Recent Flashcards
(34 cards)
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)
Phosphate and ammonium buffer
Phosphate
- hydrogen phosphate concentrated in tubule
- when excess H compared to HCO3, it combines with hydrogen phosphate to form dihydrogen phosphate
- excreted as Na salt
- net gain of one HCO3
Ammonium
- glutamine derived from amino acid metabolism in liver enters tubule cell
- metabolised to form two HCO3 and two ammonium ion
- HCO3 reabsorbed (net gain two)
- ammonium ion secreted into lumen by Na antiporter
- HCO3 and H produced by H2CO3 in tubule cell. H secreted into lumen and combines with ammonia to form ammonium ion
- ammonia permeable but ammonium ion is not and is excreted
- represents net gain of one HCO3
RTA pathophy
Type 1
- distal H secretion impaired
- defective H pump or increased luminal membrane permeability to H
- Na wasting
- hypokalaemia as Na is usually exchanged for K or H. Since H secretion impaired, K secretion increased.
Type 2
- proximal HCO3 reabsorption impaired
- abnormalities in any of transporters involved in HCO3 resorption
- acidosis reduces proximal Na reabsorption –> increased distal delivery, water loss and RAS activation –> increase K secretion and hypokalaemia
Hyperkalaemic RTA
-decreased Na reabsorption decreases luminal negative charge and decreases K secretion by principle cells and H secretion by intercalated
-leads to hyperkalaemia and acidosis
voltage dependent
-decreased distal Na delivery or defective (inherited or aquired) Na reabsorption
-occurs in UTO, hypovolaemia, lupus, drugs
hypoaldosteronism
-decreased distal Na resorption
-rare inherited conditions, hyporeninaemic and UTO
Fanconis syndrome
Proximal (Type 2) RTA, with impaired HCO3 reabsorption as well as impaired (PLUG) reabsorption due to generalised proximal tubule dysfunction:
-phosphate
-LMW proteins
-uric acid
-glucose
Inherited enzymatic disorders, drugs such as valproate and monoclonnal gammopathy
Investigations nephrolithiasis
urinalysis
- nitrits/leuks
- pH
- haematuria
- stones
- WC
FBC -leukocytosis (pyelonephritis/UTI) EUC -eGFR -Na -calcium -uric acid -phosphate
Imaging
- non contrast KUB (location, density, size)
- ultrasound/x ray (KUB)
if stone passed
- stone analysis
- 24 urine analysis
bone pain RCC
Metastasis decouples bone remodelling
- tumor humoral products such as PTH-RP increase osteoclast activity and is insensitive to serum calcium
- metastatic deposits may activate inflammatory cells with release of cytokines such as TNF alpha that increases osteoclast activity and suppresses osteoblasts
- tumour cells may directly destroy bone
Pain
- not correlated to size or degree of bone involvement
- may be due to release of chemicals within marrow
- decrease in density and disruption of architecture leads to fractures
- collapse and mechanical stress irritate local nerves
- stretching of periosteum by tumor expansion
- secondary effects might come from reactive muscle spasm or nerve root entrapment
Hx and exam testicular torsion
Hx
- sudden onset, severe scrotal pain (determine onset –> best results before 4-6 hours, irreversible damage after 12 and unsalvageable after 48)
- diffuse or focal?
- no relief with elevation of scrotum
- associated nausea, vom, abdo pain
- several hours after exercise or trauma
- may be hx of intermittent pain and relief (with de-torsion)
- often occurs during night
- fever, dysuria and discharge are not typical –> suggest infective or inflammatory aetiology
- urgency, frequency and dysuria often accompany epidymitis/orchitis
Exam
- bell clapper deformity, high riding
- diffuse tenderness
- swelling (reactive hydrocele)
- erythematous
- negative cremaster reflex
- relief with detorsion away from midline
- hernia exam (bowel sounds in scrotum)
Investigations testicular torsion
Priority is to quickly assess need for surgery.
ultrasound with doppler/colour
-whirlpool sign (swirling appearance of spermatic cord as probe is moved down it perpendicularly)
-anatomy/ fluid etc
-blood flow
scintigraphy can be done (but urological consultation should happen first)
Urinalysis
Urine culture and PCR for gon/chlam
FBC
-ESR/CRP
DDx testicular mass
Touching His Swollen Testicles Gets Her Hairy Vagina Excited
- Tumour (germ cell, sex chord stromal, gonadoblastoma, lymphoma)
- Hernia
- Spermatocele (epididymal cyst)
- Torsion
- Gumma (syphilis)
- Haematoma/haematocele
- Hydrocele
- Varicocele
- Epididymitis/epididymo-orchitis
why no testicle biopsy
Due to concern of seeding into scrotal sac and change in lymphatic drainage with possible spread to inguinal nodes.
This might necessitate groin dissection or adjunctive chemotherapy, which is totally unnecessary without scrotal violation and carries substantial morbidity.
Some studies report a higher recurrence rate in patients with scrotal incisions
