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Year 3 - Met3b > Before exam > Flashcards

Before exam Flashcards

1
Q

What are the normal ranges for Haemoglobin A1c( HbA1c)

A

Normal range <42 mmol/mol

Good control varies from individual to individual (depending on age, co-morbidities etc.)

Generally HbA1c < 53 mmol/mol indicates well controlled diabetes

if HbA1c is greater than 48 mol/mol for two times then you have diabetes

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2
Q

For an individual who has no diabetes symptoms how many tests do you have to do

A

two diagnostic tests are required (eg 2x FPG, or HbA1c, but only one abnormal OGTT is required)

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3
Q

list the numbers needed for diagnosis of diabetes for each test

  • Fasting plasma glucose
  • 2 hour plasma glucose
  • random plasma glucose
  • HbA1c
A
  • Fasting plasma glucose = greater than 7 mmol/L
  • 2 hour plasma glucose = greater than 11.1mmol/L
  • random plasma glucose = greater than 11.1mmol/L
  • HbA1c = greater than 48mmol/mol(6.5%)
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4
Q

what do you use to measure impaired glucose tolerance and what does it mean

A

can only be diagnosed using an oral glucose tolerance test

  • so the 2 hour plasma glucose
  • this is between 7.8-11 mol/L - the is not a diagnosis of diabetes but it is abnormal
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5
Q

What is used to measure impaired fasting glucose and what does it mean

A
  • Slightly higher than normal which is less than 6 but it is not quite in the diabetes range yet
  • measured by using fasting plasma glucose
  • between 6.1-6.9 mol/L
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6
Q

what autoimmune antibodies are present in type 1 diabetes

A

GAD and ICA antibodies

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7
Q

what drug causes NODAT

A

Tacrolimus (used in transplantation – may cause “New Onset Diabetes after Transplantation” [NODAT])

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8
Q

At what glucose level do the two symptoms for hypoglayemia occur at

A
  • autonomic symptoms - 3.6 mmol/L

- neuroglycopenic symptoms - 2.7 mmol/L

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9
Q

Name neuroglycopenic symptoms of hypoglycaemia

A
  • Confusion
  • soured speech
  • visual disturbances
  • drowsiness
  • aggression
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10
Q

Name the autonomic symptoms of hypoglycaemia

A
  • Sweating
  • Shaking or tremor
  • anxiety
  • palpitations
  • hunger
  • nausea
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11
Q

How do you treat mild hypoglycaemia

A

Mild - conscious, lucid and able to self treat

 Sugary drink, e.g. lucozade, ordinary coke, orange juice
 5-7 glucose tablets, or 3-4 heaped teaspoons of sugar in water

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12
Q

How do you treat moderate hypoglycaemia

A

Moderate - conscious, but cannot self administer and needs help
 Glucogel® – 1-2 tubes buccally (into the cheek), or jam, honey, treacle massaged into the cheek.
 Intramuscular glucagon

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13
Q

How do you treat severe hypoglycaemia

A

Severe - unconscious

  • Do not put anything in the mouth
  • Place the person in the recovery position
  • Administer 0.5-1mg glucagon IM
  • If carer is unable to administer glucagon, call 999
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14
Q

What happens in hospital when you present with severe hypoglycaemia

A

Ideally 75mls of 20% glucose or 150mls 10% glucose over 15 mins

50mls 50% glucose can be given, but take care with veins – extravasation can cause chemical burns

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15
Q

What should you take after the hypoglycaemic episode

A

Post hypo once glucose above 4.0 mmol/L, must have some longer acting carbs, eg:
 Two biscuits
 One slice of bread/toast
 200-300ml glass of milk (not soya)
 Normal meal if it is due (but must contain carbohydrate)

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16
Q

What is the definition of diabetic ketoacidosis

A

A state of absolute or relative insulin deficiency resulting in hyperglycemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis

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17
Q

What are the clinical features of DKA

A

 Often a short history
 Abdominal pain and vomiting is common – can present as an acute
abdomen - can be very severe
 Kussmaul’s respiration – deep sighing respirations due to acidosis
 Ketones on breath (remember ~40% people cannot smell these)
 Drowsiness, confusion
 Dehydration and Tachycardia
- polyuria and polydipsia
- vomiting

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18
Q

What fluid therapy should you give in DKA

A

Sodium chloride 0.9%

  • 1 Litre stat
  • 1 Litre in 1 hour
  • 1 Litre over 2 hours (+20 mmol potassium chloride)
  • 1 Litre over 4 hours (+potassium chloride)
  • 1 Litre over 4 hours (+potassium chloride)

5% or 10% Glucose

  • Start when the CBG is <12 mmol/L and continue at 125ml/hr
  • 10 % glucose may be necessary to increase insulin infusion
  • Increase infusion rate if glucose falls below 6.0 mmol/L
  • given glucose so you can given insulin - insulin has a short half life so when it switches of you can become ketoacidotic again
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19
Q

describe the potassium regime you give in DKA

A
  • For the first 1-2 bags fluid, give no potassium as fluid is given too rapidly
  • For every subsequent bag of NaCl 0.9% or glucose 5% use a bag of fluid containing KCl as follows according to serum K+:
  • less than 3.5 - may need additional potassium and delay insulin - cause potassium to plummet further and can cause arrthymia
  • 3.5-5.5 - 20-40mmol/L
  • greater than 5.5 - none
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20
Q

describe the insulin regime in DKA

A
  • If the patient is known to be diabetic continue their normal long acting insulin on admission
  • commence insulin infusion by intravenous syringe pump - contains 50 units of actrapid made up to 50mlin sodium chloride 0.9%

fixed rate IV insulin infusion

  • 0.1u/kg - around 6-8 u/hour for most patients
  • aiming for bicarbonate rise of 3mmol/hour and glucose fall by 3 mol/hour
  • if not achieved increase the rate by 1u/hour
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21
Q

