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Exam T year > Clinical > Flashcards

Clinical Flashcards

1
Q

Severity Assessment Mild to Moderate CDI

A
  • WCC < 15 x109/L

* < 5 stools of type 5 to 7 on the Bristol Stool Chart.

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2
Q

Severe CDI is associated with the following

A
  • WCC > 15 x109/L
    • An acute rising serum creatinine (i.e. >50% increase above baseline) a temperature of > 38.5°C
    • Evidence of severe colitis (abdominal or radiological signs)
    • The number of stools is a less reliable indicator of severity.
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3
Q

Life-threatening CDI includes:

A
  • hypotension,

* partial or complete ileus, toxic megacolon or CT evidence of severe disease.

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4
Q

What do you put patient on if suspected CDI (what Is SIGHT)

A

Vancomycin oral or IV if not tolerated- start empircally

Clinicians should use this mnemonic (SIGHT) when managing CDI:
S- Suspect a case may be infective when there is no other obvious cause for diarrhoea
I- Isolate the patient & consult the Infection control team while determining the cause of diarrhoea
G- Gloves and apron must be used for all contacts with the patient and their environment
H- Hand washing with soap and water should be carried out before and after each contact with patient and their environment
T- Test the stool for C. difficle toxin by sending a specimen immediately to Microbiology.

Other:
· Severity assessment
· Review the need to continue antibiotics for other indications (if any) in conjunction with medical microbiology
· Look for signs of acute abdomen, ileus or toxic megacolon and order abdominal X-ray and refer to surgeons urgently if required.
· Stop contributory agents (i.e. laxatives)
· Stop antimotility agents where possible (i.e. loperamide, opiates)
· Need for fluid resuscitation and electrolyte replacement,
· Nutritional status
· Presence of signs of increasing severity of disease - refer to ITU early as patients may deteriorate very rapidly

Once confirmed

Fidaxomicin oral
If impossible give metrondizaole IV
May do surgical colectomy

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5
Q

Vitamin D metabolism what are the 3 ways that vitamin D gets in

A

3 ways of getting in vitamin D:
1. Vitamin D is formed from7-dehydro-cholesterol –via UV light> this forms cholecalciferol (vitamin D3)
(NOTE need 20 mins of sunlight)
2. Ergocalciferol (Vitamin D2)is formed from the diet supplementation
3. Via natural sources such as fish can getcholecalciferol (vitamin D3)

  1. Within the liver- Hydroxylation on C25 occurs–>calcidiol 25-hydroxy vitamin D3
    Happens all the time viavitamin D 25 hydroxylase
  2. Within the kidney
    Hydroxylation on C1 via1a hydroxylaseoccurs–>1,25 dihydroxy vitamin D3which is active
    This is the regulatory step which is controlled via PTH and calcium- this regulates how much vitamin D we need
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6
Q

What is 1mv equal to in mm and small squares on an ECG

A

10MM WHICH IS 10 SMALL SQUARES

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7
Q

What is the speed of an ecg

A

25mm/s

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8
Q

What is a large square equal to in mm and secs

A

5mm and 0.20 sec

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9
Q

What is a small square equal to in mm and secs

A

1mm which is 0.04s

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10
Q

What is an R wave

A

R wave is defined as the first POSITIVE deflection of a QRS complex (regardless if it preceded by a downwards peak (Q) or followed by a downwards peak (S)

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11
Q

What is a Q wave

A

Q wave is defined as the negative deflection before the R wave (i.e it is the first negative deflection of a QRS complex that is not preceded by a positive deflection but is then followed by a positive deflection (i.e an R wave)

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12
Q

What is an S wave

A

It is the negative deflection after the R wave

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13
Q

How to check the rhythm on an ECG- Regular/irregular/sinus (3 conditions)

A

Can be regular or irregular
If irregular is it regularly irregular (current pattern of irregularity) or irregularly irregular (completely disorganized)
To do this look at the R-R intevals

Sinus rhythm - cardiac impulse starts in the sinus node
P wave must be +v in I, II, AVF
P wave must be -ve in AVR
QRS must be after P

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14
Q

How to count the rate on an ECG

A

If its regular: 300/big boxes between R-R or 1500/small boxes
○ If it is irregular: No of QRS complexes x6 in the rhythm strip- As a rhythm stirp is 10 seconds, therefore x6, is rate for 60 seconds

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15
Q

Draw the cardiac axis chart what is the normal adult range

A

-30 to +90 but this is different from children

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16
Q

What leads do you look at for AXIS

A

AVF and I

Look at the QRS

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17
Q

What is normal for axis

A

The QRS should be going up in both leads.- positive

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18
Q

What is right axis deviation?

A

If leads 1 and AVF are reaching towards eachother i.e down in 1 and up in AVF
suggests RVH

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19
Q

What is left axis deviation- how to test for true

A

Lead I is positive, lead AVF negative: LA DEVIATION: LEEEEEAVING EACHOTHER
If there is apparent LAD check in lead II
If lead II +ve= normal axis
If lead II-ve= true lad
Suggests LVH

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20
Q

What should you consider with P waves

A

Amplitude
- Less than 2.5mm tall (<2.5small squares) in the limb leads
- Less than 1.5mm tall (<1.5small squares) in the chest leads
• Duration
- Less than 120ms long (0.12s; <3 small squares) within any lead
Morphology
- Should be upright in leads I, II, AVF and inverted in AVR (i.e sinus)
- Should be bisphasic in V1

Abnormal P Waves:
 Peaked P waves (P pulmonale)
 Bifid P wave (P mitrale)
Absent P waves
 Flutter waves
Inverted P waves
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21
Q

What is peaked P waves- what does it suggest?

