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Med > Internal Medicine > Flashcards

Internal Medicine Flashcards

1
Q

What is ACS?

A

Acute Coronary Syndrome, a spectrum of clinical presentations including Stable Angina, Unstable Angina, NSTEMI, STEMI and Sudden Cardiac Death

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2
Q

What is the primary cause of ACS?

A

Atherosclerosis - most cases occur from the disruption of a previously non-severe lesion.

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3
Q

What is angina?

A

The result of myocardial ischaemia caused by an imbalance between myocardial O2 supply and demand resulting from a narrowing or spasm of the coronary arteries.

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4
Q

Describe the pathophysiology of angina.

A

Decreased blood supply –> decreased O2 –> switch from aerobic to anaerobic respiration –> ischaemia -> ATP degraded to adenosine. Adenosine diffuses to extracellular space causing arteriolar dilation and anginal pain.

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5
Q

What are the types of angina?

A

Stable angina
Prinzmetal’s Angina
Angina Decubitus
Unstable Angina

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6
Q

What are the hallmarks of stable angina?

A

It is brought on by exertion and relieved by rest.

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7
Q

What is Prinzmetal’s angina?

A

Angina symptoms commonly occurring at rest caused by vasospasm of the coronary arteries. Can be associated with ST elevation.

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8
Q

What is angina decubitus?

A

A variant of angina that occurs at night when the patient is recumbant.

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9
Q

What is Unstable angina?

A

ACS in the absence of biochemical evidence of myocardial damage. Characterised by:
- Prolonged >20 mins
- Not relieved by GTN
- Onset at rest
- Angina post recent MI

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10
Q

What are the precipitants of Angina?

A

Exercise, mental and emotional stress, sexual activity, tachycardia, increased metabolic demands (fever, thyrotoxicosis, hypoglycaemia).

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11
Q

What are some causes of angina?

A

Coronary atherosclerosis
Coronary artery spasm
Coronary syndrome X (Microvascular angina - angina in the presence of normal coronary arteries)
Systemic collagen vascular disease: Scleroderma, SLE
Inflammatory vascular diseases: Kawasaki, Polyarteritis nodosa, Takayasu arteritis

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12
Q

Describe the symptoms of Angina

A

Chest pain, discomfort, radiating to the neck, jaw, arms, back. Pain is often preceded by exertion or stress. Typically relieved by rest or GTN. May be SOB, Levine sign - Placing fist on centre of chest.

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13
Q

What are the clinical features of angina?

A

Tachycardia. ECG: may be normal, but may show ST segment depression or inverted T waves.

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14
Q

What investigations should be done for Angina?

A

ECG
Troponin, Lipids, HbA1c, Hb
Stress test, coronary angiogram

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15
Q

How to diagnose Angina?

A

Clinically, ECG and trop to rule out AMI

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16
Q

How to treat angina?

A

Risk factor modification
Statins, BP management, Antiplatelet and anticoagulation, nitrates
revascularisation.

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17
Q

Define AMI

A

Irreversible myocardial cell death secondary to prolonged ischaemia

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18
Q

In an AMI, what vessels are normally occluded?

A

LAD 40-50%, RCA 30-40%, LCx 15-20%.

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19
Q

Describe the pathophysiology of AMI and how the resulting acute heart failure, cardiogenic shock, and arrhythmias occur.

A

AMI: Disruption of cholesterol-laden plaque, exposure of pro-thrombotic substances that promote rapid platelet aggregation, thrombin generation and thrombus formation causing an interruption to blood flow. Or embolus.
HF: If significant amount of myocardium is damaged, LV pump functions is depressed: CO, SV and BP are reduced and systolic volume is increased. Results in acute HF and cardiogenic shock.
Arrhythmia: Ischaemia disrupts the normal biochemistry and depolarisation of the cell. VF and VT can occur.

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20
Q

Define NSTEMI

A

Myocardial infarction that does not show diagnostic ECG changes but does have a troponin rise

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21
Q

What can be found on ECG for NSTEMI?

