WEEK 7 Flashcards
What is potter syndrome?
Bilateral renal agenesis
- no kidneys present
- infant will be squashed
What is the Vesicoureteric reflux?
Valves from ureter into bladder, bladder refluxes back into ureter increasing risk of irritation and infection
What are examples of (i) primary (ii) secondary glomerular disease?
(i) Glomerulonephritis, glomerulonephrirides
(i) vascular, autoimmune e.g. SLE, amyloid, diabetes, acquired
In Goodpasture syndrome, crescents can be seen hostologically, what are these crescents?
Proliferation of parietal epithelium and inflammatory cells
What is goodpastures syndrome?
A type II hypersensitivity reaction of kidney failure
What type of infection if proliferative glomerulonephritis?
Type III hypersensivity reaction
What is the difference between nephrotic and nephritc?
Nephrotic syndrome
Nephritic = blood, pain, less proteinuria, oliguria
What are 2 other causes of proteinuria?
diabetes
amyloidosis
What is tubulointestinal disease?
Typically caused by drug hypersensitivity
How many mmHg in 1kPa?
7.5 mmHg
What are the normal values for (i) pH (ii) pO2 (iii) pCO2 (iv) bicarb (standard)
(i) 7.35 - 7.45
(ii) 12-13 kPa
(iii) 4.5 - 5.6 kPa
(iv) 22-26 mmol/L
How is standard bicarb calculated? What does it reflect?
From the actual bicarb assuming 37 degrees celsius and a pCO2 of 5.3 kPa
- reflects the metabolic component of acid base balance
What does a P/F ratio of (i) greater than 50 (ii) less than 40 (iii) less than 26.7?
(i) healthy
(ii) acute lung injury
(iii) ARDS
What is compensation?
altering in fucntion of the resp or renal system to change the secondary variable in an attempt to minimise an acid-base imbalance
What are the 4 steps to the assessment of ABGs?
- Asses pO2 and oxygenation
- assess pH
- determine primary problem (think about pt)
- is compensation occurring?
If pH and pCO2 are changing in the SAME direction what does this suggest?
That the primary problem is metabolic
If pH and pCO2 are changing in OPPOSITE directions what does this suggest?
That the primary problem is respiratory
What does it suggest if pCO2 and bicarb are moving in the (i) same (ii) opposite direction?
(i) compensation likely to be occurring
(ii) suspect a mixed disorder
What is the anion gap?
It is calculated from venous blood
- it is the sum of routinely measured cations in venous blood minus routinely measured ions (sodium + potassium) - (chlorine + bicarb)
What use is the anion gap?
- an increased anion gap signals the presence of a metabolic acidosis
- helps differentiate the cause of a metabolic acidosis
What is the value of the normal anion gap?
16
What are the 3 reasons that metabolic problems most commonly occur from?
From an overwhelming acid load
- bodies own production
- ingestion (exogenous source)
- failure of excretion by the kidneys
How does the bodies own production of acid cause metabolic problems?
Any condition causing hypoperfusion
- of the whole body = shock
- of part of body = femoral artery embolism
this will result in increased anaerobic metabolism with subsequent increased production of lactic acid (lactic acidosis)
What are 3 other causes of lactic acidosis?
- severe acute hypoxia
- severe convulsions (respiratory arrest)
- strenuous exercise (dehydration)
How is lactate metabolised? Why is this significant?
In liver and overall there will be no net production of acid
BUT this process needs oxygen
- so production of lactate increases (marker for shock) when oxygen delivery falls and consumption of lactate by the liver falls
What is ketoacidosis? How does it arise?
Situations of decreased insulin and increased glucagon
- uncontrolled DM (severe, life-threatening)
- alcoholic ketoacidosis (common clincially)
- starvation ketoacidosis (mild)
How/what causes an exogenous acid load?
Accidental/deliberate ingestion
- methanol (industrial solvent, windscreen wash)
- ethylene glycol (anti-freeze)
What are the renal causes of metabolic acidosis ?
Functions of the kidney re bicarb
1) reabsorbs filtered bicarb
2) regenerates bicarb consumed by buffering
3) renal failure both acute and chronic (increased anion gap)
4) renal tubular acidosis (normal gap)
If you have a normal anion gap but have metabolic acidosis, what are the causes?
