14 - Renal Medicine Flashcards

1
Q

What are the different ways that renal disease can present?

A

1. Asymptomatic: non visible haematuria, asymptomatic proteinuria, abnormal eGFR, HTN, electrolyte abnormalities

2. Renal tract symptoms: urinary symptoms, loin poin, visible haematuria, nephrotic syndrome, symptomatic CKD

3. Systemic disorder with renal involvement: DM, sickle cell, SLE, infection, malignancy, pregnancy, drugs

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2
Q

How do you take a renal history?

A
  • If being dialysed ask them what mode, what access and when they were last dialysed
  • Important to ask if NSAIDs being taken OTC
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3
Q

How do you perform a renal examination on a patient?

A

https: //www.youtube.com/watch?v=PPhwQgsebKY
- General inspection
- Hands
- Arms
- Face
- Chest
- Abdomen
- Legs and Sacrum
- Further tests

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4
Q

What are some of the different modes of renal replacement therapy?

A

- APD (Automated peritoneal dialysis via peritoneal catheter)

- CAPD (Continuous ambulatory peritoneal dialysis)

- Assisted PD (Can perform at home with help of district nurses)

- UHD (Unit based haemodialysis)

- HHM (Home haemodialysis)

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5
Q

What are the different ways of access for dialysis? (both peritoneal and haemodialysis)

A
  • PD catheter
  • AV fistula
  • Tunelled (Perm-Cath)
  • Non-Tunelled (Vas-Cath)
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6
Q

What are some signs on examination of advanced renal disease?

A
  • Brown nails
  • Yellow brown uraemic skin
  • Uraemic frost from sweat on skin
  • Hyperreflexia
  • Pericardial rub
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7
Q

What are some different renal function tests?

A

Bloods: FBC, U+Es, bone profile, CRP, HbA1c

Urine: dipstick, protein-creatinine ratio, albumin-creatnine ration, urine culture

Imaging: US KUB

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8
Q

How does a metabolic alkalosis show on a VBG and what are some causes of this?

A

- GI losses: vomiting and diarrhoea

- Renal losses: primary hyperaldosteronisms, diuretics

- Intracellular shift: hypokalaemia

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9
Q

How does a metabolic acidosis show on VBG and how can you work out the cause?

A

Anion Gap!!!!

Na - (Cl + HCO3)

Normal is 8-12

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10
Q

What is the cause of the derangment of this patients blood gas?

A
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11
Q

What are some of the symptoms of hypernatraemia and what is the number one cause of this electrolyte abnormality?

A

Thirst, irritability, weakness, confusion, seizures, hyperreflexia, spasticity, coma

Usually due to dehydration which causes cellular dehydration and vascular shear stress so bleeding and thrombosis

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12
Q

What are some causes of hypovolemic, euvolemic and hypervolemic hypernatraemia?

A

Hypovolemic: vomiting, diarrhoea, diuretics, osmotic diuresis

Euvolemic: diabetes insipidus, hypodipsia, inadequate water intake, heatstroke

Hypervolemic: hypertonic dialysis, sodium bicarbonate administration, hypertonic saline administration, hyperaldosteronism, Cushing’s

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13
Q

What are some causes of central and nephrogenic diabetes insipidus?

A

Central (impaired release of ADH)

  • Trauma
  • Tumours
  • Cerebral sarcoid/TB
  • Infection e.g meningitis
  • Cerebral vasculitis e.g SLE

Nephrogenic: (resistance to ADH)

  • Congenital
  • Drugs (lithium, amphotericin)
  • Hypokalaemia
  • Hypercalcaemia
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14
Q

How is hypernatraemia managed?

A

Free water

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15
Q

What are some of the symptoms of hyponatraemia?

A
  • Headache
  • Decreased perception
  • Confusion
  • Seizures
  • Gait disturbance
  • Reversible ataxia
  • Nausea
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16
Q

What is pseudohyponatraemia?

A
  • Sodium <135 but with a normal serum osmolality

- Due to either high lipids, myeloma, hyperglycaemia, uraemia

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17
Q

What are some causes of hypovolemic, euvolemic and hypervolemic hyponatraemia?

A

Hypovolemic: diuretics (thiazides), osmotic diuresis, Addison’s disease due to mineralcorticoid deficiency, diarrhoea

Euvolemic: Hypothyroidism, Glucocorticoid deficiency, SIADH

Hypervolemic: CCF, nephrotic syndrome, liver cirrhosis, renal failure

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18
Q

What are some investigations you should do when a patient has hyponatraemia?