A

ST depression, T wave inversion, arrhythmias and other non-diagnostic ischaemic changes.

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22
Q

What is the pathophysiology for an NSTEMI?

A

It’s a subendocardial infarct. Iner 1/3 of myocardium is permanently damaged, not transmural. The inner 1/3 is subject to higher pressure and the last part to receive perfusion, so often the first part that is damaged.

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23
Q

What are the characteristic ECG changes for a STEMI?

A

ST elevation over 1mm in chest leads, over 2 in limb leads in at least 2 contiguous leads.
Reciprocal depression
Arrhythmias

(It’s a transmural infarct)

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24
Q

What are ten risk factors for AMI?

A

HTN
DM
Dyslipidaemia
Obesity
Chronic renal insufficiency
Smoking
Male
Female post-menopause
Age
Metabolic syndrome
CAD
FHx AMI under 50
Cocaine use

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25
Q

What doest ST depression in leads V1-V4 suggest?

A

A posterior STEMI

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26
Q

When does a troponin rise, and how long does it stay up?

A

Elevated within 4-6 hours of injury, remains elevated for around 10 days.

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27
Q

What is the treatment for AMI?

A

O2 with sats under 94%
Aspirin
GTN
Analgesia: Morphine, fentanyl
Antiemetics: Ondansetron
Heparin
Clopidogrel / Ticagrelor
B-blockers decrease myocardial workload
Symptomatic management
PCI is gold standard within 90 mins. If over 120 mins, consider fibrinolysis.

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28
Q

When should a PCI be done?

A

Within 90 mins for STEMI. 12-24 hours for NSTEMI.

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29
Q

What is PCI?

A

Where catheter inserted in femoral or radial artery to assess coronary arteries. Dye is injected to visualize patency of coronary arteries and area of occlusion is visualized. The clot is removed, the area ballooned and stented.

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30
Q

What medications should be started following an MI?

A

DAPT
B blocker
ACEI
Statin
GTN
Aldosterone Antagonist (EF <40%) - do ECHO.

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31
Q

What are the complications of AMI?

A

Death
Arrhythmia
Rupture (ventricular, septal, papillary)
Tamponade
Heart failure
Valve disease
Aneurysm of ventricle
Dressler’s syndrome
Embolism
Recurrence / mitral regurgitation.

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32
Q

What is Beck’s triad of acute cardiac tamponade?

A

3 Ds: Distant heart sounds, Decreased arterial BP, Distended neck veins.

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33
Q

What is Dressler’s Syndrome?

A

Post MI syndrome. Develops 2-10 weeks after MI or heart surgery. Results in recurrent fever, chest pain, pericarditis. Possibly due to formation of autoantibodies against cardiac muscle post trauma.

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34
Q

What is cardiac failure?

A

When the heart due to an abnormality in cardiac function , fails to pump blood at a rate sufficient to meet the bodies metabolic demands or is only able to do so with an elevated diastolic filling pressure.

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35
Q

What are the types of cardiac failure?

A

Right heart failure
Left heart failure
Biventricular failure
HFpEF
HFrEF
Acute decompensated HF
Chronic compensated HF

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36
Q

How is heart failure classified?

A

Class I - No limitation of physical activity
Class II - Slight limitation of physical activity
Class III - Marked limitation of physical activity
Class IV - Sx occur at rest and discomfort with any physical activity.

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37
Q

What are the types of diuretics?

A

Thiazide diuretics, Loop diuretics, Potassium sparing diuretics

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38
Q

What are the types of anti-hypertensives?

A

ACE-I/ARB
B-blockers
a-blockers
CCBs

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39
Q

Describe the physiology of the RAAS.

