Needs work Flashcards
UC severity classification
Montreal classification
Mild:
- <4 stools
- no systemic symptoms (fever, weight loss)
- normal ESR
Moderate:
- > 4 stools
- some systemic symptoms (fever, anaemia, abdo pain)
- no weight loss
Severe:
- > 6 stools
- systemic features (fever, tachycardia, anaemia, abdo pain)
- elevated ESR
Define pyuria and sterile pyuria
pyuria is defined as the presence of 10 or more white cells per cubic millimeter in a urine specimen, 3 or more white cells per high-power field of unspun urine, a positive result on Gram’s staining of an unspun urine specimen, or a urinary dipstick test that is positive for leukocyte esterase.1 Sterile pyuria is the persistent finding of white cells in the urine in the absence of bacteria, as determined by means of aerobic laboratory techniques (on a 5% sheep-blood agar plate and MacConkey agar plate).
Viral hepatitis clinical features
A -symptomatic in 70% -acute onset (1 month) -lasts 2 months -faecal oral -rarely fulminant -never chronic or cancer -vaccine outcome -cholestatic (prolonged jaundice) -relapsing
B
- baby making, babies and blood
- DNA virus
acute
- insidious/acute onset (2 months)
- 70% asymptomatic
- resolution within 3-4 months
- rarely fulminant (more with coinfection)
- ongoing fibrosis and detectable HBV DNA despite seroconversion
chronic
- 90% of neonatal
- 5% of adult acute
- polarteritis nodosa
- membranous GN
- aplastic anaemia
- associated with hepatic cancer
D
- Chronic Hep B with sudden decline/severe Hep B with demographic features
- often fulminant
- chronicity dependent on Hep B clearance
- some association with hepatic cancer
C
- blood borne and sexual
- acute lasts 3-4 months
- approx 90% develop chronic
- 30% develop cirrhosis
- high rate of cancer
- extrahepatic in chronic = LLAMP (lichen planus, lymphoma, auto-antibodies, mixed cryoglobinaemia, porphyria cutanea tarda)
E
- same as A but usually asymptomatic
- faecal oral, endemic
- acute onset of 1 month
- lasts approx 2
- can be fulminant and cholestatic
- doesn’t progress to chronicity or cancer
Hep A, D, C virology
HEP A
Anti-HAV IgM
- lasts approx 3 months
- represents acute
Anti-HAV IgG
- lasts indefinitely
- represents past infection
- protected from re-infection
HEP D
- defective RNA virus
- requires HBsAg for envelope
- co-infection and super-infection (change from donor to recipient HBsAg)
- delta antigen present in serum briefly following infection then intra-hepatocyte
acute
- HBsAg positive
- anti-HBc IgM positive
- may have serum delta antigen or HDV RNA or anti-HDV
chronic
-total anti-HDV
HEP C
- RNA virus
- antibodies do not provide protection
- HCV RNA within days of exposure, persists for duration of infection
- RNA levels don’t correlate with prognosis
Medical conditions with bleeding
you can CHAALK it up to:
- Cancer
- Alcohol
- Autoimmune (SLE)
- Liver disease
- Kidney disease (uraemia)
MRI brain mass
Primary brain tumour:
- low grade glioma (no uptake)
- high grade glioma (heterogeneous uptake)
- meningioma (homogeneous uptake)
- primary CNS lymphoma (homogeneous)
Metastatic tumour (homogenous):
- breast
- lung
- melanoma
Vascular: infarct -cortical emboli -venous thrombus (bleeding, oedema) haemorrhage (subacute intraparenchymal) anamoly -cavernous malformation -AV malformation -posterior reversible leukoencephalopathy syndrome
Infection:
- granuloma
- progressive multifocal leukoencephalopathy (JC virus)
- abscess
Inflammatory:
- demyelination (MS)
- autoimmune encephalitis (para/non neoplastic)
DDx for bone lesion
COPIIED
- congestion (vertebral venous)
- osteiod osteoma
- pagets
- infarct
- island
- enchondroma
- dysplasia (fibrous)
Define nephritic syndrome
Characterised by glomerular inflammation (glomerulonephritis) resulting in haematuria, red blood cell casts and dysmorphic RBCs, variable degrees of proteinuria (can be nephrotic range) and pyuria. Often have renal insufficiency (decreasing GFR and azotemia/uremia) leading to HTN and oedema.