This is less common
- diarrhoea
- renal tubular acidosis
What are the GI causes of metabolic acidosis with a normal anion gap?
Much of the gut below the pylorus secretes bicarbonate into gut lumen, for every bicarb ion into the gut a H+ ion enters ECF
- in diarrhoea this process increases, along with volume depletion
- therefore renin/angiotensin/aldosterone axis stimulated retaining chloride
What are 3 other reasons for metabolic acidosis with a normal anion gap?
- laxative abuse
- ileostomy
- colostomy
When are the 2 reasons you use slow metabolic (renal) compensation for metabolic problems?
- the metabolic acidaemia is of non-renal origin
2. the kidneys are functioning effectively
What must occur to compensate for a metabolic acidosis?
pCO2 must fall therefore minute volume must increase
What is Kussmaul respiration?
A laboured deep, rapid pattern of breathing
Why is metabolic alkalosis (alkalaemia) the least common of the acid base disturbances?
The kidney is very good at excreting excess bicarb
What 2 processes have to happen for metabolic alkalosis to occur?
- an initiating process
2. a maintaining process
What is the most common initiating process of metabolic alkalaemia?
LOSS OF H+ IONS
- from gut (above pylorus)
- from kidney (furosemide and thiazide)
How is the metabolic alkalosis maintained? (the maintenance process)
A process which impairs the kidneys ability to excrete bicarbonate
- chloride depletion group
- potassium depletion group
What is the chloride depletion group?
chloride and bicarb are the only anions present in appreciable quantities in ECF
- if chloride is low in renal tubular fluid, bicarb must be reabsorbed to maintain electrical neutrality
How do you compensate for a metabolic alkalosis?
because bicarb is increased, pCO2 must increase and therefore the minute volume must fall
- but it is difficult to predict the extent partly because so many pts are babies
What can disrupt your U & E’s?
Haemorrhage - accidents, surgery Diarrhoea and Vomiting Poor intake - elderly Increased losses - pyrexia, heat Diabetes insipidus Diabetes mellitus Diuretic therapy Endocrine disorders - ADH, aldosterone
What happens in haemorrhage if a pt loses blood (isotonic fluid)?
Loss if from ECF
- there is no change in [Na]
- no fluid redistribution
What happens if a pt is dehydrated and loss of hypotonic fluid?
Greater loss from ICF than ECF
- small increase in [Na]
- fluid redistribution between ECF and ICF
What happens if you gain 2L of isotonic fluid e.g. saline drip?
Gain is to the ECF
- no change in [Na]
- no fluid redistribution
What happens if you gain 3L of hypotonic fluid e.g. water, dextrose?
Greater gain to ICF than ECF
- small decrease in [Na]
- fluid redistribution between ECF and ICF
What does the body do compensatory wise with regards to (i) physiological and (ii) therapeutic mechanisms?
(I) thirst, ADH, renin angiotensin system
(ii) IV therapy, diuretics, dialysis
What is ADH produced by? What is its function? How do you measure ADH status?
Produced b median eminence and release increases when osmolality rises
- decreases renal water loss and increases thirst
TESTS = measure plasma and urine osmolality
- urine greater than plasma suggests ADH active
What is the renin-angiotensin system activated by? What does it cause? What test is done to ascertain R/A/A status?
Activated by reduced intravascular volume (Na depletion or haemorrhage)
- causes renal Na retention
TEST = measure plasma and urine Na. If urine is less than 10mmol/L then R/A/A system active
What is urea? Describe it. What/where is elevated urea found in?
Normal breakdown product of protein metabolism
- normally filtered at glomerulus and major component of urine
- in dehydration it is often first to show any change
- sodium and urea conc. will often parallel each other during fluid correction
- elevated urea is often found in CCF, shock, MI, severe burns
- checking renal function is often necessary prior to starting certain drug treatments
What is creatinine? Where is it filtered? Is there any difference in males and females?
Breakdown product of protein and muscle
- usually freely filtered at the glomerulus
- plasma and urine values typically reflect muscle mass - and creatinine concentrations tend to be higher in males
What is the best overall measure of kidney function?