A

Decreased perfusion to JGC in macular densa leads to increased renin secretion
Renin converts angiotensinogen (from the liver) to angiotensin I
Angiotensin I converted to Angiotensin II in lungs by ACE.
Angiotensin II:
- Increased aldosterone secretion from adrenal cortex: increased Na and water reabsorption and K excretion
- Increased ADH secretion from the posterior pituitary which increases H2O reabsorption in the CD
- Increased tubular reabsorption of Na, Cl, H2O and excretion of K
- Arteriolar vasoconstriction
- Increased sympatethic activity.

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40
Q

Give two examples of ACEIs and their dosages

A

Ramipril - 2.5-10mg/qd
Perindopril 5-10mg/qd

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41
Q

How do ACEIs work?

A

Reduce the synthesis of Angiotensin II by inhibiting the action of ACE. Results in: Vasodilation, decreased Na and water reabsorption, decreased Aldosterone and ADH secretion, net decrease in BP.
Constriction of efferent glomerular arteriole, decreased myocardial workload, increased renin secretion.

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42
Q

What are ACEIs indicated for?

A

HTN, HF, Renal failure, oedema.

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43
Q

What are the side effects of ACEIs?

A

Hypotension, angiotensin induced cough, angioedema (bradykinins are also dependent on ACE for their breakdown, may occur after years), hyperkalaemia (decreased aldosterone: responsible for K secretion.

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44
Q

What is the normal BUN?

A

1.5-10.7 mmol/L

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45
Q

What is BUN?

A

Blood urea nitrogen is a measure of the amount of urea in the blood. It is produced by the liver as apart of protein catabolism and primarily renally excreted. It is a marker of renal function but is affected by others.

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46
Q

What is the normal creatinine?

A

62-106 umol/L

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47
Q

What is creatinine and what is it used for?

A

It is formed by skeletal muscle and excreted in relatively constant amounts by the kidney. It is not reabsorbed by the kidney so estimates GFR. It is a good measure of renal function. Levels will become abnormal when over 50% of the nephron units have been damaged.

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48
Q

What is the normal Urea:Creatinine ratio?

A

40-100:1

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49
Q

What does a Urea:Creatinine ratio of 40-100:1 indicate?

A

Normal or post renal AKI

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50
Q

What does a urea:creatinine ratio over 100:1 indicate?

A

A pre-renal cause - urea absorption increased compared to creatinine

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51
Q

What does a urea:creatinine ratio under 40:1 indicate?

A

Intrinsic renal damage (urea unable to be absorbed, ecomes more similar to creatinine and the ratio gets closer to 1).

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52
Q

What are causes of increased U:C Ratio?

A

Drivers can use GPS
Dehydration
Corticosteroids
GI haemorrhage
Protein rich diet
Severe catabolic state

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53
Q

What are causes of decreased U:C ratio?

A

I am a Simple SR:
Severe liver dysfunction
Intrinsic renal damage
Malnutrition
Pregnancy
Low protein diet
SIADH
Rhabdomyolysis

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54
Q

What is the definition of polyuria?

A

Over 3L/day production

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55
Q

What is the definition of oliguria?

A

Less than 0.5 ml/kg/hr

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56
Q

What is the definition of anuria?

A

Less than 50ml / day

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57
Q

What is the level for microalbuminuria?

A

30-300 mg/L

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58
Q

How much protein is required for nephrotic syndrome?

A

Over 3 g per day

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59
Q

What is azotaemia?

A

Increase of BUN

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60
Q

What is uraemia?

A

Azotaemia associated with clinical signs, Sx and biochemical abnormalities

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61
Q

What is nephritic syndrome?

A

A clinical entity caused by glomerular disease with acute onset:
Haematuria with dysmorphic RBCs, renal casts
Decreased GFR
Proteinuria
HTN

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62
Q

What is nephrotic syndrome?

A

Also due to glomerular disease, characterised by marked proteinuria:
Hypoalbuminaemia
Oedema
Hyperlipidaemia
Lipiduria

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63
Q

What are the different types of UTI?