A

- Plasma osmolality: rule out pseudohyponatraemia

- K+ and Mg2+: hypoK and hypoMg can potentiate ADH release

- Urine Na: if <20 then non-renal salt losses, if >40 then SIADH

- TSH and 9am Cortisol

- Calcium, Albumin, Glucose, LFTs

- CT head if suspect SIADH

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19
Q

How do you diagnose SIADH?

A
  • Hyponatraemia with low serum osmolality
  • Urine osmolality >100 with urine Na>20
  • Euvolemia
  • Not on diuretics

PROCESS OF ELIMINATION: normal renal, thyroid and adrenal function

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20
Q

What are some causes of SIADH?

A
  • Malignancy
  • Meningitis
  • Subarachnoid haemorraghe
  • Drugs e.g SSRIs, morphine, amitriptylline
  • Hypothyroidism
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21
Q

What is the management for SIADH?

A

- Fluid restrict: <800mls day

- Furosemide

- Demelocycline or Tolvaptan to induce ADH release (can reverse too far to DI)

  • PO NaCl
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22
Q

What is the management of hypovolemic and hypervolemic hyponatraemia?

A

Hypovolaemic: (renal or GI losses of Na) IV fluids 0.9% NaCl at 1-3ml/kg/hr and add K+ if needed

Hypervolaemic: (increased water lowering Na) fluid restrict and consider furosemide

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23
Q

Why should you not correct hyponatraemia rapdily?

A

Risk of central pontine myelinolysis, correct by <12 mmol/day

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24
Q

How should acute and chronic hyponatraemia be managed?

A

Acute and Symptomatic (<48hours)

  • 3% HYPERTONIC SALINE BOLUSES +/- Furosemide)

Chronic and Symptomatic (>48 hours)

  • If seizures hypertonic saline boluses
  • Otherwise isotonic saline and furosemide

Chronic and Asymptomatic

  • Water restriction
  • Stop offending drug
  • If dehydrated give water
  • If fluid overloaded give water restriction, furosemide and Na
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25
Q

What drugs can cause hyperkalaemia?

A
  • ACEi/ARBs
  • Spironolactone
  • Amiloride
  • NSAIDs
  • Heparin
  • Trimethoprim
  • Betablockers
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26
Q

What are some causes of hyperkalaemia?

A
  • CKD/AKI
  • Drugs (ACEi, spironolactone, NSAIDs, etc)
  • Hypoaldosteronism
  • Addison’s disease
  • Rhabdomyolysis
  • Metabolic acidosis e.g DKA
  • Hyperkalaemic periodic paralysis
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27
Q

What are some causes of artifact hyperkalaemia?

A
  • Haemolysis
  • Raised WCC
  • Raised platelets
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28
Q

What can hyperkalaemia do to the pH of the blood?

A

Metabolic acidosis

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29
Q

When is a patient having Type IV RTA and what are some common causes of this?

A

Due to issue with distal tubule not being able to respond to aldosterone

- Hyperkalemia

- Hypochloraemic metabolic acidosis

- HTN

Causes: hyporeinaemic hypoaldosteronism, diabetic nephropathy, hypertension, NSAIDs, lupus nephritis

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30
Q

How is hyperkalaemia due to type 4 RTA treated?

A
  • Low K diet
  • Fluid restrict
  • Loop diuretic if overloaded
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31
Q

What are some ECG changes with hyperkalaemia?

A
  • Tented T’s
  • Prolonged QRS
  • Slurring ST segment
  • Loss of p waves
  • Sine then asytole
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32
Q

What is the first investigation you should do when a patient has hyperkalaemia on their blood results?

A
  • VBG to check correct
  • ECG to look for changes
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33
Q

How is hyperkalaemia with ECG changes treated?

A

Stabilise myocardium to prevent arrhythmias: 10mls of 10% Calcium Gluconate over 5-10 minutes

Shift potassium back into extracellular space: IV fast acting insulin with glucose or Salbutamol neb

Eliminate potassium from body: Calcium resonium

Dialysis: if treatment resistant

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34
Q

What are some of the symptoms of hypokalaemia?

A
  • Fatigue
  • Constipation
  • Proximal muscle weakness
  • Poor glucose control
  • Cardiac arrhythmias
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35
Q

What are some of the causes of hypokalaemia?

