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MANCHESTER YEAR 3 > TCD Cases 13-24 > Flashcards

TCD Cases 13-24 Flashcards

1
Q

What are the 4 functions of your kidneys?

A
  • make urine
  • produce hormones
  • activate vitamin D
  • clean your blood
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2
Q

What are the steps involved in the SALFORD checklist?

A
  • Sepsis + other causes: treat
  • ACEI/ARBs + NSAIDs: review/suspend drugs
  • Labs (repeat creatinine within 24 hours) + Leaflets (for pts)
  • Fluid assessment + response (history + exam, fluid chart, daily weights)
  • Obstruction: USS performed within 24 hrs of non-resovling AKI3
  • Renal/critical care referral: non resolving AKI3, or CKD 4-5
  • Dip urine + record it
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3
Q

What is seen on an ECG if a patient has severe hyperkalaemia? (HINT three things)

A
  1. No discernable p waves - regular rhythm
  2. Wide QRS complexes (more than 3 small squares)
  3. Peaked T waves
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4
Q

What 3 symptoms raise suspicion of hyperkalaemia?

A
  • arrhythmias
  • muscular weakness
  • paraesthesiae
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5
Q

How is hyperkalaemia treated?

A
  1. IV calcium chloride/calcium glucoronate given to pts with hyperkalaemia + ECG changes supporting this
  2. Insulin-glucose by infusion. Nebulised salbutamol as an adjunct in severe (more than 6.5) or as monotherapy for moderate (6-6.4)
  3. Cation exchange resins only considered in mild to moderate
  4. Serum K+ monitored 1, 2, 4, 6 + 24hrs after identification. Blood glucose measured at regular intervals for a min of 6hrs after administering insulin-glucose infusion
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6
Q

What is the definition of acute kidney injury?

A

clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes

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7
Q

What are the 3 stages of AKI? List the SCr and urine output criteria for each stage.

A

STAGE 1: SCr increase of more than 26 micromols in 48 hrs or an increase of 1.5-1.9x reference SCr. Urine output of less than 0.5ml/kg/hr for more than 6 hrs.
STAGE 2: SCr more than 2-2.9x reference SCr. Urine output of less than 0.5ml/kg/hr for min 12 hrs.
STAGE 3: SCr more than 3x reference SCr OR increase of 354 micromols OR started on RRT. Urine output of less than 0.5ml/kg/hr for more than 24 hrs OR anuria for 12 hrs

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8
Q

What are the pre renal causes of AKI?

A

Are the cause of 85% of AKIs

  • dehydration
  • sepsis
  • hypotension
  • shock
  • hepatorenal syndrome
  • severe HF
  • intra-abdominal hypertension/compartment syndrome
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9
Q

What are the renal causes of AKI?

A

Cause of 10% of AKIs

  • NSAIDs, ACEI, ARBs
  • Gentamicin
  • Glomerulonephritis/Vasculitis
  • Contrast
  • Interstitial nephritis
  • Myeloma
  • Rhabdomyolysis
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10
Q

What are the post renal causes of AKI?

A

Make up 5% of AKIs

  • prostate enlargement
  • renal stones
  • pelvic cancer
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11
Q

What is the importance of the urine dip in AKI?

A
  • More than 3+ proteinuria indicates intrinsic renal disease
  • send urine PCR/MSU if dip +ve
  • if -ve it excludes intrinsic renal disease
  • if blood and protein +ve, consider glomerulonephritis
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12
Q

What patients with an AKI need a discussion with the renal team?

A
  • pts with transplant
  • AKI 3
  • AKI with blood + protein on dip
  • all with unknown cause of AKI and deteriorating function
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13
Q

When is dialysis an appropriate treatment for AKI?

A

If the following conditions cannot be controlled:

  • hyperkalaemia
  • pulmonary oedema
  • metabolic acidosis
  • uraemic encephalopathy (confusion, myoclonic jerks, seizures, coma) or uraemic pericarditis (inflammation of pericardial sac)
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14
Q

Describe the function of RAAS, briefly.

A

Tries to prevent ischaemia and maintian renal blood flow by increasing overall effective circulating volume by increasing reabsorption of salt and water. Also protects nephron locally by vasoconstricting efferent renal arteriole to maintain GFR
- ACEI, ARBs and NSAIDs all prevent this protective mechanism

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15
Q

What are the 3 phases of Acute Tubular Necrosis?