Describe the presentation of hyperosmolar hyperglycaemic syndrome

A

 Hyperglycaemia often >40 mmol/L

Osmolality >340 (275-295)
 Can be estimated by the formula 2x[Na+K]+Ur+Glu
 Patient is often hypernatraemic

 They may or may not have ketonuria – frequently “+” if not eating

 No (keto) acidosis, but may have lactic acidosis

 Severe dehydration

 66% previously undiagnosed DM

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22
Q

What is the treatment of hyperosmolar hyperglycaemic syndrome

A

 IVI as for DKA – but consider slower fluids if elderly / heart failure

 NO INSULIN BOLUS - for first 12 hours

 Much lower dose insulin – maybe no insulin for 1st 12 hours, then very low doses – perhaps 1 u/hr

 Rapid shifts in glucose should be avoided due to risk of rapid fluid / sodium shifts, and risk of central pontine myelinolysis (CPM)

 Correct BG at maximum 2 mmol/L/hr

 Central venous pressure monitoring may be required

 s/c Low Molecular Weight heparin may help reduce thrombosis

 K+ tends to decline rapidly

 Avoid 0.45% N Saline

 Accept that biochemistry will be abnormal for days or risk hypernatraemia, CPM, cerebral oedema

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23
Q

What is the management of hyperosomolar hyperglycaemic state

A

Rehydrate slowly (consider age and CCF) over 48hrs with 0.9% NaCl (IVI)

  • Typical deficit = 110-220ml/kg (~8-15L)
  • Avoid 0.45% NaCl

No insulin bolus – Only use insulin if blood glucose is not falling by 5mmol/L/hr with rehydration or ketonuria; Slow infusion of 0.05units/kg/hr (max 1unit/hr); Avoid in first 12hrs
- Rapid shifts in glucose should be avoided due to risk of rapid fluid/Na+ shits and central pontine myelinosis (CPM)

Replace K+ when urine starts to flow

  • May need CVP monitoring
  • K+ ↓ rapidly
  • Keep plasma glucose at 10-15mmol/L for first 24hrs to avoid cerebral oedema
  • Look for cause, eg bowel infarct, drugs, etc.
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24
Q

Describe the NICE guidelines for glucose lowering

A
  1. Lifestyle changes
  • ↓ HbA1c ≥48mmol/L
    2. Metformin standard release – modified release if not tolerated
  • Slow titration, take after meals
  • Care with dose of metformin if eGFR<45, stop if <30
  • Consider sulfonylurea if not overweight, metformin CI or not tolerated↓ HbA1c ≥58mmol/L
    3. Dual therapy (aim = 53mmol/L)
  • Metformin + Sulfonylurea (if hypoglycaemia a problem or metformin not tolerated:
    DPP-4 inhibitor/Pioglitazone)
  • Once daily if concordance is problematic
    Consider PGRs if erratic lifestyle↓ HbA1c ≥58mmol/L
  1. Triple therapy
    - Metformin + SU + DPP-4 inhibitor/Pioglitazone/Insulin
    - Consider GLP-1 analogue if: BMI>35, problems from weight gain
    - Continue >6 months if HbA1c drop >1% and weight loss >5%
  2. Intensify insulin or add Pioglitazone
    - Warn re oedema
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25
Q

What are the side effects of biguinides - metformin

A

nausea
diarrhoea
lactic acidosis in patients with renal failure - stop at EGFR of 30

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26
Q

What are the side effects of glitazones e.g. pioglitazone

A 
Weight gain 
oedema 
heart failure contradicted
post menopausal fractures
bladder cancer
(giving less now)
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27
Q

What are the side effects of Sulfonylureais e.g. gliclazide and prandial glucose regulators e.g. Repaglinide

A

Hypoglycaemia

Weight gain

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28
Q

What are the side effects of alpha glucosdiase inhibitors such as acarbose

A

flatulence

diarrhoea

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29
Q

What are the side effects of DPP-IV inhibitors such as sitagliptin

A

Nasopharyngitis

pancreatitis

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30
Q

What are the side effects of GLP-1 agonists such as exenatide

A

Nausea
diarrhoea
pancreatitis and pancreatic cancer (evidence is minimal)

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31
Q

What is the blood pressure control in management in diabetes

A
  • 140/80 or 130/80 in CVD or renal disease
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32
Q

How should cholesterol be compared

A
  • diabetic >40 years or Diabetic <40 years + 1 risk factor = statin
  • aim: total cholesterol <4mmol/L, LDL <2mmol/L
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33
Q

When should you stop giving biguanides (metformin)

A
  • Tissue hypoxia e.g. sepsis or MI
  • general anaesthesia (GA)
  • Before contrast medium containing iodine - risk of renal failure and subsequent lactic acidosis - restart no earlier than 48 hours after test of renal function which shows no deterioration
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34
Q

What are the sick day rules of insulin

A
  • drink lots of fluid (3L)
  • If unable to eat - sugary fluids
  • monitor glucose regularly >4 times/day
  • never stop tablets or insulin (may increase insulin)
  • oral agent users may require insulin during course of illness
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35
Q

What is non proliferative retinopathy differentiated into

A
  • Mild
  • Moderate
  • Severe - where there may also be cotton wool spots (called soft exudates)
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36
Q

What are cotton wool spots (soft exudates)

A

areas of retinal ischaemia

- also called soft exudates

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37
Q

what are hard excudates made out of

A

lipid deposits

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38
Q

What is proliferative retinopathy

A

Ischaemic retina leads to production of growth factors (such as VEGF) and to new vessel formation (neovascularisation)
- caused by VEGF

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39
Q

what are the two difference characteristics of proliferative retinopathy

A
  • new vessels on disc (NVD)

- new vessels elsewhere (NVE)

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40
Q

What is maculopathy

A

is the presence of any retinopathy within 1 disc diameter around macula.

