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Phase 3b > General medicine > Flashcards

General medicine Flashcards

1
Q

Where is ALP found in high concentrations?

A

Liver, bone, kidney, intestines, placenta
Circulating ALP usually from bone/liver (can be distinguished by isomers)

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2
Q

Name 3 causes of raised ALP

A

Hepatobiliary disease
Bone disease
Pregnancy
Vitamin D deficiency
Drugs

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3
Q

How might polymyalgia rheumatica present?

A

Bilateral shoulder and/or pelvic girdle aching
Morning stiffness lasting > 45 mins
Abrupt onset
Age > 50
Assessment of response to 15mg prednisolone

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4
Q

What is stage 1 AKI?

A

Creatinine 1.5x baseline
Urine output < 0.5ml/kg/hr over >6 hours (can just be in bladder as long as not in kidney)

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5
Q

What is stage 2 AKI?

A

Creatinine 2x baseline
Urine output < 0.5ml/kg/hr over > 12 hours

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6
Q

What is stage 3 AKI?

A

Creatinine 3x baseline
Urine output < 0.4ml/kg/hr > 24 hours
Anuria > 12 hours

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7
Q

What is renal replacement therapy?

A

Anything trying to replace function of the kidney eg dialysis

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8
Q

What are the 3 types of AKI?

A

Pre-renal
Renal
Post-renal

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9
Q

What can cause a pre-renal AKI?

A

Sepsis/shock
- Hypovolaemic shock (less fluid circulating)
- Septic shock (leaky capillaries due to inflammation so intravascularly depleted
- Cardiogenic shock (blood vessels constrict so normal BP but reduced SV from heart)
Pressure optimisation (low BP)

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10
Q

What can sepsis cause to the kidneys?

A

Acute tubular necrosis

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11
Q

How is sepsis/shock generally treated in terms of AKI?

A

Fluids

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12
Q

What does a low BP mean in terms of the kidney?

A

Hypoperfusion of the kidney

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13
Q

What can cause a renal AKI?

A

Toxins

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14
Q

Name some toxins that can cause an AKI

A

NSAIDs - acute interstitial nephritis
Contrast - tubular toxicity
Gentamicin - tubular toxicity

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15
Q

How is a renal AKI often treated?

A

Stop the medication

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16
Q

What can cause a post-renal AKI?

A

Obstruction
- Stones (acute)
- Cancer (chronic)

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17
Q

How is a post-renal AKI often treated?

A

Nephrostomy

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18
Q

What does STOP stand for in terms of AKI?

A

Sepsis/shock
Toxins
Obstruction
Pressure optimisation

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19
Q

What happens during hypoperfusion of the kidney?

A

Less K+ and H+ removed from blood so hyperkalaemia and acidaemia

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20
Q

What happens during tubular damage?

A

Na stays in urine and K+ and H+ stay in blood
Hyperkalaemia and acidaemia

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21
Q

What is continuous venvenous haemofiltration?

A

Variation of dialysis

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22
Q

What are the 5Rs of fluids?

A

Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment

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23
Q

How can you work out ideal weight? Why is this important for fluids?

A

Men 0.9xH - 88
Women 0.9xH - 92
If over this, difference will almost entirely be lipid

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24
Q

What is osmolality?

A

Osmoles per kg of solvent (usually water)

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25
Q

What is osmolarity?

A

Osmoles per L of solvent (usually water)

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26
Q

What is tonicity?

A

The ability of a solution to cause water movement

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27
Q

What happens during rhabdomyolysis/other types of mass cell death?

A

K+ leaves cells as cells break down
Hyperkalaemia
Sudden cardiac death if not treated

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28
Q

What are the two types of crystalloids?

A

Salty water
- 0.9% saline
- Hartmann’s = balanced salt solution, ions more closely resemble blood plasma, K+
Not salty
- 5% dextrose
- 10% dextrose

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29
Q

What are colloids?

A

Large molecules suspended in a liquid medium

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30
Q

What are the two types of colloids?

A

Artificial
- Gelofusine
- Hetastarch
Organic
- Blood
- Albumin solutions
- Milk

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31
Q

What does saline have in terms of electrolytes compared to humans?

A

More Na
No K+
More Cl
No Ca/glucose
Lower pH
Higher osmolarity

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32
Q

What fluid should you use for resuscitation?