A
  1. OLIGOURIC PHASE = kidneys produce less than 500 mls of urine per day. Pts vulnerable to fluid overload + electrolyte balance (K+). Creatinine rises rapidly
  2. MAINTENANCE PHASE = pt no longer oligouric + increased urine output helps maintain fluid and electrolytes. Creatinine stable or rising v slowly
  3. POLYURIC RECOVERY PHASE = large volumes of dilute urine, pts can become hypovolaemic. Cause is distal tubules and collecting tubules are last to recover (AQP) so damaged AQP channels don’t allow water reabsorption. Pt susceptible to electrolyte loss (K+). Creatinine falls swiftly
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16
Q

What are the risk factors for sepsis?

A
  1. V young (under 1) or old (over 75) or frail people
  2. Impaired immune system
  3. Surgery in past 6 weeks
  4. Any breach of skin integrity
  5. IVDU
  6. People with indwelling lines/catheters
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17
Q

How is SIRS defined?

A

When 2 or more of the following are present:

  • temp less than 36 or more than 38
  • tachycardia (greater than 90 bpm)
  • RR more than 20/min OR PaCO2 less than 4.3kPa
  • WCC less than 4x10^9 or more than 12x10^9
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18
Q

How is (i) sepsis (ii) severe sepsis (iii) septic shock defined?

A

(i) 2 or more of the signs of SIRS resulting from infection
(ii) sepsis along with signs of organ hypoperfusion eg hypoxaemia, oliguria, lactic acidosis or acute alteration in mental state
(iii) severe sepsis with hypotension (systolic less than 90) OR the requirement for vasoactive drugs despite adequate fluid resuscitation

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19
Q

What tests are done in patients with suspected sepsis?

A
  • Blood gas (glucose and lactate)
  • Blood culture
  • FBC
  • CRP
  • U+Es
  • Clotting screen
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20
Q

What is the immediate treatment for sepsis?

A

Broad spectrum antibiotics at a max dose plus IV fluid bolus without delay

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21
Q

What are raised lactate levels a marker of?

A

Poor tissue perfusion, or shock, and will result in organ damage and can result in multi-organ failure. The body’s defence mechanism maintains oxygen to vital organs so the skin kidneys + gut (incl. liver) are affected first

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22
Q

What is there a risk of with colloids? Give 2 named examples.

A

Risk of anaphylaxis

- isoplex, volplex

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23
Q

What can omeprazole and furosemide cause?

A

Hyponatraemia

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24
Q

What type of drug is (i) diclofenac (ii) losartan (iii) ramipril?

A

(i) NSAID
(ii) ARB
(iii) ACE-I

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25
Q

What are the causes of haematuria ?

A
  • bladder cancer (classically painless)
  • renal cancer
  • UTI
  • stones
  • prostate disease
  • nephrological disease
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26
Q

What do most patients over 45 with haematuria have? (investigation wise)

A

Cystoscopy and upper tract scan

- except females with a simple UTI

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27
Q

What investigations are done for pts under 45 with microscopic haematuria?

A

They don’t need urological investigation

- check GFR, BP, urine protein excretion

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28
Q

What is TURBT?

A

transurethral resection of bladder tumour

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29
Q

What imaging is done in patients with loin pain and haematuria?

A
  • plain x-ray (KUB)
  • intravenous pyelogram (IVP)
  • USS
  • CT urogram
  • MR urogram
  • angiography
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30
Q

What is the triad of symptoms of urological stones? Who do they tend to affect?

A
  • pain (colic), haematuria, infection

- present in 3rd to 5th decade, affect males more than females

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31
Q

How are urological stones managed?

A
  • increased fluid intake
  • Dietary modifications = decrease animal protein, sugar and oxalate
  • treat infection
  • alkalise urine
  • specific therapies (bendroflumethazide for hypercalciuria, allopurinol for hyperuricosuria, pencillamine for cystinuria)
  • surgery
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32
Q

What are the 2 examples of (i) benign (ii) malignant kidney tumours?

A

(i) angiomyolipomas, oncocytoma

(ii) renal cell carcinoma (80%), transitional cell carcinoma

33
Q

Who do renal cell carcinomas commonly affect? What are the triad of symptoms? How is it treated?

A

Males:females 2:1 in 4th to 6th decades
- triad of haematuria, pain, mass
Management = surgical for resectable disease or immunotherapy

34
Q

What are the symptoms of transitional cell carcinoma? Who does it affect? What are risk factors and how is it managed?

A

Haematuria, pain and LUTS
- males more than females, aged over 45
- risk factors = smoking, cyclophosphamide, schistosomiasis, radiotherapy, occupational exposure
Management = surgical resection, intravesical chemo

35
Q

What are the risk factors for papillary necrosis? What can it cause? What treatment is required?

A

Risk factors = analgesia (acetaminophen, NSAIDs), DM, sickle cell, infection

  • can cause obstruction and pyelonephritis
  • URGENT drainage and antibiotic treatment essential
36
Q

What is ADPKD? How is it managed?

