS: Pyelonephritis/Obstruction/Sickle Cell Disease/Tuberculosis/Cirrhosis/Analgesics/Renal transplant rejection/Diabetes Mellitus/Systemic Vasculitis) causing ischaemia resulting in necrosis and papilla sloughing. Sloughed papillae then obstruct ureters and sclerosis may occur.
List the signs and symptoms of Renal Papillary Necrosis.
• Flank/colicky pain
- Oliguria/Anuria
- Fever
- Albuminuria (proteinuria)
Outline the investigations you would order in a patient with suspected Renal Papillary Necrosis.
- Urinalysis: Proteinuria/Haematuria/ WBC Casts/Sterile pyuria
- U+E: Uremia/Low bicarbonate/alkalosis
- FBC: Anaemia
- US-Kidney: Obstruction and hydronephrosis (sloughing off papillae)
Describe Nephrolithiasis.
formation of stones (calculi; composed of calcium oxalate/calcium phosphate/ uric acid/cysteine/struvite) present in the kidneys (nephrolithiasis) or ureters (ureterolithiasis) causing renal colic (colicky pain) due to dilation, stretching and spasm due to acute ureteral obstruction
List the 5 main types of Renal Calculi.
- Calcium oxalate: Low urine volume/ hypercalciuria/ hypocitraturia
- Calcium phosphate: Low urine volume/ hypercalciuria/ hypocitraturia/ high urine pH
- Uric acid stones
- Cystine stones (inborn metabolic errors -> cysteinuria)
- Struvite stones (Magnesium, ammonium phosphate)
Outline the pathophysiology of Nephrolithiasis.
• Renal papillary plaques of calcium phosphate/apatite deposits erode through uroepithelium as adhesion site for stones; OR intra-tubular stones form obstruction of collecting system with intraluminal pressure increased + stretching giving afferent sensory input generating pain (renal colic)
List the signs and symptoms of a patient with Nephrolithiasis.
- Renal colic: Severe, acute, loin-to-groin radiation
- Testicular pain
- Obesity
- Hx nephrolithiasis
- Urinary urgency
- Haematuria
- Abdominal distension (hydronephrosis)
Mrs Horin, a 43 year old patient presents with severe, acute pain. She says it is in her upper right abdomen, on the side. She says it comes on randomly, the type of pain is sharp and it radiates from her flank to her groin. It is made to feel much worse with urinary urgency and she fears enuresis which would be devastating as she is a primary school teacher. Her diet is balanced but she says she likes a meat platter with Red Wine and cheese every evening to relax.
O/E you notice abdominal distension, guarding on palpation and the kidneys are heavy when balloting on an Abdomen exam.
What investigations would you order? State the anticipated finds for each investigation.
Give your DDx and outline a management plan for Mrs. Horin.
• Urinalysis: Leukocytosis/Haematuria/Nitrates
• FBC: Leukocytosis/Variable
• Serum U+E and creatinine: Variable
• Urine pregnancy test: Negative
• CT-KUB (non-contrast): Calcification, hydronephrosis, perinephric stranding
- Uric Acid Stones are radiolucent –> not visible on CT
• Stone analysis: Stone composition
DDx: Nephrolithiasis
–> Suspected Uric Acid Stone
Management:
• Conservative management: Hydration/Pain control/Anti-emetics (metoclopramide)
• ABX: Nitrofurantoin 100mg PO BD 1-2/52
• Medical Expulsive Therapy (MET): Tamsulosin 0.4mg OD
• Surgical removal: Percutaneous nephrostolithotomy
State the most common type of renal calculi.
What are these caused by?
What do these appear like?
Calcium oxalate ≈ 75%
- Hypercalciuria
- Hyperoxaluria
- Hypocitraturia
- Low urine pH
Appearance: Biconcave dumbbells/bipyramidal envelopes
What is the appearance of calcium oxalate stones?
A. Coffin-lid appearance
B. Rounded rhomboids/needle-shaped
C. Biconcave dumbbells/bipyramidal envelopes
D. Hexagon-shaped
C. Biconcave dumbbells/bipyramidal envelopes
What is the appearance of uric acid stones?
A. Coffin-lid appearance
B. Rounded rhomboids/needle-shaped
C. Biconcave dumbbells/bipyramidal envelopes
D. Hexagon-shaped
B. Rounded rhomboids/needle-shaped
What is the appearance of struvite stones?
