Nephrology Flashcards
How should hypokalemia be treated?
Treatment of hypokalaemia depends on severity. Any causative agents should be removed. Gradual replacement of potassium via the oral route is preferred if possible.
Mild to moderate hypokalaemia 2.5 - 3.4 mmol/l can be treated with oral potassium provided the patient is not symptomatic and there are no ECG changes.
Severe hypokalaemia (<2.5mmol/l) or symptomatic hypokalaemia should be managed with IV replacement. The patient should be managed in an area where cardiac monitoring can take place. If there are no contraindications to fluid therapy (e.g. volume overload, heart failure) potassium should be diluted to low concentrations as higher concentrations can be phlebitic. The infusion rate should not exceed 20mmol/hr. In this case, 3 bags of 0.9% Saline with 40mmol KCL is the correct answer.
Suggest four causes of hypokalemia?
1.) Increased potassium loss:
Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics
GI losses: diarrhoea, vomiting, ileostomy
Renal causes: dialysis
Endocrine disorders: hyperaldosteronism, Cushing’s syndrome
2.) Trans-cellular shift
Insulin/glucose therapy
Salbutamol
Theophylline
Metabolic alkalosis
- ) Decreased potassium intake
- ) Magnesium depletion (associated with increased potassium loss)
What would you see for hypokalemia on an ECG?
ECG changes seen in hypokalaemia include:
Greater
U waves
T wave flattening
ST segment changes
How can you differnetiate between pre-renal, renal and post renal AKI?
1s there protein. If so = renal
Is there an obstruction/ ultrasound = post renal
What are the features of AKI?
High blood creatinine
Low urine ouput
What are 3 main issues of AKI?
K+ high
acidosis (metabolic)
Pulmonary oedema
How do you treat the high potassium in AKI?
Stabilise membrane using calcium glucoronate
desxtrose to stimulate insulin
insulin
salbutomol
potassium binder
diuretics
dialysis
How can you treat peripheral oedema?
Fluid restriction
How can you treat metabolic acidosis?
Bicarbonate
What is CKD?
CKD is defined as abnormalities of kidney structure or function, present for >3 months, with implications for health.
What does the diagnosis of CKD involve?
Heamaturia test
ACR - albumin creatinine ratio
Dipstick blood
eGFR < 60 mL/min/1.73 m2
Scan
[HADES]
What does MDRD stand for? What does it involve?
Modification of Diet in Renal Disease (MDRD)
CAGE - Creatinine, age, gender, ethnicity
What is refeeding syndrome?
Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. The metabolic consequences include:
hypophosphataemia
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
=What type of kidney disease is linked with eisonophilia?
Acute interstitial nephritis causes an ‘allergic’ type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function
What is minimal change disease?
What drug should be stopped in diabetics undergoing CT angiography?
Metformin
Glomerular lesions: What are the four types?
Glomerular lesions can be focal, diffuse, segmental or global.
Glomerular lesions: What is the difference between a focal and diffuse glomerular lesion?
Foc(ALL) affects less than 50% of ALL of glomeruli, whereas diffuse affects more than 50% of ALL glomeruli
Glomerular lesions: What is the difference between segmental and global lesions?
These correspond to one glomerulus and how much is affected e.g. segmental is less than 50% of one glomeruilus whereas global is the whole glomerulus.or more than 50%
What type of lesion is this?
Segmental
What type of lesion is this?
Global is more than 50%
What are the causes of acute glomerulonephritis?
Post-infectious or post streptococcal (did they have a throat infection?). Anti-streptoccal antibodies. 95% of children recover.
Necrotising/ crescenteric. Anti GBM. ANCA.
What is membranous nephropathy?
Capillary wall thickening. Thickened membranes and spikes.
Membranous nephropathy is an immunologically mediated disease of the glomerular basement membrane that is often associated with nephrotic syndrome. It is one of the MOST common causes of nephrotic syndrome in the adult population. It can be described as either idiopathic (primary) or secondary to an underlying cause.
anti-phospholipase 2 receptor or antiPLA2R 85%
[spikes and PLA2R]
What appearance is seen using a silver stain in membranous nephropathy?
Spikes
What is minimal change disease?
Common in children/ Treat with steroids (it’s minimal change)
Common in 2-6 yo after infection
related to infections, leukemias and NSAIDs
What is seen in minimal change disease?
Podocyte foot effacement
What causes focal segmental glomerulosclerosis?
FSGS involves damage to the renal podocytes such that larger molecules, most notably proteins, are filtered and lost through the kidney
APOL1 gene
Africans
Podocytopathies
Trypanosomiasis protection
What is this showing?
Thin GBM disease
What causes haematuria?
Thin GBM
IgA nephropathy
Alports
What are these showing? What disease are they seen in?
Kimmelstein-Wilson nodules
Amyloidosis detection in kidney?
Congo red stain + bifringence polarised light
What does the AKI patient look like?
Hyperkalaemic metabolic acidosis • Malaise, nausea • Hyponatraemia (early sign of fluid retention) • Fluid overload
Metabolic acidosis
Hyperkalaemia
Pulmonary oedema
Fluid overload
My Happy Pony Flies
How do you treat AKI?
DASIE
Distinguish type
Ask for help
Stop drugs
IV fluid
Electrolyte and pH correction
Whay are the types of renal acidosis?
Type 1 = can’t get rid of protons (H+ -1 distal), type 2 (bicarbonate leaks - proximal), type IV –low aldosterone therefore high potassium
What is AKI characterised by?
MAKI F(or) M(y) D(inner)
Metabolic
acidosis
K (high potassium)
Interstitial fluid
Fluid overload
Malaise
eDema
What is the symptoms and signs of AKI?
What is renal acidosis?
Distinguish types of AKI.
What is CKD and how do you measure?