A
  • Commonest genetic renal disease. Approx 50% reach ESRD by 60 years
    MANAGEMENT = monitor renal function (kidney size), family screening, BP control
  • no role for surgical/radiological decompression. Nephrectomy occasionally needed for severe pain + poor function
37
Q

What is VHL? What can it cause?

A

von Hippel-Lindau disease

  • autosomal dominant, 20% familial. 2nd-3rd decade onset
  • risks include developing CNS haemangioma, retinal angioma, retinal lesions
  • 75% become cortical renal cysts, 20-45% develop renal cell carcinomas
38
Q

What is the chance of a patient over 60 with microscopic haematuria having significant pathology?

A

5%

39
Q

Who are UTIs more common in?

A

post-menopausal women

- due to alteration in normal vaginal bacterial flora

40
Q

What is an upper UTI called? What are the symptoms?

A

Pyelonephritis
- begins with lower UTI (cystitis) symptoms followed by increasing loin pain that’s unilateral. Patient feels pyrexial and systemically unwell

41
Q

What are the treatments for UTIs?

A
  • simple lower UTI = trimethoprim or cephalexin or nitrofuratonin
  • pts with pyelonephritis and pyrexia = 24-48 hrs IV gentamicin or temocillin followed by a 10 day course of oral antibiotics
42
Q

What is a complicated UTI?

A

anatomical or pathological abnormality that predisposes to developing UTIs eg vesico-ureteric reflux, urinary tract stones, urinary tract tumours, or incomplete bladder emptying

43
Q

When are UTIs classed as recurrent?

A

If you have more than 3 in one year

44
Q

What % of bladder cancers don’t involve the muscle wall? How are these treated?

A

75-80

- treated by TURBT

45
Q

What is the treatment for pts with superficial invasion of the bladder wall (T1) or histologically aggressive disease (grade 3)?

A

BCG therapy into bladder and some eventually require total surgical removal in the form of a radical cystectomy

46
Q

What is the (i) grading and (ii) staging of bladder cancers?

A

(i) GRADE 1 = least aggressive/well differentiated histologically
GRADE 2 = intermediate
GRADE 3 = most aggressive/least differentiated
(ii) pTa = tumour cells confined to epithelium
cis = aggressive cells confined to epithelium, flat ‘tumout’
T1 = tumour cells in sub-epithelial connective tissue
T2/3 = tumour cells in bladder wall muscle
T4 = tumour cells in adjacent organs (prostate or uterus)

47
Q

What are normal prostate levels? What is used to treat BPH?

A

Normal is less than 4ng/ml, but less than 4.5 in men 60-69

- tamulosin is used to treat BPH

48
Q

How is gleason score calculated? What do the grades mean?

A

= most common grade + highest other grade in samples
grades 1 and 2 aren’t cancer
grades 3-5 are cancer. Higher grade = more chance of cancer spreading

49
Q

When is urine cytology used?

A

It is not a 1st line investigation in 65 YO man with painless frank haematuria
- reserved for patients with recurrent haematuria where initial investigations were -ve or especially high risk (aka prev bladder cancer)

50
Q

What is the chance of an asymptomatic man with a serum PSA of 7.0ng/ml and a normal DRE having prostate cancer diagnosed on one set of transrectal prostate biopsies?

A

20% chance

51
Q

What drug is used to treat bladder outflow obstruction?

A

Alpha adrenoreceptor blocker

- doxazosin, terazosin, tamulosin

52
Q

When is intravesical BCG therapy useful?

A

Pts with superficially invasive (stage pT1) bladder tumour

- ineffective if there’s muscle invasion

53
Q

What investigations are required in a female over 50 years old with persistent bloating?

A
  • USS of ovaries

- Ca125 level to rule out ovarian cancer

54
Q

What is the definition of IBS?

A

Syndrome comprising of abdominal pain, bloating and altered bowel habits. Pain is colicky + associated with bowel movements. Sub-typed into diarrhoea or constipation predominant
- in the past it was considered a ‘diagnosis of exclusion’ but now we are encouraged to make a +ve diagnosis based on the typical symptoms, exclusion of red flags, and simple tests

55
Q

What are the various drug types used in IBS? Give named examples for each. (HINT there’s 5 categories)

A
  1. ANTICHOLINERGICS = dicycloverine (merbentyl), hyoscine (buscopan) and propatheline (probanthine)
  2. ANTI-SMOOTH MUSCLE = mebeverine (colofac), alverine (spasmonal), peppermint (colpermin)
  3. ANTI-DIARRHOEALS = loperamide, diphenoxylate, codeine phosphate
  4. LAXATIVES = polyethylene glycol, NOTE avoid lactulose in IBS
  5. ANTIDEPRESSANTS = tricyclic (amitriptyline) and SSRIs (citalopram, fluoxetine, sertraline), note only use tricyclics in diarrhoeal IBS but SSRIs in both
56
Q

What is another form of very successful treatment used in IBS?