A. Coffin-lid appearance
B. Rounded rhomboids/needle-shaped
C. Biconcave dumbbells/bipyramidal envelopes
D. Hexagon-shaped
A. Coffin-lid appearance
What is the appearance of cystine stones?
A. Coffin-lid appearance
B. Rounded rhomboids/needle-shaped
C. Biconcave dumbbells/bipyramidal envelopes
D. Hexagon-shaped
D. Hexagon-shaped
What is the appearance of calcium phosphate stones?
What is the cause of calcium phosphate stones?
A. Wedge-shaped crystals
B. Rounded rhomboids/needle-shaped
C. Biconcave dumbbells/bipyramidal envelopes
D. Hexagon-shaped
A. Wedge-shaped crystals
Causes:
- Hyperparathyiridism
- Type 1 renal tubular acidosis
What type of renal calculi may not be seen on a CT-KUB and why?
Uric Acid stones are radiolucent thus may not be seen on a CT-KUB
What is the cause of uric acid stones?
Low urine pH
Gout
Hyperuricemia
Hyperuricosuria
What is the cause of struvite stones? State the crystal appearance of these stones
- UTI with urease-producing bacteria
Rectangular prisms (Coffin-lid appearance)
Describe Pyelonephritis.
inflammation of the kidney due to a bacterial infection
State 3 risk factors for pyelonephritis.
- Acute pyelonephritis
- Vesicoureteral reflux
- Obstruction
- Renal calculi
- Diabetes Mellitus
Outline the pathophysiology for Pyelonephritis.
Chronic inflammatory process (failure to treat acute pyelonephritis; infection with E. coli, Klebsiella, Proteus spp.) –> thinning of renal cortex with deep, segmental, coarse cortical scarring –> Club-shaped deformity of renal calyces occur at papilla which retract into scars.
Give two types of Pyelonephritis. Outline the key difference.
• Xanthogranulomatous pyelonephritis (XGP): severe, atypical rare form of chronic pyelonephritis
- Unilateral
- Causative pathogen mainly Proteus
• Emphysematous pyelonephritis (EPN): severe, life-threatening infection of renal parenchyma
- main pathogens: E. coli, Proteus, Klebsiella
- Occurs mainly in patients with poorly controlled diabetes
List the signs and symptoms of pyelonephritis.
- Nausea
- Fever
- Flank pain: Severe, loin-to-groin
- Fish-smelling urine
- Dysuria
- Hypertension
- Hx of acute pyelonephritis
- Hx of renal obstruction
- Pyuria
- Leukocyturia
A 53 year old male painter presents with nausea, fever and flank pain. He describes the pain as a 9/10 which is present on his right flank and moves towards his genitals. He also says that he has notices a foul-smelling, fish smell to his urine as well as it being painful when urinating. He has a history of gout and nephrolithiasis/ The latter of which was left undiagnosed as the renal calculi could not be seen on the CT-KUB.
O/E you notice a blood pressure of 185/113mmHg. Additionally, you notice abdominal distension on his right hypochondrium which the patient displays signs of guarding on palpation.
What stage of hypertension does this patient have?
Outline the investigations you may order and state the anticipated finds for each.
Give a DDx and outline the management plan.
Stage 3 Hypertension
Investigations:
• Urinalysis: Haematuria/Proteinuria/Leukocytes/WBCs
• Renal function: Hypercreatinemia/Reduced eGFR
• Urine culture: Positive or sterile
• Electrolyte panel: Hyponatremia/Hyperkalemia/Acidosis (low bicarbonate)
• FBC: Anaemia/Leukocytosis
• US-renal: small, irregular, scarred kidneys; echogenic parenchyma; hydronephrosis; renal stones; peri-renal fluid collections
• XR-KUB: Renal calculi/kidney size
DDx. Nephrolithiasis and Pyelonephritis
Management:
• Treat underlying cause
XGP
• Ceftriaxone: 1g/24 hours IV
• Nephrectomy
EPN
• Percutaneous drainage + ABX + Supportive therapy: Ceftriaxone 1g/24 hours IV
• Nephrectomy
Describe hydronephrosis.
kidney enlargement due to water accumulation as a result of improper urine excretion from the kidney to the bladder secondary to another disease e.g. nephrolithiasis, CAKUT, vesicoureteral reflux, urethral stricture and stenosis
Outline the pathophysiology of hydronephrosis.