A

Lower UTI: Infection of the bladder and the lower urinary tract
Cystitis: Infection of the bladder
Pyelonephritis: Infection of the parenchyma and collecting system of the kidney.

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64
Q

What is the most common pathophysiology of UTIs?

A

Colonisation of the vagina followed by ascension into the urinary tract

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65
Q

What are the risk factors for UTIs?

A

Age (F - infants, preschool, sex, old; M- Infants and old)
Female gender (due to urethral length)
Hx of recurrent UTI
Spermicide
Pregnancy
Congenital abnormalities eg vesico-urethral reflux
Urinary tract obstruction, eg renal calculi
Residual urine in bladder eg neurogenic bladder, BPH
Instrumentation of bladder eg IDC

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66
Q

State 7 possible symptoms of a UTI

A

Dysuria
Frequency
Urgency
Difficulty urinating
Dark urine
Strong odour
haematuria
sensation of bladder fullness
suprapubic tenderness
Fever
Confusion and sepsis

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67
Q

What are 3 common organisms for UTIs?

A

E. coli
Staphylococcus saprophyticus (in YA female)
Enterobacteriacea and pseudomonas (second in hospital)

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68
Q

What are you likely to see on a UA for someone with a UTI?

A

Cloudy
Haematuria +
Leucocytes +++
Proteinuria +
Nitrites
Alkaline

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69
Q

How would you treat a UTI?

A

ABx should cover GM- (ecoli): Trimethoprim

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70
Q

What is acute pyelonephritis?

A

Infection of the renal tissue, calyces and renal pelvis.

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71
Q

What symptoms would distinguish acute pyelonephritis from UTI?

A

Flank / back pain / costovertebral angle
Fever, chills, rigors
N+V
Confusion

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72
Q

What investigations would you do for suspected acute pyelonephritis?

A

UA, Urine MCS,
Renal US
2nd line, CT (not standard)

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73
Q

How much blood needs to be present in 1 L urine for macroscopic haematuria to be visible?

A

Approx 1 mL

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74
Q

What is the diagnostic limit for microscopic haematuria?

A

over or equal to 3 RBCs/HPF.

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75
Q

State 8 causes of haematuria

A

Menstruation contamination
Trauma
Infection
Stones
Malignancy
Coagulation abnormalities
Nephrotoxic medications
Instrumentiaon
Exercise induced haematuria

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76
Q

How would you treat acute pyelonephritis?

A

Trimethoprim / augmentin
Surgical drainage
Fluids

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77
Q

What are the different types of proteinuria?

A

Isolated proteinuria
Glomerular proteinuria
Tubular proteinuria
Overflow proteinuria
Post renal proteinuria

78
Q

What is the cause of glomerular proteinuria?

A

Increased filtration of macromolecules across glomerular-capillary wall. Often due to glomerular disease - glomerulonephritis, diabetic nephropathy, hypertensive nephrosclerosis

79
Q

What is the cause of tubular proteinuria?

A

Interference with tubular reabsorption of small proteins due to tubulointerstitial disease - heavy metal intoxication, AI or allergic inflammation, medication induced.

80
Q

What is the cause of overflow proteinuria?

A

Overproduction of protiens other than albumins (immunoglobin light chains) resulting in increased excretion in the urine. Eg myeloma, haemolysis, rhadomyolysis

81
Q

What is the cause of post-renal proteinuria?

A

inflammation of the urinary tract causing increased protein excretion. Eg UTIs, nephrolithiasis, genitourinary tumour.

82
Q

What is orchitis?

A

Inflammation of the testes

83
Q

What is epididymitis?

A

Inflammation of the epididymis

84
Q

What is orcho-epididymitis?

A

Orchitis can occur as a result of epididymitis that has spread to the testes.

85
Q

What are the symptoms of orchitis?

A

Gradual onset testicular pain
Testicular swelling and inflammation
Haematospermia
Haematuria
Same side lymph node swelling

86
Q

What are the symptoms of epididymitis?