GFR
- statement of functions of kidney in numerical expression
- a decrease in GFR precedes renal failure in all forms of progressive kidney disease
What is the GFR defined as? What is it influenced by? What is the normal range? When can values rise/fall and be normal?
GFR = the volume of fluid passing through the glomerulus, in a given period of time
- influenced by renal perfusion pressure, renal vascular resistance, glomerular damage, post glomerular resistance
NORMAL = 90 - 150 mL/min
- a larger healthy person has a higher GFR and the GFR values fall with increasing age
What is the eGFR? What is its use? What is it based on?
‘e’ is for estimated
- used to aid ‘staging’ of kidney disease and intended to flag up incipient AKI
- various formulae are available and some are specific for say known renal impairment or cancer
- based on creatinine
What is (i) hyponatraemia (ii) hypernatraemia (iii) dehydration?
(i) too little sodium or too much water in ECF
(ii) too little water or too much sodium in ECF
(iii) water deficiency or fluid (Na and water) depletion
What are the potassium reference ranges? What values are potentially dangerous?
3.6 to 5.0 mmol/L
Values of less than 3 or greater than 6 are potentially dangerous (abnormal neuromuscular excitability)
Why does plasma potassium levels not reflect body potassium? How is the total body potassium determined?
As a small proportion of the total body potassium is in the plasma
- the total body potassium is measured by total cell mass
What is the relationship between potassium and hydrogen ions?
They are exchanged across cell membrane
- and both bind to negatively charged proteins (e.g. Hb)
What happens to potassium in (i) acidosis (ii) alkalosis?
(i) potassium moves out of cells (hyperkalaemia)
ii) potassium moves into cells (hypokalaemia
What are 3 artefactual causes of hyperkalaemia?
- delay in sample analysis
- haemolysis
- drug therapy - excess intake
What are the causes of hyperkalaemia?
- Acute and chronic renal failure
- acidosis
- mineralocorticoid dysfunction
- cell death (cytotoxic therapy)
What is the treatment of hyperkalaemia?
- correct acidosis if this is the cause
- stop unnecessary supplements/intake
- give glucose and insulin (as drives potassium into cells)
- ion exchange resins (GIT potassium binding)
- dialysis (short and long term)
What are the causes of potassium depletion?
- low intake
- increased urine loss i.e. diuretics, tubular dysfunction or mineralocorticoid excess
- GIT losses e.g. vomiting, diarrhoea/laxatives, fistulae
- Hypokalaemia w/out depletion e.g alkalosis, insulin/glucose therapy
What are the effects of potassium depletion?
- acute changes in ICF/ECF ratios e.g neuromuscular - lethargy, muscle weakness, heart arrhythmias
- chronic losses from ICF e.g. neuromuscular (again)
- kidney e.g. polyuria, alkalosis (increased renal bicarb production)
- vascular
- gut
How is potassium depletion detected?
HISTORY - diarrhoea, vomiting, drugs - symptoms of lethargy/weakness - cardiac arrhythmias ELECTROLYTES - hypokalaemia
What is the treatment of potassium depletion?
Prevention via supplements
Replace deficit either oral or IV
What is the primary example of a loop diuretic? What is their MoA?
Furosemide - acts within 1 hr
Act on the thick ascending limb of the loop of henle to inhibit reabsorption
- inhibit the Na/K/2Cl carrier in luminal membrane, inhibiting the transport of NaCl out tubule into interstitial tissue, this dissipates the osmotic gradient in the medulla of the kidney and are no longer able to recover water in the collecting tubule and ducts, increasing delivery of sodium to distal tubule (loss of H+ and K+) note that this may produce a metabolic alkalosis
When are loop diuretics used?
- pulmonary oedema due to LVF
- chronic heart failure
- resistant hypertension
- oedema
Why are loop diuretics used for cardiac failure?
A decrease in cardiac filling leads to decreases in the SV and CO which leads to a fall in arterial pressure
- a decrease in venous pressure leads to a decrease in capillary hydrostatic pressure and capillary fluid filtration leading to reabsorption and reduction in oedema
- loop diuretics reduce preload and contribute to venodilation, which helps afterload
What are the side effects of loop diuretics?