• Obstructive condition intrinsic or extrinsic reducing urinary flow –> reduced renal blood flow, reduced GFR and up-regulation of RAAS causing atrophy and apoptosis in tubules and interstitial fibrosis with macrophage infiltration of interstitial spaces
List the signs and symptoms of hydronephrosis.
- Flank pain: Severe, local, loin-to-groin
- Fever
- Urinary urgency/Enuresis
- Reduced force of stream
- Incomplete emptying
- Distended/palpable bladder
- Anuria/dysuria
- Enlarged nodular prostate on PR
- Costovertebral angle tenderness
A 37 year old women, Mrs James, presents with a fever and extreme flank pain. She describes the pain as 8/10, at the site of her right flank and it moves to her groin. She says she has had issues with urinary continence (enuresis). She has a PMHx of varicose veins, fibromyalgia, anxiety and gout.
O/E you observe a distended and palpable bladder with costovertebral angle tenderness.
What investigations would you order? Give the anticipated find for each.
State your DDx. Outline your management.
Investigations:
• Urinalysis: Leukocytes/Nitrites/Haematuria
—> Rule out Pregnancy with ß-hCG test urinary (preferably blood) ≈ Ectopic pregnancy
• US-Renal: Hydronephrosis
• Urea + Creatinine: Normal/elevated
• FBC: Leukocytosis/Anaemia
• CT-Pyelogram: nephrolithiasis/ureterolithiasis
• IV-Pyelogram: Delayed nephrogram/Delayed obstruction
Hydronephrosis secondary to potential nephrolithiasis (uric acid stone?)
Management:
• Passage with analgesia and rehydration: Ketorolac 30mg IM
• Alpha-blockers: Tamsulosin 0.4mg PO OD
• Active stone removal: Percutaneous nephrolithotomy
A 3 year old boy presents with abdominal distention, abdominal pain and nausea and vomiting. He was born with a congenital syndrome but had the omphalocoele surgically corrected. His parents cannot remember the name of the condition.
O/E you notice early onset obesity, brachydactyly, hypogonadism, macroglossia but his growth is normal as checked by the growth chart.
What investigations would you order and state any anticipated finds you may expect.
What is your suspicion for the DDx of the syndrome this child may have? State the DDx of the presenting condition.
Outline the management plan.
Outline the pathophysiology of the presenting condition.
Investigations: • FBC: Anaemia <110g/L • Renal function: Reduced eGFR • Hypercreatinemia • Urinalysis: Haematuria/Proteinuria • Serum protein: Hypoalbuminemia • US-Abdomen: Echogenic/Heterogeneous/Solid mass • CT/MRI: Renal mass with heterogeneous enhancement
DDx: Wilm’s Tumour
Prader-Willi Syndrome
Management:
• Surgery: Radical nephrectomy
• Post-operative chemotherapy: Dactinomycin + Vincristine
Pathophysiology:
WT1 TS gene ∆ in children with oncology referral (surgery, radio + chemo)
What is the most common type of kidney cancer?
Renal Cell Carcinoma
= most common type of kidney cancer originating in the lining of the proximal convoluted tubule
List 3 risk factors for renal cell carcinoma.
- Smoking
- Male
- Age: 55-84 years
- Developed countries
- Obesity
- Hypertension
Outline the pathogenesis of renal cell carcinoma.
• VHL protein∆ –> elevated HIF ≈ transcription promotion of VEGF, PDGF, EGFR and MMPs (aiding oncogenesis and tumour invasion) –> tumorigenesis and invasion
Mr. James, a 76 year old gentleman from America presents with flank pain, weight loss, fever and malaise. He says the pain has only recently come on but he notices its in the same location (right flank) as where he has had a lump for quite some time. He says he didn’t want to bother the busy doctors with his lump which he noticed 3 years ago. He has coronary artery disease, has had two strokes, has gastritis. He doesn’t drink alcohol since quitting but still smokes 10 cigarettes a day with 40 pack years.
O/E you notice a palpable mass in the abdomen and a blood pressure of 187/117mmHg.
i) What stage of hypertension does Mr James have?
ii) What are the red flags in Mr. James’ history?
What investigations would you order? State the anticipated findings for each.