A

P waves are taller and are pointy (peaked) in appearance.
- Duration unchanged (still <120ms)

Indicates presences of right atrial enlargement/abnormality (aka P pulmonale)
Best seen in lead II
> 2.5 mm tall in lead II (or III/AVF), satisfying criteria of right atrial abnormality (RAA)
> 1.5 mm tall in V1 (or V2), satisfying criteria for right atrial abnormality (RAA)

RAE classically seen with Pulmonary Hypertension

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22
Q

What does bifid P waves suggest

A

Indicates presences of Left atrial enlargement/abnormality (aka P Mitrale)

Best seen in lead II and V1 – LAA Criteria:
Lead II: Bifid and ≥120ms (Interpeak interval of ≥0.04s)
Lead V1: -Ve deflection of P wave wide (> 0.04 s) and deep (> 1 mm),

LAE classically seen with left sided valvular disease - mitral stenosis but can be benign

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23
Q

What is the PR interval how long is it normally, when it is shortened, when it is prolonged?

A 
Normal value is 0.12-0.2 (3-5 small squares)
Can be:
Shortened <0.12 s (3 small squares)
Normal 0.12-0.2 (3-5 small squares)
Prolonged >0.2 s (5 small squares)
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24
Q

What are the 4 things to check on the QRS

A

QRS - check the width, the amplitude, pathological q waves, R wave progression

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25
Q

What should the width be on the QRS

A

Width
• Under 0.12 seconds (3 small squares)- narrow complex originates above the ventricles
○ Narrow complex is normal - usually the bundle of his purkinje fibres
• Wide is over 0.12 second (3 small squares)
○ Wide because of a slower speed of ventricular depolarisation due a problem with:
• With HIS purkinje system
• Relying on muscle- muscle spread via gap junctions which is slower
Look at the ones which are entirely positive and negative to look at the width

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26
Q

What should the amplitude be on the QRS

A

Amplitude
• Mainly used to identify LVH and RVH
• Tall
○ Left ventricular hypertrophy
Criteria: sokolow lyon: look at the S wave in V1 (largest measurement) and the R wave in V5 or V6 (whichever is larger)
If the sum= +33mm (> 7 large squares)= LVH
○ Right ventricular hypotrophy
• Right axis deviation
• Dominant R wave in V1 (>7mm tall or R/S ratio>1)
• Dominant S wave in V5 or V6 (>7mm deep or R/S <1)
• QRS duration <120ms (i.e changes are not due to RBBB)

• Shorter suggests Impedance e.g fat, fluid etc

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27
Q

What are the features of a normal Q wave on the QRS

A

Remember Q wave is the first negative deflection before the R wave:
• <2mm deep
• <1mm wide (<40ms)
• Absent in V1-V3

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28
Q

What are features of a pathological Q wave on the QRS

A 
• Features
	○ >1mm wide (>40msec)
	○ >2mm in height 
	○ >25% of the R wave amplitude 
	○ Seen in V1-V3
Usually indicate current or prior MI
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29
Q

What is the R wave progression in the QRS?

A

• As you go from V1-V6 the electrodes are progressively more left on the chest meaning they will get more in line with the major ventricular depolarisation- therefore R wave progression from negative to positive
○ If get early- suggests that it is RVH
• Transition point is between V3/V4, also normal between V2/V3

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30
Q

What is the ST segment?

A

ST Segment
Should be isoelectric in every lead
If more than 1mm elevated in limb leads (1 small square)
If more than 2mm elevated in chest leads (2 small squares)
Suggests an MI
If more than 1mm depressed= myocardial ischaemia

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31
Q

What is the QT interval?

A

QT is related to heart rate- therefore need to correcte it
As a general rule if QT is less than half of the RR interval: it is probably normal, usually works for normal heart rates (60-100)
Corrected QT interval: Bazett’s formula= QTC=QT/ square root of RR
Depends on the sex
> 440ms in men
> 460ms in women

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32
Q

What should the T wave be?

A

• The T wave is a positive deflection after each QRS complex and represents the ventricular repolarization
• Normal: Upright in all leads except AVR and V1
Check +ve in I, II, III, AVL, AVF, V2-V6
• Lots of shapes:
○ T wave inversion- ischemia
○ Peaked T waves- hyperkalaemia
○ Hyperacute T waves
○ Inverted T waves
○ Biphasic
○ Camel hump

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33
Q

Easy way to do BBB

A

Abnormally wide QRS complexes = > 0.12 s (> 3 small squares width)
- Indicates abnormality in conduction through ventricles à Slow Depolarisation through the Parts of Ventricles.
• An abnormally wide QRS without a tachycardia - Most likely a Bundle branch block (BBB)
Widened QRS without tachycardia is a BBB, Then LOOK AT V1:
• If V1 is mainly positively deflected it is a Right Bundle Branch Block
If V1 is mainly negatively deflected it is a Left Bundle Branch Block

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34
Q

More complex way to find left bundle branch block

A

Widened QRS without tachycardia is a BBB, Then LOOK AT V1- negative= left bundle branch

WiLLiaM – in LBBB there is a ‘W’ in lead V1 and an ‘M’ wave in lead V6.