  • suspect if visual acuity is reduced
  • leads to oedema and significant visual loss
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41
Q

How do you treat proliferative or maculopathy diabetic retinopathy

A

Proliferative
- Laser photocoagulation

Maculopathy

  • laser photocoagulation
  • intravitreal steroids
  • anti-angiogenic agents
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42
Q

What are the symptoms of peripheral sensory neuropathy

A 
- Glove and stocking distribution 
▪ Numbness
▪ Pins and needles
▪ Burning
- sensory loss may be patchy
▪ Shooting
- median neuropathy/carpal tunnel syndrome
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43
Q

What is the clinical triad of nephropathy

A

 Hypertension

 Albuminuria (preceded by microalbuminuria)

 Declining renal function
- on renal biopsy: Kimmelstein-wilson lesion

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44
Q

what does diabetic nephropathy look like on renal biopsy

A

On renal biopsy, the pathological lesion is the “Kimmelstein-Wilson lesion”

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45
Q

What is the management for diabetic nephropathy

A

 Most important to maintain blood pressure < 130/80 mmHg

  • ACEI first line (ACEI is given even if BP normal)
  • Consider angiotensin receptor blocker if ACEI not tolerated
  • Often more than one anti-hypertensive is needed to achieve this BP

 glycemic control = (HbA1c < 53 mmol/mol)

 Stop metformin when eGFR < 30 mls/min

 Refer to specialist if eGFR below 45 mls/min and falling

 Renal replacement therapy may be needed
- e.g Peritoneal Dialysis / Haemodialysis / Transplant

  • In type 1 diabetes consider simultaneous pancreas and kidney (SPK) transplant
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46
Q

What do blood results look like for haemochromatosis

A
  • Serum iron is raised
  • serum ferritin is raised
  • TIBC is decreased
  • transferrin is decreased but transferrin saturation is increased

Transferrin saturation is the most useful marker

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47
Q

What is the definition of acute kidney injury

A

Acute kidney injury is a syndrome of decreased renal function, it is measured by serum creatine or urine output over hours-days.

  • rise in creatine of >26umol/L within 48 hours
  • rise in creatine > 1.5 x baseline within 7 days
  • urine output <0.5mL/kg/h for >6 consecutive hours
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48
Q

Define stage 1, 2 and 3 of acute kidney injury (RIFLE)

A

Stage 1
• Rise in serum creatinine of ≥ 26 μmol/L within 48 hours or
• 1.5-1.9 x increase in serum creatinine known or presumed to have occurred within in the last 7 days or
• 6 -12 hours oliguria (urine output < 0.5ml/kg/hour)

Stage 2

  • Serum creatine = 2-2.9 x baseline
  • Urine output <0.5ml/kg/hour for >12 hours

Stage 3

  • Serum creatine = >353.6umol/L or > 3 x baseline or having renal replacement therapy
  • Urine output = anuria for >12 hours
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49
Q

What is the minimum GFR rate for solute removal

A

• 6 hours oliguria (urine output < 0.5ml/kg/hour) - minimum GFR for solute removal

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50
Q

Describe the causes of an AKI

A

Pre-renal

  • infection
  • hypoperfusion due to stenosis or sepsis
  • dehydration
  • toxicity - drugs

Renal

  • Polycystic kidneys
  • infection of the kidneys
  • nephrotic syndrome
  • congenial issue

Post renal

  • obstruction - stones, carcinoma, catheter in wrong position
  • UTI
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51
Q

What should you do if the patient is hypovalaemic in fluid management of AKI

A

If hypovolaemic renal perfusion will improve with volume replacement
• give bolus fluids (250 – 500 mls) with regular review until volume replete
- give further boluses of 250-500mL crystalloid with clinical review after each
• If you have given ≥ 2 L Stop + remains hypoperfused consider further circulatory support e.g. something to increase CO such as isotonic compounds or something to cause vasoconstriction

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52
Q

once there euvolaemic and passing urine what should you do - fluid management of AKI

A

• If euvolaemic + passing urine give maintenance fluids (estimated daily output + 500 ml)

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53
Q

Which type of fluid should you give in fluid management of AKI

A
  • Isotonic crystalloid fluids - E.G. plasmalyte, Hartmann’s) - these contain potassium (5mmol/L) - if your giving a low concentration of potassium to someone who has a high concentration of potassium you reduce the plasma potassium but risk of hypokalaemia is low yet you are increasing there whole body potassium if they are not passing urine
  1. 9% saline
    - safe
    - can worsen metabolic acidosis if large volumes are infused rapidly
    - as the chloride can cause a hypercholermic acidosis

Colloids

  • high molecular weight states
  • dextran can worsen AKI
  • therefore they are not used anymore
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54
Q

Name some nephrotic drugs

A 
NSAIDs
ACE
ARB
metformin
potassium-sparing diuretics
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55
Q

Name the complications of acute kidney injury

A 
Hyperkalemia 
Pulmonary oedema 
Acidosis 
severe uraemia 
insufficient urine output
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56
Q

How do you manage hyperkalemia

A
  • If the ECG changes you should give calcium gluconate - 10mls and 10% over 10 minutes

• If K > 6.5 mmol/L or ECG changes insulin dextrose
(effective for lowering the potassium for about ≤ 4 hrs) - 10 units in 50mls of 50% dextrose
- Monitor for blood glucose for hypoglycaemia

• If bicarbonate < 22 mmol/L + not overloaded give 1.26% bicarbonate IV 500 ml 1-4 hrs (N.B. hypocalcaemia)

  • this will rise the pH and lower the level of potassium
  • calcium binds to albumin when pH goes up so can lead to hypocalcamia
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57
Q

What is the pathology of pre renal acute kidney injury

A
  • decrease in vascular volume = due to haemorrhage, burns, pancreatitis
  • decrease cardiac output = Cardiogenic shock and MI
  • systemic vasodilation = sepsis and drugs
  • Renal Vasoconstriction = NSAIDs, ACE-i, ARB, hepatorenal syndrome
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58
Q