Diabetic nephropathy ddx
Both proteinuria and oedema suggest glomerular disease.
Primary glomerular disease (My Girlfriend Is Mega Fit):
- Approx. 25% of diabetics have concurrent or isolated other glomerular disease
- minimal change
- glomerulonephritis
- IgA nephropathy
- membranous
- FSGS
Secondary: infective -Hep B/C inflammatory: -amyloidosis neoplastic: -lymphoma -multiple myeloma drugs: -NSAIDS autoimmune: -lupus -cryoglobinaemia
Oedema (CATCH ME)
- cirrhosis
- artery (renal artery stenosis)
- thiazolidinediones
- congestion (venous hypertension)
- heart failure
- myxedema
- enteropathy (protein losing, such as crohn’s)
DDx intrinsic AKI
Glomerular (Mindful Sailors Invest In A Good Anchor):
- membranoproliferative
- SLE
- IgA
- infectious (eg. post strep)
- anti GBM
- good pastures
- ANCA (polyangitis with granulomatosis, microscopic polyangitis, eosinophilic granulomatosis with polyangitis)
Vascular (Some Honest Virgins Admit Masturbating Every Day They Can):
small:
- Scleroderma
- Hypertension (malignant)
- Vasculitis
- Atheroemboli
- Microangiopathies
large:
- Embolus (systemic/renal)
- Dissection (aortic)
- Thrombosis (renal vein)
- Compartment syndrome (abdo)
Tubulointerstitial (Indoor Dogs Should SIT on their MAT)
interstitial nephritis:
- Infections (legonella)
- Drugs (antibiotics, NSAIDs)
- Systemic (sarcoid, srjogens, SLE)
ATN:
- Sepsis
- Ischaemia
- Toxins (vanc, aminoglycosides, contrast)
tubular obstruction:
- Myeloma
- Acyclovir
- Tumor lysis syndrome
DDx reflux nephropathy case
Provisional:
UTI’s + nocturia + HTN = UTO
Childhood Hx = congenital cause
- UPJ obstruction/narrowing
- UVJ obstruction/narrowing
- UVJ reflux
- Uretercele
- Bladder outlet obstruction
- Neurogenic bladder (spina bifida)
DDx:
Acquired:
- most likely functional secondary to anatomic or neurogenic
- carcinoma (kidney, ureter, bladder) = too young
- calculi/papillae = no pain
Vascular:
- nephrosclerosis due to HTN
- renal artery stenosis
Glomerular (nephrotic)
- My Girlfriend Is Mega Fit
- Secondary causes
- Diabetic nephropathy
Tubulointerstitial
- PCKD
- SLE, Srjogens, sarcoid
Pre-renal:
- CCF
- Cirrhosis
Smoking effects on vessel wall
Association between smoking and atherosclerosis well established but mechanism unclear
Damage to endothelium
- sympathetic activation -> increase HR and TPR
- increases LDL and triglycerides, decreases HDL
- free radicals that oxidise LDL
- > impairs endothelium dependent vasodilation (generation of NO)
- impaired prostacyclin production
- elevation of homocysteine also causes vascular damage
-also prothrombotic (decrease tPA, increase tissue factor, elevated fibrinogen and platelet activation)
path uc
Almost always involves the rectum (proctitis), commonly sigmoid (proctosigmoiditis) and up to left colic flexure. Can involve entire colon (pancolitis), with backwash ileitis.
Continuous lesions with sharp demarcation between healthy and diseased tissue.
Macroscopic: In mild disease, mucosa is erythematous with granular appearance (wet sandpaper). In severe disease, it may be haemorrhagic, oedematous and ulcerative (broad based). Regeneration leads to formation of pseudopolyps which may form mucosal bridges. In chronic disease, mucosa may be atrophied with loss of features.
Microscopic: Inflammation (mixed) is confined to mucosa or superficial submucosa. Disorganisation of crypts with crypt abscesses. There may be pseudopyloric or Paneth cell metaplasia. Shallow ulcers may be visible. There may be fibrosis of submucosa. No serositis or granulomas.
path of cd
Can involve any section of alimentary canal. 75% of cases involve small bowel, and of those, 90% involve terminal ileum. Often spares rectum. There may be skip lesions.
Macroscopic: Erythematous, longitudinal (serpinguous) ulcers giving cobblestone appearance. May be deep fissures or sinus tracts that can fistulate. Wall is thickened and there are commonly strictures. Wrapped by mesentary, creeping fat.