Hypokalaemia
Hypotension
Urinary retention (if enlarged prostate)
Gout
What are thiazide diuretics? Where do they act? What are the main examples? What is their MoA?
moderately powerful diuretics that act on the distal tubule
Ex = bendroflumethiazide, indapamide
- they decrease reabsorption of Na and Cl by binding to Na/Cl transport system, inhibiting co-transporter’s action. They also have additional extra renal actions - producing vasodilation
When are thiazide diuretics used?
- hypertension
- mild heart failure
- severe resistant oedema
- nephrogenic diabetes insipidus
What are the side effects of thiazide diuretics?
Metabolic and electrolyte disturbances
- increased cholesterol, glucose, uric acid and calcium
- decreased potassium, sodium, magnesium, BP
- metabolic alkalosis
What are the function of potassium sparing diuretics? What are the main examples? What is the MoA of these examples.
They are weak diuretics which act in the collecting tubules
EX = amiloride and spironolactone
AMILORIDE and triamterene act by blocking Na channels controlled by aldosterone’s protein mediator
SPIRONOLACTONE and eplerenone are antagonists at the aldosterone receptor
What are the indications for K+ sparing diuretics?
- alongside K+ losing diuretics (loop or thiazide) to prevent K+ loss
- Spironolactone for heart failure, Conn’s or secondary hyperaldosteronism
What are the side effects of K+ sparing diuretics?
- hyperkalaemia
- GI upset
- metabolic acidosis
What are the 3 additional types of diuretics? Give an example for each and their indications.
- OSMOTIC DIURETICS e.g. mannitol
- cerebral oedema and raised intra-ocular pressure - DIRECT COMBINATIONS e.g. co-amilofruse
- oedema and issues with medication compliance - CARBONIC ANHYDRASE INHIBS e.g. acetazolamide
- mountain sickness, glaucoma
What is SIADH? What is it associated with? What is it caused by?
An inappropriate ADH secretion from the posterior pituitary or fro mectopic source despite low serum osmolarity
- associated with a decreased Na, increased urine osmolality and euvolaemia
CAUSES =
- neurological (tumour, trauma, infection, GBS, MS, SLE)
- pulmonary (lung SCC, mesothelioma, pneumonia)
- malignancy (stomach, pancreas)
- drugs (thiazide and loop diuretics, PPis, SSRIs, ACE-is
How does Syndrome of inappropriate ADH secretion (SIADH) present?
Nausea, vomiting, cramps/tremors, depressed mood, irritability, personality change, memory change, hallucinations, seizures, coma
What is erythropoietin (EPO)?
Hormone produced by the kidney that promotes RBC formation in the bone marrow - this process is driven by anoxia
- when someones kidneys don’t work the kidneys produce less EPO so person becomes anaemic
- the drug erythropoietin is an artificial version of this hormone which can boost the body to make RBCs (nearly half people on dialysis take this)
What are the 2 categories of naturally occurring adrenal hormones? Give examples.
- CORTICAL HORMONES
- glucocorticoids e.g. cortisol
- mineralocorticoids e.g. aldosterone
- androgens - MEDULLARY HORMONES (catecholamines)
- adrenaline and noradrenaline
What are the 2 types of synthetic agents? Give examples for each.
- GLUCOCORTICOIDS
- topical steroids e.g. beclomethasone
- inhaled steroids e.g. budesonide
- oral or parenteral steroids e.g. hydrocortisone, prednisolone, dexamethasone - MINERALOCORTICOIDS
e. g. fludrocortisone
When would certain types of glucocorticoids be used?
- TOPICAl steroid for inflammatory skin conditions e.g. eczema, psoriasis
- INHALED steroid for asthma
- ORAL steroid for IBD, asthma, acute transplant rejection, congenital adrenal hyperplasia, cerebral oedema/raised icp, acute hypersensitivty and anaphylaxis, autoimmune conditions, PMR, TA
What are the side-effects of synthetic glucocorticoids?
- topically can thin the skin
- adrenal suppression/atrophy so withdrawal risk
- psychiatric effects
- diabetes
- osteoporosis
- Cushing’s syndrome
- growth restriction (children)
- peptic ulceration
- increase susceptibility to infections
Lead to suppressive action on hypothalamic-pituitary-adrenal axis
When are mineralocorticoids used? What are their side effects?