What is the pathology of renal acute kidney injury

A
  • Glomerular damage = glomerulonephritis, ATN
  • Interstitial damage = drug reaction, infection, infiltration
  • Vessels damage = vasculitis, HUS, TTP, DIC
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59
Q

What is the pathology of post-renal acute kidney injury

A
  • Within renal tract = stone, renal tract malignancy, stricture, clot
  • Extrinsic compression = pelvic malignancy, prostatic hypertrophy, retro-peritoneal fibrosis
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60
Q

In what situations are colloids given for acute kidney injury

A
  • hepatorenal syndrome
  • septic shock
    Under specialist advice
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61
Q

What is CKD

A
  • abnormal kidney structure or function present for greater than 3 months with implications for health
  • A GFR less than 60 for more than three months
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62
Q

What are the causes of CKD

A
  • Diabetes
  • Glomerulonephritis
  • Hypertension
  • Renovascular disease
  • Polycystic kidney disease
  • Pyelonephritis
  • urinary tract obstruction
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63
Q

Whey should you offer ACE or ARB treatment in chronic kidney disease

A
  • DM and A:CR >3mg/mmol
  • hypertension and A:CR >3mg/mmol
  • any CKD with A:CR >70 mg/mmol
  • check potassium and renal function prior to and 1-2 weeks after starting treatment
  • stop if potassium is >6mmol/L, eGFR is decreased by >25%, or creatine decreased by >30%
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64
Q

Describe the classification of CKD by albuminuria

A

A1

  • Albumin excretion (mg/24hr) = <30
  • Albumin creatine ratio (mg/mmol) = <3

A2

  • Albumin excretion (mg/24hr) = 30-300
  • Albumin creatine ratio (mg/mmol) = 3-30

A3

  • Albumin excretion (mg/24hr) = >300
  • Albumin creatine ratio (mg/mmol) = >30
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65
Q

What should the target blood pressure be for someone with CKD

A

Target blood pressure is 140/90

- if they have an ACR of 70mg/mmol or more or diabetes keep below 130/80

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66
Q

How do you control restless legs/cramps in CKD

A
  • check ferritin (low levels may worsen symptoms)
  • Clonazepam 0.5-2mg/daily or gabapentin
  • Quinine sulphate 300mg note can help with cramps
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67
Q

what affects GFR

A
  • serum creatinine
  • age
  • sex
  • race
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68
Q

What is the diagnosis for nephrotic syndrome

A
  • Proteinuria > 3g/24hr
  • Hypoalbuminaemia <30g/dL
  • Oedema
  • Raised cholesterol
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69
Q

How do you assess proteinuria

A

Urine dipstick

24 hour urine collection - gold standard

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70
Q

Describe underfill hypothesis (oedema development in nephrotic syndrome)

A
  • Decrease in intravascular colloid osmotic pressure due to low serum albumin - Intravascular volume depletion
  • Activation of the renin angiotensin system and retention of salt and water
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71
Q

Describe overfill hypothesis (oedema development in nephrotic syndrome)

A

Primary sodium retention

  • due to the predominant mechanism of oedema in nephrotic syndrome, heart failure and liver failure
  • as you retain sodium in the kidneys you thus retain water
  • this means that water follows sodium into the intravascular compartment and this then moves into the extravascular compartment
  • when the extravascular compartment expands, ANP is released to excrete water but ANP resistance develops
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72
Q

What are the three most commonest nephrotic syndromes

A
  • Minimal change disease
  • focal segmental glumerulosclerosis
  • Membranous nephropathy
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73
Q

Name the primary and secondary causes of nephrotic syndrome

A

Primary

  • Minimal change disease
  • focal segmental glumerulosclerosis
  • Membranous nephropathy

Secondary

  • Diabetic nephropathy
  • lupus nephritis
  • pre-eclampsia
  • amyloid
  • congential nephropathy
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74
Q

How do you diagnose membranous nephropathy

A
  • Anti-phopsholipase A2 receptor antibody in 70-80% of idiopathic disease
  • diffusely thickened GBM due to sub epithelial depostis
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75
Q

What are the complications of nephrotic syndrome

A
  • Infection (in children)
  • Thromboembolism
  • Renal Impairment
  • Dyslipidaemia
76
Q

What is the treatment for minimal change disease

A
  • prednisolone 1mg/kg for 4-16 weeks

- can relapse

77
Q

How do you treat focal segmental glomerulosclerosis

A
  • ACE/ARB and blood pressure control
  • corticosteroids only in primary idiopathic disease - remission in 25%, partial remission in up to 50%
  • Calcineurin inhibitors considered 2nd line
78
Q

How do you treat membranous nephropathy

A
  • ACE/ARB and blood pressure control

- immunosuppression only in those at high risk of progression

79
Q

What is the clinical presentation of nephritic syndrome

A
  • High blood pressure
  • mild oedema
  • urine dip - blood/protein
80
Q

In glomerulonephritis what is the difference between early and late stages of the disease

A

Early

  • red cell class
  • proteinuria
  • haematuria

Late

  • hypertension
  • oedema
  • acute renal impairment
81
Q

What are the 3 common forms of glomerulenephritis

A
  • Autoimmune
  • Infections
  • malignancies
82
Q

Name the forms of glomerulonephritis

  • autoimmune
  • infections
  • malignancies
A

Autoimmune

  • Small vessel vasculitis e.g ANCA associated vasculitis
  • SLE
  • Anti-GBM disease[Goodpastures]
  • IgA nephropathy
  • Cryoglobulinaemia

Infections

  • Viral- Hepatitis C, Hepatitis B, HIV
  • Post-streptococcal
  • Subacute bacterial endocarditis

Malignancies

  • Lymphoma
  • Multiple myeloma
83
Q

Name the common types of glomerulonephritis

A
  • IgA nephropathy
  • SLE
  • Anti-glomerular basement membrane disease (good pasture’s)
  • post-streptococcal diffuse proliferative GN
  • rapidly progressive GN (RPGN)
84
Q