• QRS Complex > 120ms
• Dominating S wave (either rS or qs) usually followed by ST elevation and prominent T Wave in V1 (/V2/V3)
• Wide Slurred R Wave in Lead I and V6
• ST-T Wave changes: T wave deflection is opposite direction to the last QRS deflection in all three of V1, V6, lead I
(LBBB usually causes LAD)
OVERALL Look at V1, V6 and Lead 1

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35
Q

More complex way to find right bundle branch block

A

Widened QRS without tachycardia is a BBB, Then LOOK AT V1- positive= right bundle branch
RBBB there is an ‘M’ wave in lead V1 and a ‘W’ wave in lead
1. QRS Complex > 120ms
2. RSR’ Wave in V1 - aka bunny ears
3. A wide/deep S-wave in V6 and/or Lead I.
4. ST-T Wave changes: T wave deflection is opposite direction to the last QRS deflection in all three of V1, V6, lead I
(RBBB does not usually cause RAD)

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36
Q

Some considerations about BBB

A

• RBBB is not always abnormal but should be flagged up, e.g. normal in athletes
• LBBB is ALWAYS abnormal. Should be investigated further.
• RBBB Severely inhibits ability to diagnose RVH
LBBB Severely inhibits ability to diagnose LVH and STEMI (As get ST elevation)

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37
Q

What is a bifascicular block?

A

RBBB with LAD= bifasicular block i.e LAFB + RBBB

RBBB with RAD= bifascicular block i.e LPFB + RBBB

Bifasicular block is conduction abnormality in the heart where two of the three main fascicles of the His/Purkinje system are blocked

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38
Q

What are the Eye’s components of GCS

A

1: does not open eye
2: opens eye in response to pain
3: opens eye in response to voice
4: opens eyes spontaneously

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39
Q

what are the verbal components of GCS?

A

1: no sounds
2: incomprehensible sounds
3: inappropriate words
4: confused, disorientated
5: orientated converses normally

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40
Q

What are the motor components of GCS?

A
  1. no movements
  2. Extension to painful stimulus (decerebrate response)- arms are like E’s (Extension)
  3. Abnormal flexion to painful stimulus (decorticate response)- arms are like C’s (towards the cord)
  4. Flexion, withdrawal to painful stimuli
  5. Localizes painful stimuli
  6. obeys commands
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41
Q

Where is Wernicke’s where is brocas?

A

Wernicke’s aphasia is due to a lesion of the superior temporal gyrus

Brocas aphasia is due to lesion in inferior temporal gyrus

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42
Q

What does UFH need to be tested with?

A

APPT

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43
Q

What does thrombin then activate

A

All odd numbers from 5 except 9 and 8 instead

44
Q

What does vit K produce

A

Protein C, S, 1972

45
Q

Where should chest drain/aspiration be?

A

Safe triangle bounded by axilla

4th ICS in mid clavicular line and base of scapula or anteriorly in the 2nd ICS

46
Q

Amber flags of sepsis

A

· Relatives or nursing concerns re mental state
· Acute deterioration in functional ability
· Trauma, surgery, procedure in last 6 weeks
· Systolic BP 91-100mmHg (or drop >40 from normal)
· HRR 111-130 or new arrhythmias
· RR 21-24 per minute or breathing hard
· Not passed urine in last 12-18hrs
Clinical signs of wound, device or skin infection

47
Q

Red flags of sepsis

A

· Responses only to voice or pain/unresponsive
· Systolic BP <90 mmHg or drop >40 normal
· HR >130
· RR>25 per minute
· Needs 02 to keep stats >92%
· Non blanching rash, mottled/ashen/cyanotic
· Not passed urine in the last 18hrs
· Urine output less than 0.5ml/kg/hr
· Lactate >2mmol/L
Recent chemotherapy in past 6 weeks

48
Q

Grey book management of sepsis red flags

A

· Sepsis 6 to be done ASAP but within 60 mins always – take blood, urine, sputum cultures if indicated
· Review by competent decision marker e.g ST3 or above IMMEDIATELY
· Telephone consultation IMMEDIATELY following initial review
· IV antibiotics reviewed within 48hrs
REFER to critical care or document why not appropriate

49
Q

Grey book management of sepsis amber red flags

A

· Sepsis 6 to be done ASAP but within 60 mins always – take blood, urine, sputum cultures if indicated
· Review by competent decision marker e.g ST3 or above IMMEDIATELY
· Telephone consultation IMMEDIATELY following initial review
· IV antibiotics reviewed within 48hrs
REFER to critical care or document why not appropriate

50
Q

Grey book management of sepsis

  1. line
  2. non severe sepsis
    3: severe/life threatening penicillin
A
  1. IV co-amoxiclav + gentamicin (if hospitalized anywhere abroad in 6 months: amikacin)
  2. Cefuroxime + gentamicin (if hospitalized anywhere abroad in 6 months: amikacin)- intrabdominal source- metronidazole
  3. Vancomycin + gentamicin i(f hospitalized anywhere abroad in 6 months: amikacin)- intrabdominal source- metronidazole
51
Q

What is the NEWS score and when it is considered?