Fludrocortisone = mineralocorticoid replacement in adrenocortical insufficiency, Addison's SE = hypertension, sodium and water retention, potassium and calcium loss
What is the definition of a chronic health condition?
conditions which can be controlled but not cured e.g. IBD, asthma, COPD, cancer, heart disease
What are the 6 quality dimensions? Describe them.
- PATIENT CENTRED = providing care that’s responsive to individual pt preferences, needs and values and assuring that pt values guide all clinical conditions
- SAFE = avoiding harm to pts from care that’s intended to help them
- EFFECTIVE = providing services based on scientific knowledge
- EFFICIENT = avoiding waste, including that of equipment, supplies, ideas and energy
- EQUITABLE = providing care that doesn’t vary in quality because of personal characteristics (e.g. gender, ethnicity, geographic location or socio-economic status
- TIMELY
What are the 3 levels of individualised stepped care? Describe them.
- SELF MANAGEMENT = collaboratively helping individuals and their carers to develop the knowledge, skills and confidence to care for themselves and their condition effectively
- DISEASE SPECIFIC CARE MANAGEMENT = providing pts with responsive, specialist services using multi-disciplinary teams and disease specific protocols and pathways (national service frameworks and quality and outcomes framework)
- INTENSIVE CARE/CASE MANAGEMENT
What is self management?
A concept where the person takes ownership and is central
- process of becoming empowered to manage life with LTC
- it requires indivuals and health professionals working in partnership
- concerned with problem solving, decision making and confidence
What are the principles of self management?
- be accountable to me and value my experience
- i am the leading partner in management of my health
- I am a whole person and this is for my whole life
- self management does not mean managing my LTC alone
- clear information helps me make decisions that are right for me
What is the role of self management programmes?
They do not conflict with existing programmes or treatment
- designed to enhance regular treatment and condition-specific education such a pain management, cardiac rehabilitation, diabetes instruction
- teach pts skills to co-ordinate all the things needed to manage health and keep active
What are the four infleunces for self-efficacy?
- the choices we make
- the effort we put in
- how long we persist when we have obstacles in our way
- how we feel
What is self-efficacy based on?
- past performance
- vicarious experiences
- verbal persuasion
- physiological cues
- it is not a stable trait. People with low self efficacy towards a task are more likely to avoid it
How do you encourage self efficacy?
- skills mastery via action planning
- modelling
- helping people to reinterpret meaning of symptoms - challenging health beliefs
- social persuasion - group work
What is the Expert Patient Programme (EPP)? How does it aim to support people? (3 things)
A self-management programme for people living with a long term (chronic) condition
Support people by
- increasing their confidence
- improving their quality of life
- helping them manage their condition more effectively
What is the Kingdom Chronic Pain Self-management programme (KPMP)? What does it aim to do?
Group format dellivered by a multidisciplinary team in primary or secondary care settings
- consists of education and guided practice on pain physiology, pain psychology, healthy function, problem-solving, goal-setting, changing unhelpful thinking patterns and relaxation skills
- use of cognitive behavioural principles to deliver components of programme
- aims to improve physical, psychological, emotional and social dimensions of quality of life of people with chronic pain
What are the contents of KPMP? (HINT: there’s 10 points)
- intro to pain management
- understanding chronic pain
- setting goals and pacing your activities
- positive responses to pain
- getting fitter and being more active
- managing your medicines and managing sleep probs
- everyday activites
- relationships and assertiveness
9 managing stress and problem solving - flare ups and maintenance
What are the effects of urinary calculi?
pyelonephritis
hydronephrosis
obstructive uropathy
What are symptoms/causes of urinary calculi?
- renal colic (classic of acute)
- haematuria
- pyelonephritis
can present acute or chronic
What are the composition of calculi? Why is this significant?
- calcium = 75%
- oxalate or phosphate - uric acid = 20+%
- infection
- proteus species - Cystine = 1%
This is important as might not see certain stones on plain x-ray (uric acid) so x-ray cannot be used to distinguish calculi
What are the causes of urinary calculi?