Microscopic: Transmural (mixed) inflammation. Disorganised crypts with crypt abscesses. May be pseudopyloric or Paneth cell metaplasia. Deep ulceration/fissures that may perforate bowel wall. Granulomas at any level. Submucosa is fibrotic, muscularis is hypertrophied and there may be serositis.
effects of acidosis
- Fall in pH detected by peripheral (carotid bodies) and central (mainly ventral surface of medulla, but now thought to be scattered throughout hind brain)
- Increase in ventilation, especially tidal volume (Kussmauls breathing)
- Impairs the function of all organs, but cardiovascular system is primarily affected
- Decreased response to catecholamines
- Increase in release of catecholamines may counter some of these effects
- Decreased myocardial contractility
- Decreased conductivity
- Vasodilation of peripheral vessels (hypotension)
- Vasodilation of splanchnic circulation, decreases perfusion
- Likewise, vasodilation of cerebral vasculature and depression of CNS function, with headache, lethargy, stupor –> coma
- Leads to constriction of pulmonary vasculature, decreased compliance and pulmonary oedema
- Decreased enzymatic activity of liver
- Impaired ATP production with decreased glucose uptake and reduction in glycolysis
-Procoagulant effect, associated with intravascular clotting
path diabetic kidney disease
- Initially thickening of GBM (as soon as 2 years from diagnosis)
- mesangial expansion, diffuse or nodular (Kimmelstiel-Wilson)
- podocyte injury
- glomerulosclerosis
- arteriolar hyalinosis and atherosclerosis (from hyperglycaemia and HTN)
- tubulointerstitial fibrosis (after initial glomerular lesion)
Class I-IV
- class 1 = GBM thickening
- class 2=mesangial expansion
- class 3= at least one KW nodule
- class 4= >50% global glomerulosclerosis
types of proteinuria
Normal total = <150mg/day
Albumin = 4-7mg/day (varies with age)
Glomerular
- increased filtration of macromolecules (albumin)
- UACR >30
- positive dipstick (>300mg/day)
Tubular
- excretion of LMW proteins such as beta2-microglobulin, IgG light chains, retinol binding protein, polypeptide chains are not reabsorbed by diseased tubules
- albumin content is low
- dipstick negative
- sulfosalysilic acid test positive
Overflow
- increased production and filtration of LMW proteins
- IgG light chains myeloma, lysozome leukema, myoglobin rhabdo, haemoglobin intravascular haemolysis
- filtration exceeds tubular resorption capacity
- dipstick negative
- sulfosalysilic acid positive
Post-renal
- inflammation can increase protein excretion
- UTI, nephrolithiasis, tumour
- IgG, IgA main proteins
- usually low albumin
- dipstick negative
- sulfosalysilic positive
pathophys diabetic kidney disease
Hyperfiltration
- greater decrease in resistance of afferent vs efferent arteriole
- due to many factors, including NO, VEGF, TGFB and renin-angiotensin system (angiotensin II)
- mechanical strain –> loss of fenestration of capillaries
- local release of cytokines and growth factors –> mesangial matrix overproduction, thickening GBM, podocyte injury
Hyperglycaemia
- mesangium critical for alteration in filtration pressure by smooth muscle activity
- hyperglycaemia associated with increase in mesangial matrix
- associated with increase in oxidative stress
- oxidative stress leads to AGE, activation of PKC, accerleration of aldose reductase pathway
Inflammatory cytokines
- VEGF –> NO –> vasodialtion and hyperfiltration; also collagen IV deposition GBM
- TGFB –> collagen deposition and glomerulosclerosis
- other cytokines, notably IL-1, IL-6 and TNF alpha also contribute
Podocyte
- nephrin (podocyte protein) is crucial for maintaining integrity of filtration barrier
- decreased nephrin expression decreased
- podocyte efacement
nephrotic syndrome definition and pathophys
Definition
- protienuria >3.5g/day
- hypoalbuminaemia
- peripheral oedema
- also HTN, lipiduria and thrombosis
Proteinuria
- glomerular type
