Needs work Flashcards

1
Q

UC severity classification

A

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
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2
Q

Define pyuria and sterile pyuria

A

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).

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3
Q

Viral hepatitis clinical features

A
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
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4
Q

Hep A, D, C virology

A

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
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5
Q

Medical conditions with bleeding

A

you can CHAALK it up to:

  • Cancer
  • Alcohol
  • Autoimmune (SLE)
  • Liver disease
  • Kidney disease (uraemia)
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6
Q

MRI brain mass

A

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)
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7
Q

DDx for bone lesion

A

COPIIED

  • congestion (vertebral venous)
  • osteiod osteoma
  • pagets
  • infarct
  • island
  • enchondroma
  • dysplasia (fibrous)
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8
Q

Define nephritic syndrome

A

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.

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9
Q

Diabetic nephropathy ddx

A

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)
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10
Q

DDx intrinsic AKI

A

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
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11
Q

DDx reflux nephropathy case

A

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
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12
Q

Smoking effects on vessel wall

A

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)

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13
Q

path uc

A

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.

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14
Q

path of cd

A

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.

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15
Q

effects of acidosis

A
  • 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

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16
Q

path diabetic kidney disease

A
  • 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
17
Q

types of proteinuria

A

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
18
Q

pathophys diabetic kidney disease

A

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
19
Q

nephrotic syndrome definition and pathophys

A

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
20
Q

define aki

A

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
21
Q

effects hyperkalaemia

A

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

22
Q

complications CKD

A

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)
23
Q

kidney stone types

A

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

24
Q

ddx nephrolithiasis

A

a TRAP for CHAPs Beginning their MD

  • Testicular torsion
  • RCC
  • AAA
  • Pyelonephritis
  • Cholecystitis
  • Herpes zoster
  • Apendicitis
  • Pancreatitis
  • Bowel obstruction
  • Mesenteric ischaemia
  • Diverticulitis
25
Q

hx and exam testicular mass

A
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
26
Q

investigations diabetic nephropathy

A
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)
27
Q

AKI investigations

A
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
28
Q

DDx haematuria

A

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
29
Q

ultrasound features DVT

A

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

30
Q

ddx MM lytic lesions

A

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
31
Q

histopath prostate cancer

A

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