A

Hartmaans

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33
Q

What should you not in terms of the kidney when prescribing fluids?

A

Trust the kidney
As long as kidney functioning well just need to give them enough fluid for them to work with
They will balance electrolytes for you

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34
Q

What are the two types of fluid loss?

A

Sensible
Insensible

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35
Q

What is sensible fluid loss?

A

Losses that are easily visible/can be measured
Eg most bleeds, vomiting, urine

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36
Q

What happens to electrolytes in vomiting?

A

Loss of H+ and Cl- along with fluid
Hypochloraemia alkalosis

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37
Q

What fluid should you give in vomiting?

A

Saline with added K+

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38
Q

What are insensible losses?

A

Fluid loss that cannot be measured
Sweating, into gut, retroperitoneal loss due to pancreatitis

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39
Q

What blood test is important to do if a patient is on IV fluids?

A

Daily U&Es

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40
Q

What is the classification of some dehydration?

A

2 or more of the following signs
- Restlessness, irritability
- Sunken eyes
- Drinks eagerly, thirsty
- Skin pinch goes back slowly

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41
Q

What is the classification of severe dehydration?

A

2 or more of the following signs
- Lethargy/unconsciousness
- Sunken eyes
- Unable to drink/drinks poorly
- Skin pinch goes back very slowly > 2 seconds

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42
Q

How do you assess dehydration status?

A

Systolic BP
HR > 90
CRT > 2 or peripheries cold to touch
RR > 20
NEWS > 5 or more

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43
Q

How do you prescribe fluids?

A

Calculate deficit
Ongoing requirements - monitor input and output
Monitor results of therapy

44
Q

What is the function of the liver?

A

Synthesis - protein, clotting factors, bile, glucagon
Detoxification - alcohol, drugs, ammonia, bilirubin
Storage - energy, vitamins, minerals
Part of immune system
+ many more

45
Q

What is acute liver failure?

A

Complex multisystemic illness that occurs after an insult to the liver

46
Q

What are the S&S of acute liver failure?

A

Jaundice
Coagulopathy INR > 1.5
Hepatic encephalopathy
Absence of chronic liver

47
Q

What are the S&S of hepatic encephalopathy?

A

Confusion
Change in personality
Slowing of cognition
Reversal of sleep-wake cycle

48
Q

How common is acute liver failure?

A

Rare
< 10 per million per year
Mortality without transplantation 10-90%

49
Q

How is acute liver failure classified?

A

Jaundice to encephalopathy time
- Hyperacute: within 7 days (best prognosis)
- Acute: 8-28 days
- Sub-acute: 29 days - 12 weeks (worst prognosis)

50
Q

What is the most common cause of acute liver failure in the UK?

A

Paracetamol

51
Q

What is the most common cause of acute liver failure in developing countries?

A

Viral hepatitis

52
Q

Name 3 other causes of acute liver failure

A

Ischaemic hepatitis
Autoimmune hepatitis
Acute fatty liver of pregnancy
Wilson’s disease
Budd Chairi syndrome
Mushrooms
Post hepatectomy

53
Q

What other drugs can cause liver damage?

A

Paracetamol, isoniazid/rifampicin, NSAIDs, ecstasy
Rarer - phenytoin, tetracycline, allopurinol, MAOIs, legal highs, anabolic steroids, chinese and herbal medicines

54
Q

What are the 2 different mechanisms of liver damage via drugs?

A

Dose dependent predictable
Idiosyncratic unpredictable

55
Q

What viruses can cause acute liver failure?

A

Hepatitis A, E, B
Rarely -> HSV, CMV, EBV, parvovirus

56
Q

What is the mechanism of paracetamol metabolism?

A

CYP450
N-acytl-p-benzoquinoneimine toxic metabolite
Detoxified by glutathione (from diet)
If too much paracetamol toxin builds up causing liver damage

57
Q

What factors can increase paracetamol hepatotoxicity?

A

Staggered overdose
Excessive alcohol consumption
Malnutrition, HIV, cancer
Chronic liver disease
Liver enzyme inducer drugs (anti-epileptics, rifampicin, spironolactone)

58
Q

What is the management of a paracetamol overdose?