A
  1. Pulse rate
    1. BP
    2. RR
    3. O2
    4. Temp
    5. Conscious level
      New confusion

> 5 THINK SEPSIS
• A low score (NEWS 1–4) should prompt assessment by a competent registered nurse who should decide if a change to frequency of clinical monitoring or an escalation of clinical care is required.
• A medium score (ie NEWS of 5–6 or a RED score) should prompt an urgent review by a clinician skilled with competencies in the assessment of acute illness – usually a ward-based doctor or acute team nurse, who should consider whether escalation of care to a team with critical-care skills is required (ie critical care outreach team).
• A RED score refers to an extreme variation in a single physiological parameter (i.e., a score of 3 on the NEWS chart in any one physiological parameter, colored RED to aid identification; e.g., heart rate
A high score (NEWS ≥7) should prompt emergency assessment by a clinical team/critical care outreach team with critical-care competencies and usually transfer of the patient to a higher dependency care area.

52
Q

How do you calculate the units in a drink

A

Total volume of the drink (ml) x ABV (alcohol by volume) %/ 1000

53
Q

What is dependency syndrome 5 key features - need 3 or more for at least 1 month or if less than 1 month, occurring together repeatedly within a 12 month period

A

• Syndrome of clinical features
• Enables the identification of physiological alcohol dependence- the clinical significance is potentially fatal withdrawal syndromes occur if blood levels drop too low
1. Strong desire/sense of compulsion to use alcohol
2. Impaired capacity to control alcohol use: onset/termination/levels of use/reduction of use
3. Physiological withdrawal state on reducing/ceasing use or use to relieve withdrawal symptoms
4. Tolerance
5. Preoccupation with alcohol use
6. Persistent use despite awareness of harmful effects
NEED three or more occurring together for at least 1 month or if less than 1 month, occurring together repeatedly within a 12 month period

54
Q

What are the CAGE questions?

A
  1. Have you ever felt you needed toCut down on your drinking?
  2. Have peopleAnnoyed you by criticizing your drinking?
  3. Have you ever feltGuilty about drinking?
    Have you ever felt you needed a drink first thing in the morning (Eye-opener) to steady your nerves or to get rid of a hangover
55
Q

How do you know what an alcohol use disorder is- questions how many suggest it

Mild, moderate, severe

A

• Had times when you ended up drinking more, or longer, than you intended?
• More than once wanted to cut down or stop drinking, or tried to, but couldn’t?
• Spent a lot of time drinking? Or being sick or getting over other after effects?
• Wanted a drink so badly you couldn’t think of anything else?
• Found that drinking — or being sick from drinking — often interfered with taking care of your home or family? Or caused job troubles? Or school problems?
• Continued to drink even though it was causing trouble with your family or friends?
• Given up or cut back on activities that were important or interesting to you, or gave you pleasure, in order to drink?
• More than once gotten into situations while or after drinking that increased your chances of getting hurt (such as driving, swimming, using machinery, walking in a dangerous area, or having unsafe sex)?
• Continued to drink even though it was making you feel depressed or anxious or adding to another health problem? Or after having had a memory blackout?
• Had to drink much more than you once did to get the effect you want? Or found that your usual number of drinks had much less effect than before?
• Found that when the effects of alcohol were wearing off, you had withdrawal symptoms, such as trouble sleeping, shakiness, restlessness, nausea, sweating, a racing heart, or a seizure? Or sensed things that were not there?
Note:The severity of the AUD is defined as: mild — the presence of 2 to 3 symptoms, moderate — the presence of 4 to 5 symptoms, severe — the presence of 6 or more symptoms

56
Q

What is Marchiafava–Bignami disease

A

progressive neurological disease of alcoholism, characterized by corpus callosum demyelination and necrosis and subsequent atrophy.

57
Q

What is Pellagra

A

Vitamin B3 deficiency- diarrhoea, dermatitis and dementia

58
Q

What is Boerhaave syndrome

A

Effort rupture of the esophagus, or Boerhaave syndrome, is a spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting)

59
Q

What repro symptoms does alcohol result in

A

Testicular atrophy- Low testosterone/progesterone high oestrogen
Fetal alcohol syndrome: low IQ, short palpebral fissure, absent philtrum, small eyes- problems in birth too

60
Q

When do withdrawl symptoms start and end

A

4-12hrs and subside 40-50

61
Q

What other 3 drugs may be given post dependency?

A

-Acamprosate- increases GABA, inhibits glutamate- may help with anxiety, insomnia, cravings- CI: pregnancy, severe liver disease, creatinine>120 SE: dv, high or low libido.
Disulfiram: blocks ADH- accumulation of acetyladlehyde
Naltrexone: opioid antagonist

62
Q

What is the framingham CCF diagnostic requirements?

A 
MAJOR
· Acute pulmonary oedema
· Cardiomegaly
· Hepatojugular reflex 
· Neck vein distention
· PNH
· Pulmonary rales
· S3 gallop rhythm 
· Weight loss >4.5Kg in 5 days in response to treatment 
MINOR
· Ankle oedema
· Dyspnoea on exertion
· Hepatomegaly
· Nocturnal cough
· Pleural effusion 
· Tachycardia (HR >120)

Require 2 major or 1 major 2 minor

63
Q

What is the NYHA 4 criteria of HF

A

· No limitation of physical activity
· Ordinary physical activity does NOT cause Sx

· Slight limitation of physical activity
· Normal physical activity causes Sx
· Comfortable at rest

· Marked limitation of physical activity
· Comfortable at rest
· Less than ordinary activity causes symptoms (fatigue, palpations, dyspneoa)

· Unable to perform physical activity without discomfort
· Symptoms at rest

64
Q

What are forward/backward symptoms?