A

Gradual onset scrotal pain
swelling
one teste hanging low in scrotum
Dysuria
Urethral discharge
Fever
Sx often only in 1 teste.

87
Q

What are the causes of orchitis and epididymitis?

A

Chlamydia or gonorrhoea
Other bacterial infections
UTI - bacterial backtrack through urinary structure to reproductive.

88
Q

RFs for orchitis and epididymitis?

A

Previous episodes
Unprotected sex

89
Q

Treatment for orchitis and epididymitis?

A

ABx

90
Q

What is testicular torsion?

A

Twisting of the spermatic cord resulting in cutting off the testicular blood supply resulting in ischaemia and gangrene if not resolved.

91
Q

What are the symptoms of testicular torsion?

A

Rapid onset severe testicular pain
may radiate to groin or lower abdo
N+V
swelling, redness

92
Q

On examination, what indicated testicular torsion?

A

Swollen, tender, high riding teste
Abnormal transverse lie
Absent or decreased cremastor reflex
Prehn’s sign negative - lifting of the teste will not relieve pain
Mild pyrexia

93
Q

What is the most common cause of testicular torsion?

A

Congenital malformation of the processus vaginalis (90%).

94
Q

What is an aneurysm?

A

A dilation of a blood vessel to over 50% of its original size.

95
Q

How many layers of the blood vessel wall does an aneurysm include?

A

All three

96
Q

What is a dissecting aneurysm?

A

When blood from the vessel lumen tracts between the intima and the muscularis propria

97
Q

What is a perivascular haematoma?

A

A collection of blood external to the 3 layers of the blood vessel.

98
Q

What is a pseudoaneurysm?

A

A false aneurysm. A collection of blood between the outer layers of an artery: the muscularis propria and the adventitia.

99
Q

What is the definition of an AAA?

A

A localised enlargement of the aorta to over 3 cm. Over 5 cm is clinically significant.

100
Q

What are the risk factors for AAA?

A

Nonmodifiable:
Over 65 years
Male
CT disorders
Previous aneurysm repair or aneurysm

Comorbidities:
Peripheral atherosclerotic vascular disease
COPD, CAD, HTN
Vasculitis

101
Q

What are the three broard causese for AAA?

A

Atherosclerosis, CT disorders such as Marfan’s, and inflammation.

102
Q

How do you classify AAA?

A

By size:
Small is less than 4
Medium is 4-5.5
Large is over 5.5
Very large is greater than or equal to 6.

By origin:
Suprarenal, pararenal, juxtarenal, infrarenal

103
Q

What are the symptoms for AAA?

A

Most asymptomatic.
Can have abdominal, flank, back or groin pain.
Lower limb ischaemia

104
Q

What are the symptoms ofr a ruptured AAA?

A

Severe sudden onset epigastric or back pain
Syncope
Absent lower limb pulses, paralysis, paraesthesia
Shock
Hypotension

105
Q

What are the clinical features of a AAA?

A

Pulsatile mass over 3 cm.
Abdominal bruit.

106
Q

How to diagnose AAA?

A

Ultrasound
CT is more sensitive, and for size evaluation and assessment.

107
Q

How and when to treat AAA?

A

3-4cm - US surveillance every 1-2 years
4.5-5 cm, US surveillance every 6-12 months
Over 5.5 cm - surgical repair
EVAR - endovascular Aneurysm / aortic repair
Open repair
managment of comorbidities / risk factors: smoking, HTN

108
Q

What is the prognosis of a AAA?

A

2-5% mortality with elective repair
50% mortality if ruptured

109
Q

What is an aortic dissection?

A

Where blood tracks between the tunica intima and the media causing a separation of the layers of the aortic wall and the creation of a false lumen.

110
Q

Describe the pathophysiology of an aortic dissection.

A

A tear in the tunica intima.
High pressures in the aorta cause blood to track between the intima and the media.
This creates a false lumen and disection of the aorta.
Most classic aortic dissections begin at one of the following three anatomic locations:
Around 2.2cm above the aortic root
Distal to the left subclavian artery
The aortic arch

111
Q

What is the classification system for aortic dissection?