What Is the management of glomerulonephritis

A

Control BP
- <130/80
- <125/75 if proteinuria is >1g/day
Include an ACEI or ARB as these reduce proteinuria and are renoprotective

Immunosuppression
- High dose IV steroids

Cytotoxic Agents

  • 1st line – cyclophosphamide
  • 2nd line – rituximab

ANCA Removal
- Possible plasma exchange

85
Q

Name some lower urinary tract symptoms

A

Storage symptoms

  • polyuria
  • nocturne
  • urgency
  • incontinence

Voiding symptoms

  • hesitancy
  • intermittency
  • involuntary interruption of voiding
  • weak urinary stream
  • straining to void
  • dysuria
  • sensation of incomplete emptying

Post-micturition symptoms
- post micturition dribbling

86
Q

What drug do you give if you have

  • Moderate to severe LUTs
  • LUTS and a prostate estimated to be larger than 30g or PSA greater than 1.4 ng/ml, and high risk of progression
  • Bothersome moderate to severe LUTS, and a prostate estimated to be larger than 30g or PSA greater than 1.4 ng/ml
A
  • Moderate to severe LUTs = offer an Alpha blocker
  • LUTS and a prostate estimated to be larger than 30g or PSA greater than 1.4 ng/ml, and high risk of progression = offer a 5-alpha reductase inhibitor (5ARI)
  • Bothersome moderate to severe LUTS, and a prostate estimated to be larger than 30g or PSA greater than 1.4 ng/ml = consider a combination treatment with an alpha blocker and a 5 alpha reductase inhibitor
87
Q

What are the risk factors of progressive disease

A
  • Age over 70 and LUTS
    • Moderate to severe symptoms i.e.IPSS>7
    • PSA>1.4ng/ml
    • Prostate volume over 30ccs (i.e. feels enlarged on DRE)
    • Flow rate < 12ml/sec
88
Q

What are the investigations of urinary tract infections

A

 Urine dipstick – leucocytes, nitrites, protein. May be false positive in elderly o Nitrite in urine – 90% sensitive, but 35-85% specific for UTI

 Mid stream urine (MSU) for MC&S – common bacteria are gram –ve such as E.Coli, Pseudomonas, Klebsiella, Proteus. Gram +ve such as strep faecalis or staph aureus are less common

 Recurrent UTI – USS renal tract or CT KUB (kidney, ureter, bladder)

89
Q

What is the presentation of pyelonephritis

A
  • flank/loin pain
  • nausea and vomiting
  • fever and rigors
  • LUTs
90
Q

Define hyperprolactinaemia

A

> 390mU/L

91
Q

what are the symptoms of hypopituitarism

A
  1. GH – central obesity, atherosclerosis, dry wrinkly skin, ↓strength, ↓balance, ↓well-being, ↓exercise ability, ↓CO, osteoporosis, ↓glucose
  2. FSH&LH
    - Women: oligomenorrhoea or amenorrhoea, ↓fertility, loss of libido, osteoporosis, breast atrophy, dyspareunia
    - Men: ED, loss of libido, ↓muscle bulk, hypogonadism (↓body hair, small testes, ↓ejaculate volume, ↓spermatogenesis)
  3. TSH – as for hypothyroidism
  4. ACTH – as for adrenal insufficiency (note no skin pigmentation as ↓ACTH
  5. PRL – rare; absent lactation
92
Q

What do blood tests show in hypopituitarism

A
  • LH and FSH ↓ or ↔
  • Testosterone or oestradiol ↓
  • TSH (↓ or ↔) and T4 ↓
  • PRL ↑
  • IGF-1 ↓
  • Cortisol ↓
  • U&Es – ↓Na+ from dilution
  • FBC – ↓Hb (normochromic, normocytic)
93
Q

what do dynamic tests show in hypopituitarism

A
  1. Short Synacthen test – to assess adrenal axis
  2. Insulin tolerance test (ITT) – to assess adrenal and GH axes
    - CI: epilepsy, heart disease, adrenal failure 🡪 glucagon stimulation test
    - Induces hypoglycaemia, causing stress to ↑cortisol and GH
  3. Arginine + GHRH test
94
Q

What is the management of hypopituitarism

A

Hormone replacement therapy and treatment of underlying cause

  • hydrocortisone - fro secondary adrenal failure before any other hormones are given
  • Thyroxine - if hypothyroid

Hypogonadism

  • men - testosterone enanthate 250mg IM every 3 weeks, daily topical gels, buccal mucoadhesive tablets or patches
  • Women - oestrogen: transdermal estradiol patches or COCP, +/- testosterone or dehydroepiandrosterone
  • gonadotrophin therapy to induce fertility
  • GH - somatotrophin mimics human GH, addresses problems of increased fat mass, decreased bone mass, decreased muscle bulk, decreased exercise capacity and problems with heat intolerance
95
Q

what is the Rotterdam criteria for PCOS

A

 i)Clinical hyperandrogenaemia
 ii) oligomenorrhoea (less than 6-9 menses per year)
 Iii) 12 or more polycystic ovaries on ultrasound. Or ovaries greater than 10ml

96
Q

What conditions is PCOS associated with

A
  • Hyperinsulinaemia and insulin resistance - prevalence of T2DM is 10 times higher than in normal women
  • hypertension, hyperlipidaemia and increased cardiovascular risk - metabolic syndrome is 2-3 times higher in PCOS
97
Q

What are the clinical features of PCOS

A
  • Hirsutism
  • Age and speed of onset – usually begins around time of menarche and increases slowly and steadily in teens and twenties
  • Menstruation – most people will have some disturbance, typically oligo-/amenorrhoea
  • Weight – many people are overweight or obese; this worsens the underlying androgen excess and insulin resistance, and inhibits the response to treatment
98
Q

describe the hormones of PCOS

A
  • Raised LH with normal FSH, Raised Testosterone (with or without reduced SHBG)
99
Q