A

IV N-acetylcysteine
IV crystalloids 100-250mls/hr
IV broad spectrum Abx + antifungal if encephalopathy
Call liver transplant centre

59
Q

Name 3 complications of acute liver failure

A

Encephalopathy
Cardio-respiratory - hypotension, ARDS, pneumonia
Renal failure
Sepsis
Malnutrition

59
Q

Name 3 complications of acute liver failure

A

Encephalopathy
Cardio-respiratory - hypotension, ARDS, pneumonia
Renal failure
Sepsis
Malnutrition

60
Q

What are the red flags for sepsis?

A

Altered mental state
SBP < 90
HR > 140
RR > 25
New O2 requirement
Lactate > 2
Recent chemotherapy

61
Q

What is the definition of sepsis?

A

Life threatening organ dysfunction caused by dysregulated host response to infection
Clinically characterised by change in SOFA score > 2 points

62
Q

What is septic shock?

A

Subset of sepsis in which particularly circulatory, cellular, and metabolic abnormalities are associated with greater risk of mortality than with sepsis alone
Clinically identified with vasopressor requirement to maintain MAP > 65 + serum lactate > 2 that persist despite adequate fluid resuscitation

63
Q

What can cause sepsis?

A

Bacterial endotoxins -> widespread leukocyte activation -> massive cytokine release
Cytokines -> haemodynamic collapse

64
Q

What is hypoxic respiratory failure?

A

Whole body O2 demand
- Leucocyte activation
- Increased metabolic rate
Pulmonary capillary diffusion defect (leaking) -> poor gas exchange
ARDS

65
Q

How can sepsis cause cardiomyopathy?

A

Toll-like receptors trigger TNF alpha and directly impair myocytes
Cytokines
- IL 1-beta/6/8
- Secreted by macrophages/monocytes
- Causes fever, hypotension, myocardial repression
NO from endothelium increased = vasodilatation
Oxidative stress - cellular damage from O + N free radicals, damage to DNA and mitochondrial enzymes
Arrhythmogenesis = SVT
Reduced contractility - inability to use Ca
RV dysfunction secondary to pulmonary HTN -> hypoxia = vasoconstriction in lungs = HTN

66
Q

How can sepsis cause renal failure?

A

Pre-renal and renal insults
Reduced CO = reduced renal perfusion
Cytokine induced tubular dysfunction = includes DAMPs and PAMPs

67
Q

What is sepsis induced coagulopathy?

A

Organ dysfunction + thrombocytopenia + prolonged PT or INR
Cytokines cause activation of clotting cascade
Also prevents fibrinolysis
DIC

68
Q

What are the signs of DIC?

A

INR/PT increased
D-dimer increased
Fibrinogen and platelets decreased as being used up

69
Q

How can you interpret ECGs?

A
  1. Rate
  2. Rhythm
  3. Axis deviation
  4. Bundle branch block
  5. Morphology
  6. Cardiac angle
70
Q

How can you work out rate?

A

Large squares 300/no. large squares in R-R interval
Or
Rate = R waves on strip x 6

71
Q

What should you look at in rhythm?

A
  1. Tachy/bradycardia?
  2. Regular/irregular? -> regularly irregular/irregularly irregular
  3. QRS morphology
    -> Narrow complex (< 120ms) -> sinus/atrial/junction origin
    -> Wide complex (> 120ms) -> ventricular/supraventricular with aberrant conduction
    Narrow = normal, if tachycardic -> narrow complex tachycardia
    Wide = if tachycardic -> wide complex tachycardia
  4. P waves -> absent (sinus arrest/AF), present (saw tooth = flutter)
72
Q

What should you look for in cardiac axis?

A

LAD -> I and II are Leaving each other
QRS = + in leads I and aVL, - in leads II and aVF

RAD -> I and II are Reaching for each other
QRS = + in lead II, III, and aVF, - in lead I

73
Q

What does L BBB look like?

A

WiLLiaM
W = V1
M = V6
(W might not be obvious)

74
Q

What does R BBB look like?

A

MaRRoW
M = V1
W = V2

75
Q

What should you look for in morphology?

A

P waves -> present/absent?
PR interval
ST segment
Delta wave?
Digoxin?
T wave?

76
Q

What should you look at the PR interval for?

A

Length
Normal = 120-200ms
> 200ms = 1st degree heart block
< 120ms = pre-excitation ?accessory pathway eg WPW

77
Q

What should you look for in the ST segment?

A

Inversion/elevation

78
Q

What does a delta wave look like and what does it signify?