A

The stanford classification:
Type A: Ascending Aorta involvement: irrespective of site of tear, 70%
Type B: Nil involvement of ascending aorta 30%

112
Q

What are the risk factors for aortic dissection?

A

HTN
Dyslipidaemia
Cocaine use
Smoking
Diabetes Mellitus
CT disease
Vasculitis

113
Q

What are some causes of aortic dissection?

A

CT disorders - Marfan’s, Ehlers-Danlos
Congenital - Coarctation of the aorta
Aortic HTN
Syphilitic aortitis
Vasculitis
Deacceleration injury
Iatrogenic

114
Q

What are some symptoms of Aortic dissection?

A

Chest pain: Sudden, severe, ripping or tearing.
Back radiation - descending aorta involvement
Abdominal radiation - with abdominal aorta involvement
Neck radiation - aortic arch and expansion into great vessels
Flank pain - renal artery involvement
Myocardial ischaemia from coronary artery involvement
Scapular radiation if diaphragmatic irritation
Neurological deficits - cerebral or IC vessels
Numbness, paraesthesia or weakness in extremities
Altered mental status
Syncope
Shock
Sudden death

115
Q

What clinical findings would you expect?

A

Asymmetrical pulses: carotid, brachial, femoral.
Unequal BP over 20 mmHg
Aortic valve regurgitation: bounding pulses, widened pulse pressure, diastolic decrescendo.

116
Q

Investigations for Aortic dissection?

A

CXR - not 1st line, but will exclude other causes
ECG - exclude AMI
Renal function tests - if perfusion compromise suspected
Type and cross
CT angiogram
MRI
Transthoracic / Transoesophageal echo in ED or ICU when CT unavailable.

117
Q

What is the treatment for aortic dissection?

A

Medical: For type B unless leaking, ruptured or compromising branches. HTN management.
Surgical: Type A or complicated TYpe B. Surgical grafts, endovascular repair, 10% mortality, 10% significant complications

118
Q

What are some complications of Aortic dissection?

A

Aortic rupture
Aortic regurgitation
AMI
Cardiac tamponade
End-organ ischaemia and death

119
Q

What is the prognosis of aortic dissection?

A

Treated: 40% mortality
Untreated: 100% mortality.

120
Q

What is simple constipation?

A

It’s a symptom rather than a disease, diagnosed clinically according to the Rome III criteria

121
Q

What are the Rome III criteria for Functional constipation?

A

2 or more of the following, for the last 3 months with symptom onset at least 6 months prior to diagnosis:
Fewer than 3 bowel movements per week
Straining
Lumpy or Hard stools
Sensation of anorectal obstruction
Sensation of incomplete defecation
Manual manoeuvring required to defecate

122
Q

What symptoms can simple constipation produce?

A

Abdominal bloating, pain, pain on defecation, PR bleeding, Diarrhoea, lower back pain

123
Q

What are the causes of simple constipation?

A

Idiopatic / Functional: Decreased fibre and increased colon transport times
Dehydration
Drugs (opioids, CCBs)
Hypothyroidism or hyperparathyroidism
Diet and exercise
Motility disorders (Hirschprung, spinal disorders)
Colon cancer
Obstruction

124
Q

What investigations for suspected simple constipation?

A

Bristol Stool form
Abdominal exam
DRE exam
Abdo XR
CT
Endoscopy

125
Q

How to treat simple constipation?

A

Activity, fibre in diet, probiotics, increased water?
Bulk forming agents
Stool softeners (Docusate)
Lubricants
Prokinetics
Stimulant laxatives (Senna)
Enema
Dietary change.

126
Q

What are 4 pharmacological treatments for simple constipation?

A

Osmotic laxatives, stimulants, 5-HT4 Receptor antagonists, Methylnaltrexone

127
Q

What are some examples of osmotic laxatives and how do they work?