How do you manage hirsutism as a symptom of PCOS

A

local - hair removal, eflornithiine cream

Systemic

  • Oestrogens (COCP) – should be used first unless CI
  • Cyproterone lactate 50-100mg daily – produces amenorrhoea so only given for days 1-14 of each cycle
  • Spironolactone 200mg daily – antiandrogen activity
  • Finasteride 5mg daily - 5α-reductase inhibitor; prevents formation of DHEA in the skin
  • Flutamide – less commonly used due to hepatic SEs
100
Q

How do you manage sub fertility in PCOS

A
  • Clomifene 50-100mg daily – given daily on days 2-6; effective in 75% in achieving ovulation; not used for longer than 6 cycles due to increased risk of ovarian cancer
  • Low-dose FSH – used for non-responders to clomifene
  • Metformin – on its own may improve ovulation and achieve conception
101
Q

Name the 4 stages of breast cancer

A

Stage 1
- confined to the breast, mobile

Stage 2

  • growth confined to the breast, mobile
  • lymph nodes in ipsilateral axilla

Stage 3

  • tumour fixed to muscle but not chest wall
  • lymph nodes in ipsilateral axilla and fixation
  • Skin involvement larger than tumour

Stage 4
- complete fixation to chest wall and distant metastasis

102
Q

Describe the T part of the TNM staging in breast cancer

A
  • TX - primary tumour cannot be assessed
  • TO - no evidence of primary tumour
  • Tis - carcinoma in situ
  • T1 - tumour 2cm or less in greatest dimension - A = 0.1-0.5cm, B = 0.5-1cm, C - 1-2cm
  • T2 - tumour 2-5cm in greatest dimension
  • T3 - tumour >5cm in greatest dimension
    T4 - a) Fixation to chest wall; b) Oedema (peau d’orange) or skin ulceration; c) Both fixation to chest wall and oedema/peau d’orange; d) Inflammatory carcinoma
103
Q

What mode is chemotherapy used in early breast cancer (stage1-2)

A
  • adjuvant
  • consider in all but excellent prognosis patients
  • neoadjuvant chemotherapy has NO SURVIVAL BENEFITs
  • Doxorubicin/epirubicin + CMF ( Cyclophosphamide + methotrexate + 5-FU)
104
Q

What endocrine treatment is used in pre-menopausal women in early breast cancer (stage1-2)

A
  • Anti-oestrogen’s (ER antagonists) such as tamoxifen 20mg/d for 5 years post-op

May also benefit from

  • ovarian ablation (oophorectomy)
  • GnRH analogues - such as goserelin
105
Q

What endocrine treatment is given to post menopausal women in early breast cancer (stage1-2)

A
  • Aromatase inhibitors (target peripheral oestrogen synthesis) such as anastrozole, letrozole and exemestane
106
Q

what treatment is used in metastatic breast cancer

A
  • Tamoxifen (ER antagonist)
  • Chemotherapy if relapse after success of tamoxifen
  • Chemotherapy + biologicals, eg trastuzumab
  • Radiotherapy for painful bony mets and bisphosphonates (supportive)
  • Chest surgery to help wall
  • Psychological care
107
Q

What can be the case of breast pain

A
  • True or referred
  • Relationship with menstruation
  • Associated swelling/nodularity
  • Perimenopausal
  • Exogenous hormone intake SE
  • Unknown cause – most common
108
Q

What is the triple assessment (investigation)

A
  1. Clinical assessment – Hx and Ex
  2. Radiology
    <35yrs USS
    >35yrs Mammography + USS
  3. Cytology & Histology – Fine Needle Aspirate (FNA) or Core Biopsy (CB)
109
Q

What are the two views in mammography

A

Two views: cranio-caudal (CC) & medial-lateral-oblique (MLO) – allowing for discrimination of abnormality position

110
Q

What are the non ANDI causes of breast lumps

A
  • breast infection
  • lipomas
  • fat necrosis
  • Montgomery’s gland
  • Mondor’s disease
  • gynaecomastia
  • intraductal papilloma
  • periductal mastitis
  • tuberculosis
111
Q

Name the ANDI (abberations of normal breast development and involution) causes of breast lumps

A
  • fibroadenomas
  • Cysts
  • sclerotic/fibrotic lesions
  • duct ectasia
112
Q

What is the commonest FUNCTIONING type of pituitary tumour

A

 Prolactinoma - amenorrhoea / galactorrhoea

113
Q

What are the signs of acromegaly

A
  • Prognathism
  • Spade hands
  • prominent supraorb ridge
  • bi-temporal hemianopia
  • hypertension
114
Q

What investigations should you carry out to test for acromegaly

A

OGTT (oral glucose tolerance test)-

  • make them fast
  • check glucose and GH
  • give 75g of glucose
  • if you dont have growth hormone excess then GH goes to 0
  • if you do than growth hormone doesnt decrease and fails to suppress = acromegaly
  • IGF-1 - not a diagnostic test
  • MRI pituitary
115
Q

What is the difference between the different hyperparathyroidism

A

Primary Hyperparathyroidism

  • Raised calcium, low phosphate
  • PTH may be raised or inappropriately normal given the raised calcium

Secondary Hyperparathyroidsm

  • PTH is elevated
  • calcium low or normal
  • phosphate elevated

Tertiary hyperparathyroidism

  • calcium is normal or high
  • PTH double elevated
  • phosphate levels are decreased or normal
116
Q

What are the causes of primary hyperparathyroidism

A
  • 80% solitary adenoma
  • 15% hyperplasia
  • 4% multiple adenoma
  • 1% carcinoma
117
Q

What is the management of hyperparathyroidism

A
  • definitive management is total parathyroidectomy

Conservative management
- may be offered if the calcium level is less than 0.25 above the upper limit of normal and the patient is greater than 50 years and there is no evidence of end organ damage