Outline the management plan for your DDx.
i) Stage 3
ii)
- Age (> 50 years old)
- Weight loss
- Lump
- Malaise
- Smoking
- Alcoholic (previously)
Investigations:
• FBC: Reduced Hb (Anaemia); RBC elevated (erythrocytosis)
• LDH: Elevated > 1.5x
• LFTs: AST elevation/ALT elevation
• Urinalysis: Haematuria/Proteinuria
• US-Pelvis: Abnormal renal cyst/mass
• CT-Abdomen: Renal mass/Regional lymphadenopathy/Visceral bone metastases
DDx: Renal cell carcinoma
Management: Stage-dependent
1-3
• Surgery: Surgical resection
• Local ablation therapy: Radiofrequency ablation (RFA)
4
• Surgery
• Chemotherapy/Radiotherapy
• Clinical trials
A 65 year old female, Mrs Jin, presents with painful urination (dysuria), urinary urgency and polyuria. Additionally, though she is concerned, she is pleased she has lost 2 stone in the last month without exercise. She also suggests flank pain. She has previously had Breast cancer which was cured with surgery and chemotherapy. She is retired after previously working in a industrial factory which was closed due to fears of chemical carcinogens and radiation exposure. She has no other medical conditions other than GORD and gastritis.
O/E you notice abdominal distension and a painless palpable mass in the suprapubic region.
i) What are the red flags in Mrs. Jin’s history?
What investigations would you order? State the anticipated find for each.
Give your DDx. Outline a management plan for Mrs. Jin.
i)
- Age (> 55 years)
- Weight loss
- PMHx Ca
- Occupational radiation exposure
- Chemical carcinogen exposure
- Mass - painless
Investigations: • Urinalysis: Haematuria/Pyuria/RBC casts • FBC: Normal/mild anaemia • US-renal and US-bladder: Obstruction • CT-urogram: Bladder tumours
DDx: Urothelial Bladder Cancer
Management:
Non-invasive
• Transurethral resection
• Intravesical chemotherapy
Locally invasive tumours
• Radical/partial cystectomy with pelvic lymph node dissection
• Preoperative + postoperative chemotherapy
Metastatic Disease
• Chemotherapy
• Surgery/Radiotherapy
• Immunotherapy
Define CKD.
Abnormality of kidney structure or function for ≥ 3 months as determined by eGFR or urinary Albumin
State the three categories of CKD in relation to the anatomy. Give an example of a disease for each.
a) Pre-Renal
• Atherosclerosis
• Real hypoplasia
• Bilateral renal agenesis (Potters Syndrome)
b) Renal • Glomerulonephritis • Focal Segmental Glomerulosclerosis • Membranous Nephropathy • Renal papillary necrosis • Minimal Change Disease • Rapidly Progressive Glomerulonephritis • Diabetes Mellitus • Hypertension • Polycystic Kidney Disease
c) Post-renal
• Obstruction
State the different stages of CKD and the eGFR values for each.
G1: > 90 G2: 60-89 G3a: 45-59 G3b: 30-44 G4: 15-29 G: < 15
State the different stages of CKD and the different Urinary Albumin Creatinine Ratios for each.
A1: < 30
A2: 30 to 300
A3: > 300
List 5 goals for prevention of CKD.
• BP management - 140/90 (< 80 years old) - 150/80 (<80 years old and HBPM/ABPM) - 130/80 (proteinuria present) • Reduce proteinuria • Cessation of smoking • Diabetes control • Reduce BMI
List 2 complications of CKD. State how each occurs.
1) Anaemia
• Reduced EPO
• Increased hepcidin
• Reduced RBC lifespan (uremic environment)
• Increased bleeding risk (uremic environment)
2) Hyperparathyroidism
i) Vitamin D:
• 7-dehydrocholesterol + UVB -> Cholecalciferol (pre-VitD) -> WAT (storage) or Liver (activation)
• Cholecalciferol + 25alpha-hydroxylase (CYP2R1) -> 25-hydroxycholecalciferol (Liver)
• 25-hydroxycholecalciferol + 1alpha-hydroxylase (CYP27B1) -> Calcitriol (Kidneys)
• Calcitriol ≈ increased Calcium resorption + inhibits PTH secretion
ii) PTH: Physiological [Ca++] of 1.1-1.3mM PTH at 50% basal secretion which changes if CaSR detects large deviations e.g. reduced calcium causes increased PTH
• Net reabsorption from bone thus increased serum [Ca2+] and Pi from HA of bone
• Increased calcium reabsorption across DCT of nephron
• Reduced Pi reabsorption across the tubules
Outline the complete pathway of vitamin D synthesis.