A
  • Poor intake
  • Gut losses e.g vomiting, NG losses, ileostomy
  • Drugs e.g alpha blockers, beta agonists, insullin, theophylline
  • Refeeding syndrome
  • Conn’s syndrome (Primary hyperaldosteronism)
  • Cushing’s syndrome
  • Diuretics
  • Hypomagnesiumaemia
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36
Q

What are some ECG changes with hypokalaemia?

A
  • Small T waves
  • U wave after T
  • Increased PR interval

HypoK is <3.5 but do not see ECG changed until moderately low <2.5-2.9

37
Q

How is hypokalaemia managed?

A
  • Replace Mg
  • Oral K replacement
  • IV replacement in 0.9% NaCl NOT dextrose
38
Q

What are the different options for renal replacement therapy?

A
  • Haemodialysis
  • Peritoneal Dialysis
  • Transplantation (best survival and quality of life)
  • Conservative Management
39
Q

When is long term dialysis started?

A

When needed to manage the symptoms of renal failure. eGFR usually <10-15. Used as a bridge to transplantation

  • Inability to control fluid status e.g pulmonary oedema
  • Inability to control VP
  • Acid-base or electrolyte abnormalities
  • Cognitive impairment
40
Q

How does peritoneal dialysis work to filter the blood?

A
  • Peritoneal membrane acts as dialysis membrane
  • Catheter inserted into peritoneal cavity and dialysate fluid is infused.

This fluid has a high osmotic gradient due to addition of glucose, which pulls water from the patient into the fluid

  • Solutes (urea, creatinine, electrolytes) move from blood across peritoneal membrane into dialysate fluid
  • Continuous process with intermittent drainage and refilling of peritoneal cavity
41
Q

What are the different types of peritoneal dialysis?

A

- Automated PD: Automatic cycler machine at night over 10hours with 10-12L exchanged. Leaves daytime free

- Continuous Ambulatory PD: 4-5 dialysis exchanges a day at regular intervals of 2L.

- Assisted Automated PD: healthcare assistants visit the patient’s home to set up machine for night

42
Q

What are the advantages of peritoneal dialysis?

A
  • Increase QOL as home based
  • Good if patient still got some residual renal function
  • Regime individualised to patient rather than HD clinics
  • Lower risk of HepC
  • No anticoagulation needed
43
Q

What are the disadvantages of peritoneal dialysis?

A

- Patient needs to learn technique

  • Unsuitable if patient has stoma or previous GI surgery

- Risk of peritonitis

- Hernia

  • Hydrothorax
  • Leaks
  • Catheter site infection
  • Loss of membrane function over time
44
Q

How does haemodialysis work to filter the blood long term?

A

Blood pumped from patient into machine where it is passed over a semi-permeable membrane containing dialysis fluid flowing in the opposite direction

Solutes diffuse across down concentration gradient. Excess fluid diffuses down hydrostatic gradient (not osmotic like PD)

Access usually via AV fistula due to risk of infection with central venous dialysis catheters

45
Q

What are the different types of HD?

A

- Unit based

- Home based: training offered so can do more frequently

  • Nocturnal

- CRRT: used in ITU/HDU

46
Q

What are the advantages of haemodialysis?

A
  • More efficient form of dialysis
  • Unit based so support from staff
47
Q

What are the disadvantages of haemodialysis?

A
  • Risk of bleeding due to heparin
  • Infection
  • Hypotension
  • Anaemia
  • AVF steal syndrome
  • SVCO from central lines
  • Time consuming
48
Q

How does haemofiltration work and when is it used?

A
  • Used in critical care patient’s BP is too low for haemodialysis
  • Waste is replaced with volume of clean fluid before (pre-dilution) or after (post dilution) the membrane
49
Q

What are some complications of renal replacement therapy in general?

A

- Cardiovascular disease: raised BP, Ca/PO4 dysregulation, vascular stiffness

- Protein-calorie malnutrition

- Renal bone disease

- Infection

- Amyloid accumulation: carpal tunnel syndrome, arthralgia

50
Q

Sometimes when a patient is in ESRF the decision is made to not carry out RRF and just have conservative management. Which patients does this occur in?

A

Decision after discussion with patient and family about risks and benefits.

- Age >80

- WHO performance of 3 or more

If the characteristics above then RRT is likely to have no survival benefit

51
Q

What are the principles of conservative management in ESRF?