A

Forward failure: reduced CO–> poor systemic perfusion –> organ dysfunction (hypotension, renal dysfunction)

Backward failure: blood congestion
• Increased LV volume and pressure- back up into the lungs- increased pulmonary capillary pressure- pulmonary edema
Reduced CO- systemic venous congestion- edema and progressive congestion of internal organs

65
Q

What level of BNP in age <50, 50-75, 75+ makes HF likely

A

> 540

> 900

> 1800

66
Q

What is levo and dextrocardia?

A

Levocardia is normal- this when the base to apex points to the LEFT
Dextrocardia- is when the base to apex points to the RIGHT- ABNORMAL

67
Q

What is dextroposition

A

When there is a shift in the heart due to extrinsic factors but the apex still points to the left
· L sided pneumothorax
· L sided diaphragmatic hernia
· R lung hypoplasia - volume loss- this is congenital
R pneumonectomy

68
Q

What is situs? What is situ solitus, invertus, totalis and ambiguus?

A

· Situs solitus= normal position
· Situs invertus= reversed
• Situs invertus totalis= means the sub diaphragmatic contents are also reversed
Situs ambiguus= it is complicated- a combination of both above

69
Q

Dextrocardia and heart failure associations

A

· Dextrocardia with situs inversus and inverted great arteries (mirror image)= most common dextrocardia in the general population- this has a low incidence of congenital heart failure (2-5%)
· Dextrocardia with situs solitus or any situ ambiguous higher incidence of congenital heart failure

70
Q

What is Kartagener’s syndrome?

A

Kartagener’s syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. ‘quiet heart sounds’, ‘small volume complexes in lateral leads’)
Autosomal recessive

Pathogenesis
• dynein arm defect results in immotile cilia- primary ciliary dyskinesia
Features
Triad of:
1. Situs inversus
2. Paranasal sinusitis
3. Bronchiectasis
Also have subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)- increased risk of ectopic pregnancy
Can get chronic ear infection, conductive hearing loss
Decreased nasal nitric oxide is used as screening test
Only 50% of those with primary ciliary dyskinesia have situs invertus

71
Q

What is the surgical seive

A 
V vascular 
I atrogenic 
T rauma 
Autoimmune 
Metabolic 
Infection 
Neoplastic
Congenital
Degenerative 
Endocrine 
Function
72
Q

What is the estimate FiO2 of room air?

A

21%

73
Q

Nasal prongs going from 1-6L/min what is the estimated Fi02?

A 
1=24%
2=28%
3=32%
4=36%
5=40%
6 max advised=44%

Preferred by patient’s but O2 delivery is imprecise and may cause nasal soreness. The flow rate is 1-4L usually and roughly defines the concentration of oxygen 24-40%. May be used to maintain SaO2 need to be run using air e.g COPD

74
Q

What does a simple face mask running at 5L/min-10L/min supply in fiO2?

A

40-60

Delivers a variable amount of O2 depending on the rate of inflow. Less precise than Venturi so do not use if hypercapnia or type II respiratory failure. Risk of CO2 accumulation (within mask and so in inspired gas) if flow rate <5L/min. Care with patients with COPD

75
Q

What FiO2 does a non rebreath face mask at 15L/min supply?

A

60-90%

have a reservoir bag and deliver high [] of oxygen (60-90%) determined by the inflow (10-15L/min and the presence of the flap valves on the side. They are used in emergencies but are imprecise and should be avoided in those required controlled o2 therapy

76
Q

What FiO2 do venturi masks provide?

A

Provides a precise % or fraction of O2 at high flow rates
Start at 24-28% in COPD. Colour of the masks
Blue= 2L/min= 24%
White=4L/min=28%, Yellow=8L/min=35%, Red=8L/min=40% Green=12-15L/min= 50-60%

77
Q

What do you do with patients who have COPD when they need oxygen?

A

start on ventir mask give most controlled give 24% blue one
Wary of COPD patient on high flow O2:
• COPD- rely on the hypoxic drive vs. normal people who rely on hypercapnic
When would repeat ABG?
30-60 min later depending on clinical picture

78
Q

When do you seek immediate senior review considering NIV or invasive in the hypercapnic Resp failure branch

A

when there is respiratory acidosis with a low PH, PCO2 is high

If they are just hypercapnic then can treat with venturi mask and aim for sats 88-92%

79
Q

What is the nose and the oropharynx/hypopharynx lined by?

A

Nose: columnar ciliated epithelium with goblet cells, submucosal seromucinous glands, BV to warm the air

Oropharynx and hypophaynx are lined by squamous which is more protective as is the true vocal cord (while the false is lined by respiratory epithelium)

80
Q

What are the parts of the respiratory system from trachea down (which parts are the conductive and which the respiratory?

A

Conduction: passage of air- cleaning and warming
Main bronchus, lobar, segment, bronchioles, terminal bronchioles,
Respiratory portion: for gas exchange
Respiratory bronchioles then alveoli

81
Q

What is the structure of the trachea and bronchus and how is this different to the bronchiole?

A

Trachea and bronchi: lined by ciliated columnar respiratory epithelium, seromucinous glands in the wall, cartilage support, dual blood supply- pulmonary and bronchial arteries. Has mucociliary escalator

Whereas the bronchiole has no glands or cartilage

82
Q

What is the structure of alveoli?

A

Thin walled sacs lined by flattened pneumocytes:
Type 1: large flattened very thin diffusion for gases
Type 2: secrete surfactant
Capillary netowkr
Elastic tissue in walls
Macrophages- remove bacteria and debris

Goblet cells become replaced by CLUB cells produce the surfactant

83
Q

What’s the deal with the anion gap when is it used?