A

They work by increasing the water content in the stool.
Polyethylene Glycol (PEG) found in Movicol and ColonLytely (Colonosopy prep)
Magnesium Citrate - some Mg is absorbed, take care to prevent electrolyte disturbances
Sodium phosphate: Main ingredient in enemas, risk of hypocalcaemia and hypokalaemia
Non-absorbable carbohydrates: Lactulose: Drink, lowers osmotic pressure in the gut drawing water out.

128
Q

What are some examples of stimulants to treat constipation and how do they work?

A

Senna - encourages bowel motility. It’s converted to active Sennosides A and B by colonic bacteria. Often it’s combined with coloxyl - a detergent that softens stool and irritates the bowel causing stimulation.

129
Q

What is a 5-HT4 Receptor antagonist and how does it work to treat simple constipation?

A

Prucalopride. Stimulates the 5-HT4 receptor resulting in colonic movements providing force for defecation.

130
Q

Can Methylnaltrexone be used for treated simple constipation?

A

It’s for opioid induced constipation, mainly in the palliative setting. Doesn’t cross the BBB, so does not reverse pain blockage. Works fast in opioid constipation.

131
Q

What is the definition for diarrhea?

A

3 or more loose stools within 24 hours or stools that are more frequent than what is normal for the individual.

132
Q

What is the rough pathophysiology of diarrhea?

A

Decreased absorption or increased secretion of fluid and electrolytes
Increase in bowel motility
May be inflammatory or
Non inflammatory:
- Secretory: altered transport of ions across the mucosa, which results in increased secretion and decreased absorption or increased secretion of fluid and electrolytes, or increase in bowel motility
- Osmotic: Presence of unabsorbed or poorly absorbed solute in the intestinal tract that causes an increased secretion of liquids into the gut lumen.

133
Q

What are some infectious causes of diarrhea?

A

Bacteria: E coli, campylobacter, salmonella, Shigella, C. Diff
Viral: Norovirus, rotavirus, adenovirus
Parasites / protozoa: entamoeba histolitica, giardia lambia

134
Q

What are some non-infectious causes of diarrhea?

A

Medications: Antibiotics, anti-arrhythmic, anti-hypertensives, anti-inflammatories
IBD, bowel ischaemia, radiation injury

135
Q

What are some pharmacological treatments for diarrhea?

A

Mu-opioid receptor agonists: Loperamide, diphenoxylate, codeine sulphate. These decrease gut propulsive activity. With IBS there is a risk of toxic megacolon if motility is slowed.
Bulking agents: Plant fibre, guar gum, methylcellulose. Can be used to increase solidity and bulk up stools in patients with IBS or stoma.

136
Q

What is antibiotic associated diarrhea?

A

It is diarrhea that results from an imbalance in the colonic microbiota caused by antibiotic use.

137
Q

What is the pathophysiology of antibiotic associated diarrhea?

A

Microbioata alteration changes the carbohydrate metabolism with decreased absorption of fatty acids resulting in osmotic diarrhea and potential for overgrowth of Clostridium difficile.

138
Q

What is pseudomembranous colitis?

A

Inflammatory condition of the colon characterised by pseudomembrane formation, typically associated with clostridium difficile colonisation and exotoxin production post ABx usage.

139
Q

What are the symptoms of pseudomembranous colitis?

A

Diarrhea, mucus in stool, blood in stool, crampy abdominal pain, anorexia, malaise, fever.

140
Q

What investigations can be done for someone with suspected pseudomembranous colitis?

A

FBC, Electrolyte levels, stool culture, ctool cytotoxin test (immunoassay for glutamate dehydrogenase, toxins A and B), stool PCR (more sensitive but higher false positive), AXR, CT.

141
Q

How to treat pseudomembranous colitis?

A

Supportive and symptomatic.
Cessation of ABx
Specific therapy to target C Diff - Metronidazole, vancomycin
Faecal transplant

142
Q

What are the complications of pseudomembranous colitis?