- hyperfiltration + hyperglycaemia –> OS + inflammatory cytokines –> loss of fenestration, mesangial matrix expansion, thickening GMB, podocyte effacement
Hypoalbuminaemia
- filtered albumin catabolised by proximal tubule cells
- low oncotic pressure leads to increase in hepatic albumin synthesis
- high levels of inflammatory cytokines such as IL-1 and TNF alpha suppress hepatic response
Oedema:
-overfill and underfill hypothesis. Both likely contribute
Underfill:
-starlings law for transcapillarly filtration is hydraulic pressure gradient - oncotic pressure gradient
-decrease in albumin would be expected to lead to increase ECV –> activation of RAS
-gradual decline in albumin means that transcapillary gradient in oncotic pressure does not increase as much as expected
Overfill:
-primary Na retention induced by renal disease –> water retention
-nephrotic patients have lower ANP and higher renin activity that expecting
-increased activity of N/K ATP-ase in collecting tubule
-resistance to ANP
-increased expression of ENaC
Hypercholesterolaemia/hypertriglyceridaemia:
- low oncotic pressure stimulates hepatic apolipoprotein B gene transcription
- increases lipoprotein production containing cholesterol
- delipidation casade of VLDL –> IDL –> LDL by lipoprotein lipase is impaired
define aki
Impairment in kidney function:
- serum creatinine >26.5micromol/L within 48hrs
- serum creatinine 50% increase from baseline within a week
- urine output <0.5mL/kg/hr for 6hrs
effects hyperkalaemia
Weakness/paralysis
- ascending muscle weakness
- beginning with legs, moving to trunk and arms
- progressives to flaccid paralysis (resembling GB)
ECG -tall peaked T waves -shortened QT worsening -prolonged QRS -prolonged PR eventually -loss of P wave -sine wave QRS -ventricular standstill with loss of electrical activity
Arrhythmias
- sinus brady
- AV block
- sinus arrest
- RBB/LBB/bifasicular block
- VT
- VF
- asystole
Reduced ammonium excretion and acidosis:
-high K competes with ammonium at Na/K/2Cl in thick ascending limb
complications CKD
Chronic Kidney Bandage
Cardiac -HTN/hypervolaemia/oedema -vascular disease (CAD,PAD) -CCF, MI, LVH -pericarditis HyperKalaemia Bone/mineral -secondary hyperparathyroidism -osteitis fibrosa cystica -osteomalacia -adynamic bone disease (with tumoral calcinosis, caliphylaxis) -vessel calcification Anaemia Neurological -restless legs -asterixis -neuropathies -memory/attention/stupor Dermatological -pruiritis -pigmentation Acidosis -normal anion gap with renal tubular acidosis -high anion gap late development GI -uremia fetor -ulcers -anorexia, nausea, vommiting -malnutrition Endocrine -impaired glucose metabolism -decreased insulin excretion -sex hormone (infertility, miscarriages)
kidney stone types
Uric acid
- Only acidic urine
- Pleomorphic
Calcium oxolate (calcium phosphate)
- monohydrate = dumbbell
- dihydrate = envelope
Struvite
- alkali urine with increased ammonium phosphate
- due to UTI with proteus or klebseilla (urease producing)
- coffin lid shape
Cystine
-hexagonal shape
ddx nephrolithiasis
a TRAP for CHAPs Beginning their MD
- Testicular torsion
- RCC
- AAA
- Pyelonephritis
- Cholecystitis
- Herpes zoster
- Apendicitis
- Pancreatitis
- Bowel obstruction
- Mesenteric ischaemia
- Diverticulitis
hx and exam testicular mass
Hx -onset and course of mass -dull ache or discomfort scrotum, lower abdo, peri-anal -10% with acute pain (haemorrhage/infarct) 10% present with mets symptoms -neck mass -cough/dyspnea -anorexia, nausea, vom, GI haemorrhage (retroduodenal) -lumbar back pain (psoas or nerve roots) -bone pain -neuro symptoms -limb swelling (iliac or IVC) risk factors extratesticular manifestations
Exam -size, contour, consistency of contralateral for baseline -firm fixed area is suspicious -rubber and ovoid = seminoma -irregular/indiscrete borders = embryonal and teratocarcinoma -hydrocele -involvement of spermatic chord, epididymus nodes -abdo nodes -inguinal nodes (local spread to scrotum) -supraclavicular chest -effusion -gynecomastia bone pain lower limb oedema neurological