A

There are two types of metabolic acidosis= anion gap (Na++ K+ - (CL- + HCO3-)-
This is used to help identify the cause of metabolic acidosis (not that this refers to serum anion gap but urine anion gap is also useful)
The anion gap is a derived variable used for the evaluation of metabolic acidosis to determine the presence of unmeasurable anions. To work out if the metabolic acidosis is due to increased acid production or ingestion vs. decreased acid excretion or loss of HCO3-. You can calculate it, the normal anion gap varies between 8-17mmol/L and is ascribable due to unmeasured anions

Other ‘minor’ anions (sulphate, phosphate, organic compounds) and cations (magnesium, calcium, paraproteins) can be measured and both contribute a further 6mmol/L to the equation.

→ INCREASED ANION GAP- suggests increased acid production or ingestion
	○ H+ from organic acids bind to  HCO3- to form H2CO3, reduced HCO3- either as a result of more organic acids (+ cations) accumulating or increased production
	○ Bicarbonate is consumed by the unmeasured cation(H+) (via its action as a buffer) resulting in a high anion gap
		- Lactic acidosis, ketoacidosis (DKA or alcohol), toxins (e.g aspirin overdose), renal failure, Ethylene gylcol (treat with ethanol), prophylene glycoll, methanol (treated with ethanol)-blindness via the optic nerve

→ DECREASED/NORMAL ANION GAP: decreased acid excretion or loss of HCO3- (This results in rise in CL therefore remains normal)
	○ The decrease in HCO3- is the main problem, since there is only one other major buffering anion, there is an increase in CL-
		- GI losses of HCO3- (diarrhoea, ileostomy, proximal colostomy)), renal loss of HCO3 and retaining H+(proximal tubular acidosis), renal dysfunction, renal hypo aldosterone (retaining H+) etc, drugs (acetazolamide), pancreatic failure, Addison's, ammonium chloride ingestion Regulation mechanisms:
· ECF/ICF: reduced HCO3- as mops up H+ 
· Lung assuming there is no respiratory disorder- hyperventilates allow pH to return to normal however if there is lung disease they are likely to get exahusted and develop severe acidosis quickly
· However [H+] remains renal compensation occurs by maximal reabsorption of HCO3- and increased generated HCO3- stimulates H+ secretion
· Ammonia is secreted too  Treatment of this depends on the disorder  . The therapeutic goal is to raise the arterial pH to about 7.20, a level at which arrhythmias are less likely and cardiac contractility is restored. Do not attempt to fully correct the pH as continuing hyperventilation will make the patient alkalotic and may precipitate tetany.  • Renal failure with acidosis and volume deplete give NaHCO3  • Renal failure acidosis and fluid overload: ma need renal replacement  • DKA treatment  • Lactic acidosis: establish reason e.g CVD, ischaemic bowel and treat • Normal anion gap secondary to diarrhoea or renal tubular acidosis: NaHCO3

When reducing the anion gap:
• Co existent Resp disease may lead to inappropriate severe acidaemia and attention needed to RT
Metabolic acidosis with normal anion gap- measure urine pH to help distinguish renal and non renal. Renal if PH>5.4

84
Q

What are some causes of metabolic alkolosis

A

Alkalosis is characterised by increased pH due to ECF with increased HCO3- caused by:
• Hyper aldosterone
• Excessive vomiting: loose H+ via the GI tract
• Ingest anti acids
• Hypokalaemia
• Burns
Excessive diuretics: loop interfere with reabsorption of Na+/K+/Cl- K+ losses as increase distal tubular Na+ stimulates aldosterone- this exchanges NA+ in exchange for K+ and H+- loss in urine= metabolic alkalosis, part of the loss of H+ and K+ occurs due to loss of RAAS

85
Q

What is associated with mixed resp/metabolic acidosis/alkalosis

A 
Mixed respiratory and metabolic acidosis
A mixed respiratory and metabolic acidosis would have the following characteristics on an ABG:
• ↓ pH
• ↑CO2
• ↓HCO3–
Potential causes include:
• Cardiac arrest
• Multi-organ failure

Mixed respiratory and metabolic alkalosis
A mixed respiratory and metabolic alkalosiswould have the following characteristics on an ABG:
• ↑ pH
• ↓ CO2
• ↑ HCO3–
Potential causes include:
• Liver cirrhosis with diuretic use
• Hyperemesis gravidarum
Excessive ventilation in COPD
86
Q

What is the relationship between calcium and alkolosis

A

TINGLING CAUSE: calcium is normally bound to albumin , as is H+, H+ comes off protein when it is alkalosis, releases binding sites for calcium, ionized calcium drops total calcium is the same
Tingling: is due to less ionized and more bound

87
Q

What is nephrotic syndrome

A

• High proteinuria (>3-5 gm/day; ACR>100)
• serum albumin is low (<30G/L)
• Decreases plasma osmotic pressure odema (patient complains of this)
filter failure lets protein through (triad of three symptoms!) may/may not drop GFR
Associated with hypercoagulapathy- anti thrombin III lost (may anti coagulant)
Frothy urine due to proteins
Rise in serum cholesterol []- we do not know if need to treat
Infections
Management: specific to disease, generic is control of fluid and intake of salt

Causes: minimal change disease (mainly in children), membranous nephropathy, focal segmental glomerulosclerosis - primary causes

88
Q

What is nephritic syndrome?