- hypercalcaemia (sarcoid, renal tubular acidosis, hyperthyroidism)
- gout
- obstruction (vesico-ureteric reflux)
- genetic
- dehydration (common acute cause)
What 4 things are signs of bladder disease?
infection
inflammation
calculi
neoplasia
What is a common cause of cystitis?
UTI
What are the (i) common (ii) less common types of urinary tract neoplasms?
(i) BLADDER - urothelial carcinoma
RENAL 4/5ths are clear cell carcinoma (ccRCC)
(ii) 1. renal carcinomas other than clear cell i.e. transitional cell
2. renal nephroblastoma (Wilms’)
3. ureter transitional cell carcinoma
4. renal/bladder sarcoma
Who do Wilms’ Tumour tend to affect? What is the underlyign cause? What is the histology? What is the survival rate?
Children usually under 3yrs
- WT1 tumour suppressor gene
- histology resembles immature or embryonal blastema
- younger pt = better prognosis
- surgery, radio, chemo leads to 90% survival
Where is renal cell carcinoma? What is the commonest type? What are risk factors/genetic causes?
Originates in the ducts, especially PCT
- commonest type = clear cell
- smoking and obesity = risk factors
- affects men more than women
- genetics = autosomal dominant RCC, hereditary papillary and von Hippel-Lindau (VHL mutation) Syndrome
How do renal cell carcinomas present? What is the 5 yr survival?
Haematuria
pain
metastases
paraneoplastic syndromes e.g. pyrexia, hormones (eg EPO)
50% five yr survival (very stage dependent)
Where do the majority of urothelial cancers arise? What is the typical pattern?
Posterior and lateral wall
- mainly papillary
What is the spectrum of malignancy of urothelial cancer?
From superficial, carcinoma in situ to deeply invasive
What is the (i) aetiology (ii) presentation of urothelial cancers?
(i) smoking industrial (aniline dyes) (ii) haematuria - even once is significant dysuria obstruction
What are the (i) pre renal (ii) renal (iii) post renal causes of ACUTE renal failure?
(i) shock, major trauma
(ii) some gomerulonephritides, toxic e.g. drugs, malignant hypertension, vasculitis, analgesics
(iii) obstruction
What are the effects of ACUTE renal failure?
High potassium and creatinine
- may be oliguria (abnormally small amounts of urine)
- hypertension
(lipids in nephrotic syndrome)
What are the (i) pre renal (ii) renal (iii) post renal causes of CHRONIC renal failure?
(i) atherosclerosis
(ii) glomerulonephritis, diabetes, HT, polycystic
(iii) obstruction
What are the effects of CHRONIC renal failure?
high potassium and creatinine
- may be oliguria (abnormally small amounts of urine)
- anaemia
- small kidneys
What are the types of bladder outflow obstruction? (post-renal renal failure)
- prostate enlargement in men
- uterine prolapse in women
- calculi
- tumours
- urethral structures
What is hydronephrosis/hydroureter caused by? When does it cause renal failure?
OBSTRUCTION
(i) extrinsic = tumours e.g. cervical cancer
(ii) INTRINSIC
- within wall = intrinsic tumour e.g. transitional cell carcinoma
- in lumen = calculi, blood clot etc
must be bilateral to cause renal failure
What are the clinical features of post-renal renal failure?
- anaemia
- immunosuppression
- neuropathy
- bone disease
- neoplasia
What renal replacement therapy is used?
- electrolytes
- fluid
- excretion
- erythropoetin
What are the risks associated with renal replacement therapy?
- diet and nutrition
- anaemia
- calcium/phosphate
- BP
- infection
What is a risk with haemodialysis - which will make dialysis less effective?
Increased fibrosis
What does continuous ambulatory peritoneal dialysis require?
a permanent catheter
What are the risks/problems with transplantation?
- donor availability
- cadaveric, live related, live unrelated - cross matching
- immunosuppression
- risk of infection
- risk of skin cancer
- risk of lymphoma
What can arise as a result of transplantation? (both acute and chronic problems)
- acute cellular rejection
- acute antibody mediated rejection
- acute vascular rejection
- chronic allograft nephropathy (chronic rejection)