118
Q

What do you find on an X ray in hyperparathyroidism

A
  • Pepperpot skull
119
Q

What are the causes of secondary hyperparathyroidism

A
  • Parathyroid gland hyperplasia occurs as a result of low calcium and almost always in a setting of chronic renal failure
120
Q

What is the cause of tertiary hyperparathyroidism

A
  • Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause
121
Q

What kind of genetics is maturity onset diabetes of the young

A
  • autosomal dominant condition

- causes the development of type 2 diabetes in patients under 25 years ol d

122
Q

What is

  • MEN type 1
  • MEN type IIa
  • MEN type IIb
A

MEN type 1

  • Primary hyperparathyroid
  • pituitary tumours
  • pancreas tumours

MEN type IIa

  • Medullary thyroid cancer
  • Primary hyperparathyroid
  • pheochromocytoma

MEN type IIb

  • Medullary thyroid cancer
  • pheochromocytoma
  • marfanoid body habits
  • Neuromas
123
Q

List causes of respiratory acidosis (hypoventilation)

A
  • Opiate causing respiratory depression
    • Pulmonary disease = asthma, COPD, pneumonia
    • Reduced resp drive = sedative drugs, CNS tumour
    • Neuromuscular disease = cervical cord lesion
      Thoracic wall disease = fail chest, kyphoscoliosis, obesity, pneumothorax
124
Q

List causes of respiratory alkalosis (hyperventilation)

A
  • Anxiety attack
    • CNS causes - stroke, subarachnoid haemorrhage
    • Asthma
    • Altitude
    • Fever
    • PE
    • drugs
125
Q

List causes of metabolic acidosis

A

Normal anion gap

- Diarrhoea 
- Renal tubular acidosis 
- Drugs - acetazolamide 
- Addison's 
- Pancreatic fistulae 
- Hyperchloremic acidosis

High anion gap
- DKA
- Lactic acidosis (shock, infection, tissue ischaemia)
- Renal failure
Drugs - salicylates, biguanides, ethylene glycol, methanol

126
Q

List causes of metabolic alkalosis

A
  • Prolonged vomiting
    • Potassium depletion
    • Burns
      Ingestion of base
127
Q

How are growth hormone and glucose linked

A

glucose inhibits growth hormone

  • therefore in the OGTT when giving glucose you expect the growth hormone to be suppressed but GH is not suppressed in acromegaly
128
Q

What is the most common endogenous cause of Cushing’s

A

Most common endogenous cause of cushings is a pituitary adenoma

129
Q

what is the most common cause of cushing’s

A

Steroids - Iatrogenic

130
Q

What can prolong the life of red blood cells leading to a raised HbA1c (due to increased red blood cell lifespan)

A
  • Splenectomy
  • Vitamin B12/folic acid deficiency
  • iron deficiency anaemia
131
Q

What can result in an lower than expected level of Hb1ac ( due to reduced red blood cell lifespan)

A
  • Sickle cell disease
  • GP6D deficiency
  • hereditary spherocytosis
132
Q

What is Nelsons syndrome

A
  • disorder charactered by abnormal hormone secretion, enlargement of the pituitary gland and development of invasive growths known as adenomas
133
Q

What is the difference between subclinical hypothyroidism and hyperthyroidism

A

Subclinical hypothyroidism

  • high TSH, normal T4
  • This can also mean poor compliance with thyroxine (check to see if patient is taking levothyroxine or previously diagnosed thyroid disorder)

Subclinical hyperthyroidism
- Low TSH, normal T4

134
Q

What is sick euthyroid results in thyroid issues

A
  • low TSH

- low T4

135
Q

For thyroid nodules what is the first line investigations

A
  • Ultrasonography
136
Q

What is the difference in Kallman syndrome and Klinefelter

A 
Kallmann's syndrome 
- Low FSH/LH 
- Low testosterone 
Features 
- delayed puberty 
- hypogonadism,, cryptorchidism 
- anosmia 
- patients are normal or above average height
Klinefelter syndrome 
- High LH 
- low testosterone 
features 
- often taller than average 
- lack secondary sexual characteristics 
- small firm testes 
- gynaecomastia  
- infertile
137
Q

What is the treatment for SIADH

A

First line treatment is fluid restriction

- if sodium is less than 120 = treatment is hypertonic saline

138
Q

What do you give if sodium is less than 120

A

Hypertonic saline

139
Q

What is Trousseau’s sign (hypocalaemia)

A

carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic

  • Wrist flexion and fingers are draw together
  • seen in patients with Hypocalcaemia
140
Q

What is Chvostek’s Sign (hypocalaemia)

A
  • Tapping over parotid causes facial muscles to twitch

- seen in patients with hypocalaemia

141
Q

What vitamin deficiency can acute pancreatitis cause

A

Hypocalaemia

142
Q

How do you treat hypophophastaremia in a DKA

A

Hypophosphatemia can be caused in DKA - need to continue with insulin therapy and initiate parental phosphate replacement

143
Q

What do the following vitamin deficiencies cause

  • Vitamin A
  • Vitamin B1
  • Vitamin B3
  • Vitamin B6
  • Folic acid
  • Vitamin B12
  • Vitamin C
  • Vitamin D
  • Vitamin K
A
  • Vitamin A = Night blindness
  • Vitamin B1 (thiamine) = Beriberi, polyneuropathy, Wernicke-Korsakoff syndrome, heart failure
  • Vitamin B3 (Niacin) = Pellagra
  • Vitamin B6 (pyridoxine) = anaemia, irritability, seizures
  • Folic acid = megaloblastic anaemia, neural tube defects if deficiency in pregnancy
  • Vitamin B12 = megaloblastic anaemia, peripheral neuropathy
  • Vitamin C = scurvy (gingivitis, bleeding)
  • Vitamin D = rickets, osteomalacia
  • Vitamin K = haemorrhage disease of the new born
144
Q

What is the maximum rate potassium can be given per hour

A

10mmol

145
Q

What does aldosterone do

A
  • increases sodium reabsorption and water reabsorption
146
Q

What is conn’s syndrome

A

is primary hyperaldosteronism caused by an aldosterone-producing adenoma.