A
  • Symptom control to enhance QoL
  • Respect patients preferred place of care
  • Advanced care plan
  • Support system for patients and family as end of life
52
Q

What are the advantages and disadvantages of a renal transplant for ESRF?

A

Advantages

  • Near normal lifestyle
  • Better mortality/morbidity

Disadvantages:

  • Lifelong medication
  • Risk of rejection
  • Risk of malignancies over time
  • Risk of infection and immunosuppression
  • Long waiting times
  • Need to fufill certain criteria
53
Q

What is the biggest cause of death in dialysis patients?

A

IHD!

54
Q

What are some contraindications for kidney transplantation?

A

- Active infection or malignancy

  • Severe heart or lung disease
  • Reversible renal disease

- Uncontrolled substance abuse

  • Non-adherance to treatment

- Short life expectancy

55
Q

What are the different types of renal graft?

A

Deceased Donor:

  • Long waiting list
  • Survival of kidney and patient lower than living

Living Related Donors

  • Best possible transplant option as higher compatibility as time to HLA march
  • Only takes few months

Living Unrelated Donor:

  • Also a best option

- 4 types: live-donor paired exchange, live-donor/deceased-donor exchange, live-donor chain, altruistic donation

56
Q
A
57
Q

How is hyper acute rejection of a renal graft avoided?

A

Induction of immunosuppression at moment of transplant

Drugs used:

- Methylprednisolone plus one of below

  • Basiliximab
  • Thymoglobulin
  • Alentuzumab
  • Rituximab
58
Q

How is long term rejection of a renal graft avoided?

A

Maintenance of immunosuppression therapy

Steroids: prednisolone or prednisone

Calcineurin Inhibitors: tacrolimus, cyclosporin

Antimetabolites: mycophenolate, azathioprin

T cell regulation: belatacept, belimumab

59
Q

What is the long term care a patient needs following a renal transplant?

A
  • For first 6 months review every few times a month
  • Monitor GFR, CNI levels, proteinuria, Ca, PO4, PTH, lipids and glucose

- Screen for infections

- Vaccinations (not live or attentuared)

  • Check for CVD and bone mineral disease

- Annual skin checks for skin cancer

- Contraception for first year then counsel about pregnancy

60
Q

What are the biggest causes of mortality following a renal transplant?

A
  • CVD
  • Malignancy
  • Infections
61
Q

What are some complications of a renal transplant?

A

Surgical (first month): bleeding, thrombosis, infection, hernia

Rejection: acute or chronic, treat with high dose steroids and increased immunosuppression

Infection: increased risk of infection

Malignancy: increased risk of skin, gynaecological and PTLD cancers

CVD

62
Q

What infections are common following a renal transplant?

A

<4 weeks: nosocomial or from donor

1-12 months: activation of latent infections or opportunistic infections e.g CMV and Pneumocystitis Jirovecci

After 12 months: community acquired

63
Q

What endocrine disorder can occur after a renal transplant?

A

New onset diabetes after transplant (NODAT)

Look at personal risk factors, medications and new gluconeogenic kidney

64
Q

What malignancies should you screen for after a renal transplant?

A
  • Skin
  • Cervix
  • Prostate
  • Renal and urothelial
  • Liver
  • Colorectal
  • Lymphoproliferative disorder (especially if have EBV)
65
Q

What are some simultaneous transplants that can occur with a kidney transplant?

A

- Liver-Kidney: if ESRF and cirrhosis

- Pancreas-Kidney: if type 1 diabetes

- Kidney transplant with ESRF: re transplanted

66
Q

What is the prognosis following a renal transplant?

A
67
Q

How do you carry out a fluid assessment on a patient?

A

- Hands: temp, cap refill, turgor

- Pulse and blood pressure

- JVP

- Face: eyes sunken and dry mouth

- Chest: heart sounds, lung bases, resp rate

- Abdomen: ascites

- Oedema

68
Q

What is dehydration?

A

Excessive loss of water from the body so that there is more water lost than being taken in

69
Q

What hormones regulate fluid balance in the body?

A

ADH

Aldosterone

ANP

70
Q

What are some signs on examination of CKD?

A

- Oedema

- Uraemic breath

- Pericardial rub

  • Pulmonary oedema
  • Palpable kidneys
  • Uraemic yellow skin
71
Q

What are some of the pros and cons of a live renal donor over a deceased renal donor?

