Recent Flashcards
X ray IBD
CD =small bowel or colonic dilation; calcification; sacroiliitis; intra-abdominal abscesses. With fluroscopy = string sign
UC = dilated loops with air fluid level. With fluro = lead pipe, loss of haustra
Medical conditions associated with bleeding
you can CHAALK it up to:
- Cancer
- Alcohol
- Autoimmune (SLE)
- Liver disease
- Kidney disease (uraemia)
Management of seizure due to tumour?
Firstly, determine whether this was a seizure or syncope due to a plateau wave suggesting high ICP.
Dexamethasone is useful for reducing vasogenic oedema.
Use of anticonvulsants as prophylaxis (phenytoin, carbamazepine, valproate), usually monotherapy.
Treatment of tumour with surgery or radiation reduces relapse.
Organisms associated with meningitis
Bacterial:
- strep pneumoniae
- haemophilus influenzae (young unvaccinated)
- neisseria meningiditis
- listeria monocytogenes (neonate, elderly, immunocompromised)
- group B
- gram negative aerobic bacilli
Virus:
- entero (coxsachie, echo)
- West Nile
- HIV
- HSV
- Lymphocytic choriomeningitis
Fungus
-cryptococcus
Mycobacterium (immunocompromised)
-TB
Syphilis
Definition CKD
KDIGO:
presence of kidney damage or decrease in function for >3 months
Damage:
- UACR >30
- urine sediment
- imaging (PCKD, hydronephrosis)
- -pathologic with biopsy
- kidney transplant
Function:
- eGFR (CKD-EPI)
- <60mL/min/1.73m2
Staging CKD
Cause of disease
GFR (6 G stages)
- 1 = >90 normal
- 2 = 60-89 mildy decreased
- 5 = <15 ESRD
Albuminuria (3 stages)
- A1, ACR <30, normal
- A2, ACR 30-299, moderately increased
- A3, ACR >300, severely increased
Stratification into 18 different categories, with specification of underlying cause
- heat map divides categories into three broad risk categories
- infer risk of all-cause mortality, cardiovascular mortality, progression to ESRD
Glomerular filter
Fenestrated endothelium
-lets everything but blood cells through
GBM
- combined endothelial and visceral epithelial basement membranes
- Type IV collagen meshwork
- negatively charged with GAGs
- prevents all but smallest proteins from passing
Podocyte
- primary process
- secondary process with slit gaps
- diaphragms across gaps
- glycoproteins and glycosaminoglycans
- LMW proteins such as beta2-microglobulin, IgG light chains, retinol binding protein, and polypeptides from albumin breakdown are filtered and reabsorbed in proximal tubule
Between is mesangial cells (stellate type).
Parietal epithelium is squamous. Space between parietal and visceral is urinary space (Bowmans).
Diabetic vs non diabetic CKD
- Onset less than 5 years since diagnosis Type 1
- Acute onset of disease
- Active urine sediment (acanthocytes) and cellular casts (dysmorphic red cells and red cell casts are rarely seen in diabetic nephropathy)
- Microscopic haematuria does not exclude diabetic nephropathy
- In type 1, absence of retinopathy (less so for type 2)
- Absence of neuropathy
- Signs and symptoms of another disease
- Significant decrease in GFR within 2-3 months of of ACEI or ARB
AKI staging
Stage 1
- serum creatinine >26.5
- serum creatinine increase 1.5-1.9 times baseline
- urine output <0.5mL/kg/hr for 6-12 hours
Stage 2
- serum creatinine increase 2-2.9
- urine output <0.5 for >12 hours
Stage 3
- serum creatinine increase >3 times baseline
- serum creatinine >353.6 micromol/L
- urine output <0.3 for >24hrs or anuria for >12
Measuring GFR
Serum creatinine
- not reabsorbed or metabolised
- 10-40% urinary creatinine comes from tubular secretion
- GFR x SCr = constant
Creatinine clearance
-ignoring tubular secretion,
GFR x SCr = UCr x V
GFR = (UCr x V) / SCr
eGFR cockroft gault -considers age and body weight CKD epi -considers age, body weight and race
Hyperkalaemia AKI pathophys
Decreased Distal Nephron Na Delivery:
- decrease in GFR leads to decrease in Na delivery to distal convoluted tubule and collecting duct
- this decreases K secretion by ROMK and Maxi K
Impaired Aldosterone Activity:
-ACEI
-ARBs
-Aldosterone receptor antagonists
-Impaired renin release (NSAIDs)
-hyporeninemic hypoaldosteronism due to interstitial disease
All decrease K secretion by ROMK and Maxi K and Na/K ATPase
Distal Tubular Defect:
impaired K secretion with mild decrease in GFR and normal aldosterone
-direct injury to K secreting cells
-K sparing diuretics impair collecting duct secretion of K
-urinary obstruction impairs electrogenic secretion of K in distal nephron
Increased in diseases with release of intracellular K:
- rhabdo
- haemolysis
- tumor lysis
Hyperkalaemia treatment
Calcium IV:
- antagonises membrane effects of hypokalaemia
- reverses depolarisation of resting potential that leads to Na channel inactivation and reduced excitability
- effects immediate but last 30-60 mins
- can be repeated while monitoring serum calcium level
Insulin and glucose IV
- insulin increases Na/K ATPase activity and drives K uptake by skeletal muscle
- glucose given to avoid hypoglycaemia
- peaks within hour and lasts 4-6hrs
Increase K excretion: loop diuretics -not to be used as monotherapy and should be avoided with poor renal function gastrointestinal cation exchangers -bind K and exchange for Na or Ca haemodialysis -preferred method, particular with poor renal function -can be delayed when no vascular access
Cease Drugs
- ACEI/ARB
- Aldosterone antagonist
- K sparing diuretics
Monitor:
- ECG
- K
- glucose
- calcium
Complications of AKI
BUMPKIN CAVE:
- bleeding (ESRD)
- uraemia
- malnutrition
- hyperphosphataemia/hypocalcaemia
- hyperkalaemia
- infections
- hyponatraemia
- cardiac (arrhythmias, ccf)
- acidosis
- volume (hyper –> hypo with resolution)
- ESRD/CDK
Pathophy UTO polyuria/nocturia
Initial obstruction –> increases pressure proximally due to continuing filtration, which decreases eventually due to back pressure
Tubular pressure –> vasoconstriction due to RAS and thromboxanes
Result is decrease in GFR and ischaemia
Infiltration by inflammatory cells
Finally leads to tubular atrophy and interstitial fibrosis
Loss of medullary hypertonicity due to downregulation of
- Na/K ATPase
- Na/K/2Cl cotransporter
- eNaC
leads to impaired naturesis and polyuria/nocturia
H and HCO3 kidney balance
HCO3
- freely filtered
- 80-90% reabsorbed proximal tubules
- remainder thick ascending limb, distal and collecting duct
- combines with H in tubule to form H2CO3 then CO2 and H2O
- CO2 enters tubule cell combines with H20 etc forming HCO3 and H
- H is secreted back into lumen (passively in proximal tubules, actively in late nephron alpha intercalated cells)
- HCO3 is transported across basolateral membrane and into blood
- for every H secreted a HCO3 is reabsorbed (titrated against each other)