A

Hypnotherapy

  • 12 sessions at weekly intervals
  • daily practice with audio tape/disc
57
Q

What is functional dyspepsia described as? What is the treatment available?

A

‘IBS of upper GI tract’

- treatment includes hypnotherapy, supportive treatment and conventional treatment

58
Q

What is non cardiac chest pain? How do you treat it?

A

Angina like pain with no evidence of heart disease

  • difficult to treat as patients fear sudden death
  • supportive and hypnotherapy treatment
59
Q

What is the difference histologically between UC and Crohns?

A

UC is superficial inflammation whereas Crohn’s is transmual

60
Q

What is a characteristic feature of UC?

A

pseudopolyps

61
Q

What is carnetts sign? What does a positive carnetts sign indicate?

A

determines whether pain originates from viscera or myfascia/abdominal wall

  • patient lies down and raises head or legs against gentle resistance from the physician
  • the test is POSITIVE if the manoeuvre exacerbates pain aka abdominal wall origin
62
Q

How is IBS diagnosed?

A

Only if the person has abdominal pain that’s:
- relieved by defecation OR - associated with altered bowel frequency or stool form
AND at least 2 of the following:
- altered stool passage
- abdominal bloating, distension, hardness or tenderness
- symptoms worse on eating
- passage of mucus

63
Q

What is the most important investigation if you suspect infectious diarrhoea?

A

Stool cultures

64
Q

What is dysentry?

A

diarrhoea with visible blood

65
Q

What are the causative organisms for infective diarrhoea? (HINT bacterial, viral and parasitic examples)

A 
BACTERIAL = campylobacter, shigella, salmonella, c.diff
VIRAL = norovirus, rotavirus
PARASITIC = giardia, crytposporidium, schistosomiasis
66
Q

Most gastroenteritis is self-limiting, but when are antibiotics considered?

A

In at risk patients if severe (bacterial) and/or systemic symptoms; for possible dysentry or enteric fever once stool samples are obtained

67
Q

What is campylobacter? How is it spread? What are the symptoms? What can it cause? What is the treatment?

A

The most common bacterial gastroenteritis in the UK

  • foodborne and is spread faeco-orally
  • abdominal pain, profuse diarrhoea, malaise, vomiting uncommon
  • usually mild but 20% are severe and are at risk of developing toxic megacolon, pancreatitis, cholecystitis, peritonitis, arthritis (HLA-B27)
  • treatment is supportive or consider use of macrolide if severe
68
Q

Name and describe (i) ETEC (ii) EHEC.

A

(i) enterotoxigenic e.coli = cholera like, affects travellers and children, experience watery diarrhoea, cramps and a low grade fever
(ii) Enterohaemorrhagic e.coli = increased risk of HUS + TTP, affects all ages and can cause outbreaks, profuse bloody diarrhoea, afebrile, AVOID antibiotics

69
Q

What types of salmonella DON’T cause dysentry? Describe the symptoms of these two types.

A

Typhi and paratyphi

  • enteric fever
  • caused by food and water
  • constipation more than diarrhoea, fever and abdominal pain
70
Q

What type of shigella is an endemic in the UK?

A

sonnei

71
Q

What can shigella.dysenteriae be associated with?

A

toxic megacolon and haemolytic uraemic syndrome

72
Q

Describe giargia lamblia. How is it treated?

A

Malabsorption type diarrhoea

  • present in upper small bowel causing cysts in stool
  • treatment = emperic trial of therapy may be indicated with metronidazole/tinidazole
73
Q

What are the symptoms of Entamoeba histolytica (amoebiasis)? What treatment is available?

A

Mostly asymptomatic

  • treatment = metronidazole and luminal cysticide
  • abscess may require drainage
74
Q

What are the 4 gastrointestinal related consequences of opiates?

A
  1. Worsening motility
  2. Increased cannula infections on parenteral nutrition
  3. Mental fogging/narcosis + drug seeking behaviour
  4. Opiate induced hyperalgesia giving risk to narcotic bowel syndrome
75
Q

What are some causes of constipation?

A
  • rectocele
  • IBS
  • dysinergic defecation
  • normal transit
  • slow transit
  • enterocele
  • drug induced
76
Q

What is countertransferance?

A

feelings evoked in you by the patient

77
Q

What condition does IBS overlap with?

A

Fibromyalgia

78
Q

What can the following drugs be used for (i) linaclotide (ii) rifaximin?

A

(i) moderate to severe IBS with constipation

(ii) treatment of travellers diarrhoea

MANCHESTER YEAR 3 (11 decks)

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