A

Pros:

  • Less chance of rejection
  • Shorter waiting time

Cons:

  • Patient may not have someone willing to donate
  • Risks to the donor
72
Q

What are some of the causes of sterile pyuria?

A
  • TB
  • Recently treated UTI
  • Appendicitis
  • Chlamydia
  • Calculi
  • Pregnancy
  • Recent catheter
73
Q

When should you not treat asymptomatic bacteriuria?

A
  • Non-pregnant women
  • Men
  • Adults with catheter
74
Q

How do you manage a UTI in the following patients:

  • Non pregnant women
  • Pregnant women
  • Men
  • Catheterised patients
A

Non pregnant women: 3 days of Nitrofurantoin or Trimethoprim if three or more symptoms of cystitis and no vaginal discharge. If pyelonephritis use co-amoxiclav

Pregnant women: Do not use trimethoprim in 1st trimester or nitrofurantoin in 3rd trimester. Risk of preterm deliver and IUGR

Men: 7 days of Nitrofurantoin or Trimethoprim. If signs of prostatitis give ciprofloxacin for 4 weeks. Send all men with UTI for urological investifation

Cathererised: Only send MSU if symptomatic as all catheters have bacteria. Change long term catheter before antibiotics

75
Q

How does urinary tract tuberculosis present?

A
  • Dysuria
  • Frequency
  • Suprapubic pain
  • Sterile pyuria
  • Negative culture
76
Q

How does diabetic nephropathy develop?

A
  1. Hyperglycaemia leads to hyperfiltration and capillary hypertension as RAAS is activated due to less Na getting to macula densa

2. GBM thickens

3. Mesangial proliferation

4. Glomerulosclerosis

77
Q

How is diabetic nephropathy diagnosed?

A
  • Screening for microalbuminuria using albustix annually

- Dipstick for overt proteinuria

- ACR ratio in urine by sending off

78
Q

What is the histology of diabetic nephropathy?

A
  • Glomerulosclerosis
  • Kimmelsteil-Wilson nodules
  • Thicker GBM
79
Q

How is diabetic nephropathy treated once microalbuminamia has developed?

A

Need to stop proteinuria developing as this is irreversible:

  • Strict HbA1c control <6.5%
  • Tight blood pressure contol using ACEi/ARB
  • Statins
80
Q

What diuretics work in each part of the kidney tubule?

A
81
Q

What are some nephrotoxic drugs?

A
  • NSAIDs
  • Rifampacin
  • Valproate
  • PPIs
  • Furosemide
  • Thiazides
  • ACEi/ARB
  • Lithium
  • Gentamicin and Tobramycin
82
Q

How may a patient with ADPKD present?

A
  • Asymptomatic
  • Abdominal discomfort due to pressure
  • Haematuria from haemoraghe into cyst
  • Hypertension
  • Renal calculi
83
Q

How is ADPKD diagnosed?

A
  • USS
  • Genetic testing
  • Screen for an ask about family history of SAH and intracranial aneurysms
84
Q

How is ADPKD managed?

A
  • Water intake 3-4L a day
  • Control BP with ACEi then thiazide then betablockers
  • Plan for RRT and future transplantiation
  • Tolvaptan
85
Q

What are some examples of loop diuretics, what is their action, when are they given and what are some common side effects?

A

Furosemide and Bumetanide

  • Block Na/K/Cl transporter
  • Fluid overload
  • HypoNa, HypoK, Diuresis, Dehydration
86
Q

What are some examples of thiazide/thiazide like diuretics, what is their action, when are they given and what are some common side effects?

A

Bendroflumethiazide and Indapamide

  • Block NaCl channel in DCT
  • Hypertension and fluid overload
  • Cause HypoNa and Hypo K and Hyper GLUC
87
Q

What are some examples of K sparing diuretics, what is their action, when are they given and what are some common side effects?

A

Amiloride and Spironolactone

Can cause hyperK and gynacoemastia

88
Q

What are some examples of carbonic anhydrase inhibitors what is their action, when are they given and what are some common side effects?

A

Acetazolamide

  • Used for glaucoma and benign intracranial HTN
  • Flushing, metabolic acidosis, agranulocytosis
89
Q

What are some of the side effects of steroids and what are some medications you should give alongside steroids?

A
  • Hyperglycaemia
  • Raised white cells
  • Cushing’s
  • Osteoporosis
  • Glaucoma
  • Muscle wasting
  • Skin thinning