investigations diabetic nephropathy
Bedside: urinalysis -proteinuria -specific gravity > = pre-renal cause of decreased GFR -leuks/nitrites = UTI -haematuria (doesn't differentiate) -casts and dysmorphic red cells (non diabetic) -fat bodies and lipid droplets ACR ->30mg/g (can be normal) -repeat 2 more times over 2-3 months VBG -acidosis (initially normal --> high anion gap) ECG -electrolyte abnormalities and HTN
Bloods: HbA1c FBC -anaemia EUC -eGFR (can be normal or raised early), <60 for 3 months diagnostic -hypernatraemia -hyperkalaemia CMP -hypocalaemia/phosphataemia Lipids -hypertriglyceridaemia Coags -venous and arterial thrombosis Albumin
Imaging:
-ultrasound (normal to large), exclude other etiologies
Consider:
- CT abdo (if ultrasound poor)
- MRangiography (renal artery stenosis) in patients recently started on ACEI
- Ultrasound doppler for same effect
- biopsy (when unusual clinical picture/other etiology suspected)
- TTE or TOE (cardiomyopathy, diastolic dysfunction)
- chest xray (pulmonary HTN batwing)
AKI investigations
VBG/ABG -high anion gap = decreased GFR and retention of acids -normal anion gap with high urine pH = renal tubular acidosis (Type 1 with impaired distal H secretion; Type 2 with impaired proximal bicarb reabsorption) Urinalysis Urine chemistries -FENa (<1 = pre-renal, >2=ATN) -FEUrea when diuretics (<35=pre-renal, >65=ATN) Urine osmolality -increased = pre-renal -decreased = ATN ECG -hyperkalaemia
FBC -anaemia (haemolysis, microangiopathies, myeloma) -eosinophilia (interstitial nephritis, emboli, vasculitides) -thrombocytopenia (microangiopathy) EUC -eGFR -urea:creatinine ratio >20 = pre-renal -hyperkalaemia CMP -hyperphosphataemia -hypocalcaemia
Renal ultrasound/CT -obstruction -architecture Chest xray -CCF -Pulmonary oedema
Consider (in glomerulonephritis)
- ANA/anti-DSDNA = lupus
- C3/4 = immune complex GN types
- anti-GBM antibodies
- ANCAs
- cryoglobin
- anti-streptolysin O (post strep), hep (membranoproliferative) and HIV serology based on Hx
- biopsy
DDx haematuria
NIICCKSS
neoplasm
- kidney (RCC, transitional)
- bladder (urothelial, squamous)
- penile (squamous)
- ureter
- prostate (BPH/cancer)
Infection
- UTI
- pyelonephritis
Inflammation
- prostatitis
- cystitis
- diverticulitis
Cysts
-PCKD
Coagulopathy
- medical (eg. von willebrand, platlete (MAID FLUID), haemophilia, vessel wall)
- drugs
Kidney injury (glomerular) -Mindful Sailors Invest In A Good ANCA
Stones
- renal
- bladder
Staining
- beets
- phenazopyridine
- rifampicin
ultrasound features DVT
presence of thrombus demonstrated by non-compressibility
- the most sensitive/specific >95
- addition of doppler does not improve sensitivity
- variation of venous size with valsava is low sensitivity and specificity and rarely performed
Iliac and calf veins cannot be compressed
-doppler
ddx MM lytic lesions
Lytic bone lesion (FOG MACHINE)
- Fibrous dysplasia
- Osteoblastoma
- Giant cell tumour
- Metastatic disease (RCC, breast, lung)
- Aneursymal bone cyst
- Chondroblastoma
- Hyperparathyroidism
- Infection
- Non ossifying fibroma
- Enchondroma
histopath prostate cancer
Cancer types
- adenocarcinoma = 95%
- also transitional, basal cell, carcinosarcoma, lymphoma..
Adeno Architecture
- microscopy with H&E staining
- small glands (smaller than benign glands)
- infiltrating in haphazard manner
- less differentiated = less well organised glandular appearance + glands grow in chords, nests or cribiform plate
Adeno Cytology
- microscopy with H&E
- purple and darker than benign cells
- large nuclei, prominent nucleoli, irregularity, hyperchromasia
Immunohistochemistry
PSA
-limited utility in differentiated benign glands from cancer
-more useful in determining prostate origin of mets
High Molecular Weight Cytokeratin
-identifies basal cells
-present in benign glands but not adeno
p63
-present in basal cells of benign glands and not adeno
AMACR
-molecular marker for adeno