A

Upstroke in QRS at beginning
Pre-excitation of ventricles
Often WPW

79
Q

What does digoxin toxicity look like?

A

Backwards tick at the end of QRS

80
Q

What might a T wave look like in hyperkalaemia?

A

Peaked
(Tall, tented)

81
Q

When might you see a hyperacute T wave?

A

Preceding ST elevation in STEMI
Prinzmetal angina

82
Q

When might you see an inverted T wave?

A

MI/infarction
BBB
PE
Hypertrophy

83
Q

When might you see a biphasic T wave and how does it differ in the two conditions?

A

Hypokalaemia/infarction
Hypokalaemia = down then up
Infarction = up then down

84
Q

When might you see a flattened T wave?

A

Hypokalaemia/infarction

85
Q

What is important to remember about T waves when interpreting an ECG?

A

Dynamic changes = active ischaemia
Fixed = previous ischaemia/infarction

86
Q

What areas of the heart at the chest leads showing?

A

V1 + 2 = septal
V3 + 4 = anterior
V5 + 6 = lateral

87
Q

What areas of the heart are the limb leads showing?

A

I = lateral
II, III = inferior
aVF (foot) = inferior
aVL (lateral) = lateral

88
Q

What is metabolic syndrome?

A

Cluster of risk factors that increase risk of heart attacks, stroke, and T2DM

89
Q

How can you prevent/reverse metabolic syndrome?

A

Weight loss
Better diet
Exercise

90
Q

What signs are required to be diagnosed with metabolic syndrome?

A

At lease 3/5 of….
1. Elevated waist circumference
2. Elevated triglycerides or on drug treatment for elevated triglycerides (statins)
3. Low HDL cholesterol or on drug treatment for low HDL cholesterol
4. Elevated BP or hypertensive drug treatment
5. Elevated fasting glucose or drug treatment for elevated glucose

91
Q

What is the mnemonic that can help with looking at the quality of CXR?

A

RIPE
- Rotation -> mid clavicular line to spinous processes should be the same distance on each side
- Inspiration -> 5 to 7 ribs should be visible
- Projection
- Exposure -> see vertebrae behind heart and L hemi-diaphragm

92
Q

What is the mnemonic for interpreting CXR?

A

A to E
A -> airway (trachea)
B -> breathing (lungs and spaces)
C -> circulation (heart) cardiomegaly in PA > 50%
D -> disability (#)/disability
E -> everything else

93
Q

What does it mean in there are > 7 ribs visible in a CXR and what condition might this be seen in?

A

Hyperinflation (barrel chest)
COPD

94
Q

What do metastases in the lungs look like on a CXR?

A

Cannonballs

95
Q

What does pulmonary oedema look like on a CXR?

A

Generalised haziness on CXR

96
Q

What is the treatment for pulmonary oedema?

A

O2
Furosemide

97
Q

What does surgical emphysema look like on a CXR?

A

Air spaces outside of lungs

98
Q

What is the mnemonic for interpreting MSK XRs?

A

ABCS
- Alignment and joint spaces (loss of alignment = fracture)
- Bone density (altered density = pathology eg osteomyelitis)
- Cortices (trace cortex round bone for #)
- Soft tissue ?effusion/foreign body

99
Q

How do you describe a fracture?

A
  1. Position on bone -> proximal/middle/distal, joint involvement intra/extra-articular
  2. Complete/incomplete (often more in children eg greenstick)
  3. Open/closed
  4. Displacement
100
Q

What are the different types of displacement in fractures?

A

Angulation (dorsal/posterior or volar/anterior)
Translation
Rotation
Distraction/impaction

101
Q

What does a NOF# look like clinically?

A

Shortened + externally rotated

102
Q

How can you see a NOF# on XR?

A

Trace Shenton’s line
Under trochanter to superior pubic rami

103
Q

How should you describe a NOF#?

A

Intra vs extracapsular
This changes management

104
Q

What is the difference between a colles and smiths fracture?

A

Colles -> extra-articular radial # with dorsal angulation and impaction. Fall onto outstretched hand (FOOSH) extended
Smiths -> distal radial # with volar angulation FOOSH flexed

105
Q

What is the weber classification for ankle fractures?

A

A -> below syndesmosis (stable)
B -> at level of syndesmosis (unstable)
C -> beneath syndesmosis (unstable)
Want weight bearing XR

Phase 3b (6 decks)

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