A

Abrupt onset of both modes of filter failure: decrease GFR (Raised creatinine, oedema, hypertension) and blood/protein in urine. Also have azotaemia, and oliguria
-Post streptococcal glomerulonephritis classic cause (10-14 days), rapidly progressive glomerulonephritis, IGA nephropathy, membranoproliferative, and alport sydnrome

89
Q

What can NSAIDS cause renally?

A

AKI
Acute allergic interstitial nephritis
Minimal change disease
And membranous nephropathy

90
Q

What is Thrombotic microangiopathy- it causes disease in the vascular compartment

A

Characterised by endothelial injury and deposition of thrombi in microcirculation including glomeruli, this damages RBC giving schistocytes and microangiopathic haemolytic anaemia
-Haemolytic uraemic syndrome
· Seen in young children and produces a triad of AKI, microangiopathic haemolytic anaemia, thrombocytopenia, classically from STEC E.coli, pneumococcal, HIV, rarer are SLE, drugs cancer, may be due to congenital
-TTP (Thrombotic thrombocytopenic purpura- blood clot within small blood vessels through the body)
· May be congenital - gives MAHA, renal failure, thrombocytopenia, CNS involvement, pyrexia
Various other microangiopathies

91
Q

What is rapidly progressive glomerulonephritis?

A

This actually nephritic syndrome (both modes of filter failure) but over weeks- month
Often due to 3 main groups:
• ANCA positive= vasculitis
• Anti glomerular BM disease (Goodpasture)
• Miscellaneous conditions-> tuft damage- fibrin in bowman’s space

Fibrin in the bowman’s space stimulates the proliferation- to get crescentic nephritis
Cannot tell the difference between anca, or anti glomerular by light but do immunofluorescence
ANCA does not see immunofluorescent but do see in anti GBM

92
Q

What is membranous nephropathy, what is it due to? What is the common appearance on immunofloruence, on silver stain? What is the most common presentation and in what population? What percentage of people get better, stay the same, get worse. What is the treatment?

A

Thickening of the glomerular basement membrane due to IGG deposition in granular pattern
Here seen thickened loops in the capillaries.
Silver stain- can see black spikes- basement membrane is growing up between the immune deposits- caused by autoantibodies. Immunofluorescence- staining for antibodies- coarse lumpy appearance

This is the most common primary glomerular cause of nephrotic syndrome in Caucasian adults
Most are idiopathic but may be malignancy, and associated with certain drugs or infections (Hep B)

1/3 get better, 1/3 stay the same, 1/3 decline- immunosuppression is specific treatment but also management of nephrotic

93
Q

What is minimal change disease? Who gets it? What is the prognosis and treatment?

A

Examination of the renal biopsy by light microscopy and immunohistochemistry is normal
The only changes: Foot processes fused- minimal change disease- light microscopy normal, no immune deposit

Common in 75% of children with nephrotic syndrome and 30% of adults
Most cases idiopathic but association with allergy, some cases with malignancy, Hodgkin’s disease and NSAIDs

Very good prognosis- manage nephrotic and steroids

94
Q

What is focal segmental glomerulonephritis? Who gets it most commonly with what presentation? What can cause it? What is the prognosis

A

Areas of sclerosis, mesangial matrix expansion, collapse of capillary loops affecting at least initially only parts (Segmental) of the glomerular.
starts in the deeper juxtaglomerular
Segmental only part of it is affected- collapse of the loops, more pink stuff, foamy macrophages- will leak more protein

Commonest cause of glomerular disease in afrocarribeans - presenting with nephrotic. Most are idiopathic but some occur in obesity, hyperfiltrations in presence of reduce nephron mass, malignancy, and number of other miscellaneous conditions. It is NOT a single entity and represents a pattern of glomerular injury produced by various insults.

This is poor prognosis- 70% will develop PKD. Management of nephrotic and also steroids and immunosuppression

95
Q

What is IGA nephropathy (Berger’s disease)? Where is it deposit? How common is it? What is the presentation typically? What is the prognosis and management?

A

Increase in mesangial matrix and cells in association with mesangial deposition of IGA
More pink stuff- can see the mesangial 6 more (matrix and cells proliferation occurs)
IGA is deposited in the mesengium- clustered in the mesenum
In the paramesengium areas

Commonest primary form of glomerulonephritis in the world up to 25% of renal biopsy. The vast majority of cases are primary, but some may occur in the setting of liver disease and spondyloarthropathies.
Presentation is usually with asymptomatic urinary abnormalities; a subset of patients have recurrent visible haematuria in association with infections (particularly respiratory infections).
E.g
• Young male, recurrent episodes of macroscopic haematuria
• typically associated with a recent respiratory tract infection

Presentations with nephritic syndrome, nephrotic syndrome or a rapidly progressive glomerulonephritis are rare. Hypertension is common.

Management is good blood pressure control with ACEi or ARB. About 20% get progressive renal impairment

96
Q

What is post infectious glomerulonephritis? What is it classically seen after? What is the pattern of injury? What is the typical presentation? What is the prognosis?

A

Classically seen in a group A streptococcal infection this pattern of glomerular injury exhibits proliferation with an increase in mesangial and endothelial cells an infiltration by PMN (polymorphonuclear cell). There are hump-shaped sub epithelial immune deposits too

Typically abrupt onset of nephritic syndrome -3 weeks after inciting infection. May also have oedema and hypertension

Supportive care. Good LT prognosis but renal impairment sene in adults

97
Q

What is mesangiocapillary glomerulonephritis (membranoproliferative). what are the two types? what is the typical presentation? What is the prognosis without treatable underlying disease?