Vitamin D:
• 7-dehydrocholesterol + UVB -> Cholecalciferol (pre-VitD) -> WAT (storage) or Liver (activation)
• Cholecalciferol + 25alpha-hydroxylase (CYP2R1) -> 25-hydroxycholecalciferol (Liver)
• 25-hydroxycholecalciferol + 1alpha-hydroxylase (CYP27B1) -> Calcitriol (Kidneys)
• Calcitriol ≈ increased Calcium resorption + inhibits PTH secretion
What is dialysis? When is it used?
Type of renal replacement therapy based on diffusion of molecules across semipermeable membrane separating blood on one side and dialysate.
- eGFR = 7mL
- Prepare patient when eGFR < 20mL
- Education
- Options: Hemodialysis, Peritoneal Dialysis, Transplantation
Explain the differences between the two types of dialysis. Give the benefits and drawbacks of each.
1) Haemodialysis: circulating blood through disposable dialyser with selectively permeable material of large SA.
• Dialysate produced by continuous combination of concentrate with highly treated tap water which has contralateral flow to blood
• Contains low concentration of factors to be removed and high concentration of bicarbonate allowing diffusion in blood and correct of acidosis.
• Removal of accumulated fluid achieved via pressure gradient across dialysis membrane resulting in controlled ultrafiltration.
• Heparin used to prevent clotting and treatment performed x3 per week.
• Adequate control of biochemistry, fluid overload, acidosis and uraemic symptoms in most patients
+ Site of access
+ Established technique: Arteriovenous fistula (arterialised vein thus flow through vein prevents collapse)
+ Less isolating
- 3x per week
- Done in hospital
2) Peritoneal dialysis: peritoneum used as dialysis membrane with pre-packaged fluid instilled into peritoneal space for exchange of products between blood and peritoneal fluid.
• Dialysate contains factors that do not need to be removed at similar levels to plasma
• Acidosis corrected by diffusion of buffer from fluid into blood and ultrafiltration occurs down oncotic gradient as fluid has higher osmolality than plasma due to high concentration of glucose in the instilled fluid.
+ Younger patients preferred
+ Less restrictions
- Complications due to high-glucose fluid e.g. Peritonitis
- Placement of tube
- Requires a virgin abdomen
- Requires 3-5 exchanges of fluid per day every day
Compare and contrast the benefits and drawbacks of renal transplants.
+ No dialysis
+ Better QoL
+ Better Survival (new kidneys)
+ Cost (17,000 per year cf 38,000 per year with dialysis)
- Optional extra (reasons below) - Cardiac disease - Respiratory disease - Malignancy - Severe PVD - BMI > 35: Delayed Graft Function + Post-operative complications - Age?
Which of the following is the gold standard investigation for upper tract calculi?
A) XR-KUB
B) CT-KUB - no contrast
C) CT Urogram with contrast
D) USSKUB
B) CT-KUB - no contrast
Upper tract calculi least commonly presents with…
A) Pain
B) Urinary retention
C) Sepsis
D) Haematuria
B) Urinary retention
In someone with proven ureteric stones, which symptom would be most concerning?
A) Haematuria
B) Nausea
C) Pain
D) Fever
D) Fever
Which is not a recognised risk factor for the development of urolithiasis?
A) Dehydration
B) High salt intake
C) High Red Meat Intake
D) Smoking
D) Smoking
Which of the following bacteria is most commonly associated with stag horn calculi?
A) S. Aureus
B) E. coli
C) Proteus
D) N. gonorrhoea
C) Proteus
Outline what must be done if sepsis is suspected secondary to nephrolithiasis/ureterolithiasis.
Sepsis 6: BUFALO
Give 3, Take 3
Bloods (take) Urine culture (take) Fluids (give) ABX (give) Lactate (take) Oxygen (give)
What feature of ureteric calculi primarily determines its management?
Size - 1cm (10mm) is the key number
ESWL if <1cm
PCNL > 1cm
What percentage of adults have a BP of above 140/90?
A. 40%
B. 50%
C. 60%
D. 70%
A. 40%
If a patient has a BP of 158/95 in your clinic (2 readings 2mins apart) should you?