147
Q

What is the most common cause of primary hyperaldosteronism

A
  • Bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases
148
Q

What is the management of primary hyperaldosteronism

A

Management

  • Adrenal adenoma = surgery
  • Bilateral adrenocortical hyperplasia = aldosterone antagonists e.g. spironolactone
149
Q

What are the stages of hypertensive retinopathy

A

Stage 1
- Silver and copper wiring

Stage II
- arteriovenous nipping

Stage III

  • cotton wool exudates
  • flame and blot haemorrhages

Stage IV
- papilloedmea

150
Q

Uraemia can cause a….

A
  • Pericardial friction rub
151
Q

How often can adnrealine be given

A
  • can be given every 5 minutes
152
Q

What tablets can reduce the absorption of levothyroxine

A

Iron / calcium carbonate tablets can reduce the absorption of levothyroxine - should be given 4 hours apart

153
Q

if you have dysregulated coagulation in sepsis what can this mean

A

DIC
Blood picture
- decreased platelets
- decreased fibrinogen
- increase PT and APTT
- increase fibrinogen degradation products
- Schistocytes due to microangiopathic haemolytic anaemia

154
Q

What is desmopressin (DDAVP)

A
  • Used in the treatment of diabetes insipidus

- replaces ADH

155
Q

What is tranexamic acid

A

antifibrolytic by reversibly binding 4 to 5 lysine receptor sites on plasminogen which decreases the conversion of plasminogen to plasmin

156
Q

What drug is used in the management of haemorrhaging varices

A

Terlipressin

157
Q

Name some SGLT2 inhibitors

A

Canagliflozin

158
Q

Name the drug causes of raised prolactin

A

metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids

159
Q

management of myxoedema coma

A

If myxedema coma is suspected, IV corticosteroids should be given alongside IV thyroid replacement until coexisting adrenal insufficiency has been excluded

160
Q

How does labetaolol work

A

Labetalol’s dual alpha and beta adrenergic antagonism

161
Q

What is the treatment for a toxic multinoudlar goitre

A

radioactive iodine

162
Q

what test should be used to assess diabetic neuropathy

A

A 10 g monofilament should be used to assess for diabetic neuropathy in the feet

163
Q

How does the short synthetic test in Addisons work

A

In a patient with suspected Addison’s disease the definite investigation is an ACTH stimulation test (short Synacthen test). Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM.

164
Q

Thyroid cancers and there markers

- Medullary carcinoma =

A
  • Medullary carcinoma = Serum calcitonin
165
Q

Name a drug that can inhibit dopamine release

A

cabergoline - dopamine agonist

166
Q

What are the biochemical abnormalities in Congenital adrenal hyperplasia

A

Increased plasma 17-hydroxyprogesterone levels
Increased plasma 21-deoxycortisol levels
Increased urinary adrenocorticosteroid metabolites

167
Q

What blood test is important in thyroid disease

A

TSH

168
Q

DKA can cause a …

A

hypokalaemia

169
Q

describe what happens to mensuration with hypothyroidism and hyperthyroidism

A

Hyperthyroidism is associated with oligomennorhoea, or amennorhoea, whereas hypothyroidism is associated with menorrhagia

170
Q

In toxic multi nodular goitre what does nuclear scintigraphy reveal

A

In toxic multinodular goitre, nuclear scintigraphy reveals patchy uptake

171
Q

What acidosis do you get in Addisons disease

A
  • metabolic acidosis with normal anion gap
172
Q

First line treatment in thyroid storm

A

In thyroid storm with IV beta-blockers are a important first-line treatment

173
Q

If breast cancer is less than 4cm first line treatment…

A

wide excision

174
Q

What is the difference in endocrine treatment for breast cancer in peri-menopausal versus post menopausal women

A

Tamoxifen is used in ER +ve women who are pre- or perimenopausal, aromatase inhibitors are used in those who are post-menopausal

175
Q

What are the causes of focal segemetnal glomerulosclerosis

A 
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport's syndrome
sickle-cell
176
Q

How can you diffenrtiate primary and secondary hyperaldosteornism

A

Primary and secondary aldosteronism can be differentiated by looking at the renin levels. If renin is high then a secondary cause is more likely, i.e renal artery stenosis.

177
Q

How does acute interstitial nephritis present

A

Acute interstitial nephritis causes an ‘allergic’ type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function

178
Q

When can you remove a fibroadenoma

A

Breast fibroadenoma: surgical excision is usual if >3cm

179
Q

What is the most common cause of peritonitis secondary to peritoneal dialysis

A

Coagulase-negative Staphylococcus is the most common cause of peritonitis secondary to peritoneal dialysis

180
Q

What does the blood marker CA15-3 measure

A

marker for breast cancer, usually secreted from the breasts and rises in breast cancer

181
Q

Serum creatinine in…

A

Serum creatinine only in AKI NOT UREA

182
Q

Hypocalcaemia is an indication that kidney disease is ….

A

Hypocalcaemia is an indication that kidney disease is chronic and not acute

183
Q

How do you test for diabetic nephropathy

A

ACR should be used to screen for diabetic kidney disease*as it has greater sensitivity than PCR for low levels of proteinuria. PCR can be used as an alternative for quantification and monitoring of high levels of proteinuria (ACR 70 mg/mmol or more)

184
Q

Define microalbuminuria

A

Microalbuminuria is the earliest, clinically detectable manifestation of classic diabetic kidney disease. It is defined by a rise in urinary albumin loss to between 30 and 300 mg a day. Timed urine collections may be inaccurate and therefore a urinary albumin/creatinine ratio (ACR)>2.5 mg/mmol in men and >3.5 mg/mmol in women is often used to define microalbuminuria.

185
Q

What is the first line management of mastitis

A

First-line management of mastitis is to continue breastfeeding

Year 3 - Met3b (26 decks)

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