A

Increase in mesangial matrix and cells, thickening of capillary loops due to peripheral extension of the mesangial cells and matrix with the latter causing apparent doubling contouring of the BM

There are two main types
Type I: immune complex disease,
driven by increased or abnormal immune complexes which deposit in the kidney and activate complement.
some cases due to recognized underlying condition e.g lupus, infectious endocarditis, cryoglobuinaemia with hep C, most are idiopathic

Type II: rarer due to due to a genetic or acquired defect in the alternative complement pathway, eg C3 nephritic factor. Progressive kidney dysfunction is common.

10% of nephrotic syndrome
asymptomatic urinary abnormalities and a rapidly progressive glo- merulonephritis may also be seen. Features of the underlying conditions mentioned above may be present.

Without treatable underlying disease the prognosis is poor
Most cases experiencing progressive renal impairment

98
Q

What is anti GBM disease (good pastures)? What does it look like? What is the autoantibody binding to? Who gets it and how does it present? What is the prognosis?

A

Autoantibody binds to collagen components present in the alveolar and glomerular basement membrane

Rare 1-2 per million per year, Presents with rapidly progressive glomerular nephrotoxicity- Pulmonary haemorrhage is not always seen: it is commoner in smokers, or those with some other cause of lung injury. Even when present, pulmonary haemorrhage may be largely concealed, with little overt haemoptysis

Very poor prognosis- treat with immunosuppression and plasma exchange to remove antibody. If they present on dialysis less than 10% chance of recovery of independent renal function

99
Q

What is Alport syndrome, what is is it associated with a defect in? what percentage is X linked, what is the presentation. What is the prognosis?

A

Inherited defect in type IV collage, key structural protein of ECM that supports epithelial membranes

1/500. 80-85% is X linked
Haematuria, proteinuria, progressive renal insufficiency
High tone sensorineural hearing loss
Anterior lenticonus

Average age of renal failure in men is 30-40
May develop Ab to glomerular basement membrane after transplant

100
Q

what is the 3,6,9 rule for the bowel dilation

A

small bowel: <3 cm
large bowel: <6 cm
caecum/sigmoid: <9 cm

101
Q

What is Courvoisier’s sign?

A

Courvoisier’s sign states that in a patient with a painless, enlarged gallbladder and mild jaundice the cause is unlikely to be gallstones. Furthermore, it is more likely to be a malignancy of the pancreas or biliary tree.

102
Q

What is needed to define an AKI? What are the three stages?

A

Causing a rise in serum creatinine 1.5 x baseline or a 26.4 μmol/L rise from baseline and/or a fall in urine outputof less than 0.5 mL/kg/h for more than 6 hours

3 stages:
Stage 1: Creatinine rise 1.5-2 fold from baseline or ≥26.4μmol/L and/or urine ≤0.5ml/kg/hr > 6h
Stage 2: Creatinine rise 2-3 fold from baseline (TWICE NORMAL) and/or urine ≤0.5ml/kg/hr > 12 h
Stage 3: Creatinine rise >3 fold from baseline or renal replacement therapy (THREE TIMES NORMAL) or ≥354μmol/L and/or urine ≤0.3ml/kg/hr > 24 h or anuria for >12hrs

103
Q

What is the way of classifying pre renal, renal, post renal based on Urine osmolality (mOsm/kg)

Urine Na (mEq/L)

A

Prerenal
>500 <20
Renal: <350 >40
Post renal: <350 varies

104
Q

What are the 3 reasons to start dialysis

A

 Life-threatening or intractable pulmonary oedema
 Uncontrollably rising K+
 Severe (pH < 7.2) or worsening acidosis

105
Q

How can you prevent AKI due to radiocontrast?

A

Identify high risk patients with CKD, Diabetes, Age>65, Heart failure and use
IV Fluids 0.9% saline 1ml/kg/hr, 3-12 hours before and 6-12 hours after procedure (to maintain urine output 150ml/hr) Sodium bicarbonate can also be used
Stop potential nephrotoxic agents eg NSAIDS, ACEi, ARB and Diuretics

106
Q

What are some other biochemical and clinical indicators for RRT?

A

· Life threatening or intractable pulmonary oedema
· Uncontrollably rising K+
· Severe (pH <7.2) or worsening acidoisis
Biochemical indicators:
o Refractory hyperkalaemia >6.5mmol/l
o Serum urea>30 mmol/l
o Refractory metabolic acidosis pH < 7.1
o Refractory electrolyte abnormalities
○ Hyponatraemia, hypernatremia, hypercalcaemia
o Tumour lysis syndrome via hyperuricaemia and hyperphosphatemia
o Urea cycle defects and organ acidurias resulting hyperammonaemia, and methylmalonic acidemia
Clinical indicators
o Urine output < 0.3 ml/kg for 24 h or complete anuria >12 hrs
o AKI with multiple organ failure
o Refractory volume overload
o End organ damage: pericarditis, encephalopathy, neuropathy, myopathy, uraemic bleeding
o Create intravascular space for plasma and other blood product infusions and nutrition
o Severe poisoning or drug overdose
o Sever hypothermia or hyperthermia
The indications are not clear cut, if you are sicker or older, you are more likely to need dialysis
Renal replacement therapy includes: haemodialysis, hemofiltration and renal transplants
The initiation of RRT may be deferred if the underlying clinical conditions is improving and there are early signs of renal recovery

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