A. Start treatment immediately
B. Organise ambulatory or home blood pressure monitoring
C. Repeat blood pressure in 6 months
B. Organise ambulatory or home blood pressure monitoring
Name 4 lifestyle changes that can reduce blood pressure
Salt reduction
Weight loss
Alcohol reduction
Increased exercise
Relaxation - mindfulness/bibliotherapy/meditation
Lifestyle changes can lower BP by the same as a single anti-hypertensive drug - true or false?
True
What are the guidelines for a sphygmomanometer cuff?
Bladder width should be 40% arm circumference, bladder length should be 80% arm circumference
Does a cuff that is too small underestimate or overestimate the BP?
overestimates
What is the definition of white coat hypertension?
Hypertension present in surgery but not home readings
Name 2 things that should be done as part of the initial assessment of a patient with hypertension
Check height/weight
Check ECG
Check urinalysis
Check U+Es
Lipid panel
You have a patient with a BP of 223/120 in your clinic – do you..
a. start treatment immediately
b. work out his 10 year risk of cardiovascular disease and then decide
c. give lifestyle advice and repeat BP in 4-6 months
a. start treatment immediately
Which BP treatment should not be given in a patient with a history of gout?
Diuretics (esp thiazides)
Which BP treatment is contra-indicated in asthma?
Beta-blockers
Which BP treatment requires u+es checking 7-14 days after starting?
ACE inhibitors
What would be the significance of a doubling of creatinine after starting this treatment (ACEi)?
Would point to a renal cause of hypertension esp renal artery stenosis
Which BP treatment is first line in Afro-Caribbean patients?
Calcium channel blockers
What is the level of increased cardiovascular risk in Afro-Caribbean patients with hypertension?
3.5x
How long should you give lifestyle measures to work?
4-6 months
You have a patient with a BP of 164/95 who has AF with a rate of 112 (no other medical problems). What type of BP treatment might be particularly effective?
Beta-blocker (might accept rate limiting calcium channel blocker)
You have a 65 year old patient who needs to commence BP treatment. What would be your first choice?
Calcium channel blocker
At which stage of CKD would you refer a patient to secondary care?
When they hit stage 4 (eGFR <30)
What are the parameters for Stage 3a (G3a) CKD?
eGFR 45-59
What level of ACR is relevant for the management of a diabetic patient?
A2 (3-30)
How would you manage a diabetic patient with an ACR at this level (A2 = 3-30)?
Prescribe ACE inhibitor (or ARB)
Symptoms of CKD are common in patients with CKD3 – true or false?
FALSE – usually asymptomatic
Is a single eGFR of 55ml/min/1.73m² diagnostic of CKD3? Justify your answer. (2 points)
No – requires 2 readings 2 months apart
Could be acute - AKI?
What is the correction factor applied to eGFR for Afro-Caribbean patients?
X 1.159
What is an alternative treatment when ace inhibitors are required, but not tolerated?
ARB
What BP treatment commonly causes swollen ankles?
Calcium channel blockers
At which level of ACR in a hypertensive (non-diabetic) patient would specific treatment be recommended?
A3 (ACR ≥ 30)
At which level of ACR in a normotensive, non – diabetic patient would specific treatment be recommended?
ACR ≥70
What 2 types of treatment might be recommended in the above scenarios? (2 points)
ACE inhibitor or ARB
What is superior for testing microscopic haematuria – dipstix or miscoscopy?
DIPSTIX (red cells may haemolyse in transport)
What should you do with a patient of 65 who has isolated persistent microscopic haematuria and dysuria and no evidence of UTI?
Refer as cancer referral to urology
Name one common side effect of ACE inhibitors
cough
ACE inhibitors lower potassium – true or false
False, they tend to raise potassium
ARBs can raise potassium – true or false?
true
Furosemide lowers potassium – true or false
true
What percentage of patients with stage 4 CKD have anaemia?
33%
What is the ideal Hb target level in a patient with CKD?
10-12g/dl (increased thrombotic risk if higher)
What does ESA stand for in the context of CKD related anaemia?
Erythropoietin stimulating Agents
What derangement of calcium occurs in patients with advanced CKD and outline why?
Failure to convert vit D to active form
Failure to convert a25-hyroxyvitamin-D to a1,25-hydroxyvitamin D in the kidney
What rate of decline in eGFR should prompt a nephrology referral?
Decrease of 25% and change in stage or drop of 15ml or more in 1 year