A

Fulminating colitis with toxic megacolon or perforation
Dehydration, electrolyte imbalance, SIRS
Relapse

143
Q

What is sepsis?

A

Life threatening organ dysfunction due to a dysrgulated host response to infection.

144
Q

What score can be used for sepsis?

A

The qSOFA:
Hypotension under 100 mmHg
Altered mental status
Tachypnoea RR over 22

145
Q

What is septic shock?

A

Persistent hypteonsion requiring vasopressor support to maintain MAP and serum lactate levels over 2mmol/l despite adequate fluid resuscitation.

146
Q

What is SIRSS?

A

Systemic inflammatory Response Syndrome:
Any 2 of:
Temp over 38 or under 36
Hr over 90
RR greater than 20 or CO2 less than 32 mmHg
WCC over 12 000 or less than 4000 / uL or over 10% bands

All septic patients have SIRS, but not all SIRS are septic.

147
Q

What is MODS?

A

Multiple Organ dysfunction syndrome. The presence of altered end organ function in acutely ill patient

148
Q

What are the symptoms of sepsis?

A

Fever, chills, rigors
Confusion
Fatigue, malaise
Decreased urination
Local Sx of infection

149
Q

What are common causes of sepsis?

A

Bacteraemia
Pneumonia
Pancreatitis
Endocarditis
Meningitis
Bone and soft tissue infections

150
Q

What investigations would you do to work up sepsis?

A

3 sets of blood cultures
FBC, CRP
Coag studies
UEC
UA and culture
Gram stain of pus
CXR or other imagine

151
Q

How would you treat sepsis?

A

Broad spectrum Abx
Targeted Abx
Resuscitation
Haemodynamic monitoring and support
Ventilatory support
Management of cause

152
Q

What complications of sepsis can occur?

A

ARDS
DIC
AKI

153
Q

What is septicaemia?

A

Presence of bacteria within the blood

154
Q

What are the causes of septicaemia?

A

Other infection
Surgery
Foreign bodies eg catheters
IVDU
Transient bacteraemia eg brushing teeth

155
Q

What bacteria are responsible for septicaemia?

A

S Aureus
Streptococcus
Enterococcus (UTI)
E coli - most common cause of community acquired
Pseudomonas
Salmonella

156
Q

What is SLE?

A

Systemic Lupus Erythematosus - Chronic AI disease of unknown cause that can affect virtually any organ of the body.

157
Q

Who gets SLE?

A

Females in their 20s-30s.

158
Q

What is the pathophysiology of SLE?

A

Abnormality of apoptosis, results in plasma and nuclear antigens being exposed to the immune system
Dysrgeulated lymphocytes begin producing anti-nuclear antibodies targeting normal intracellular antigens
There is defective clearing of the apoptotic cell debris allowing for the persistenc eo fantigen and immune complex production
Accumulation of immune complexes results in many problems
Can be deposited in glomeruli - renal failure; the skin or in BVs.

159
Q

What are the symptoms of SLE?

A

Constitutional Sx - fever, fatigue, weight loss, lymphadenopathy
Photosensitivity - rash
Painless oral ulcers
Hair loss
Raynaud
Arthritis
Livedo Reticularis

160
Q

What are the criteria for SLE?

A

SOAP BRAIN MD
Serositis - pleurisy, pericarditis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders (anaemia, thrombocytopaenia)
Renal involvement - proteinuria
ANA
Immunologic phenomena (Other ABs)
Neurologic disorder
Malar rash - butterfly
Discoid rash - plaque

161
Q

Investigations to work up SLE?

A

FBC, ESR and CRP, ANA< DsDNA, Smith antigen, APA, Complement levels, Proteinuria, CXR

162
Q

Treatment for SLE?

A

Diet, exercise, immunisation, avoid sun
Acute flare: steroids
Maintenance: Methotrexate, hydroxychlorquine, azathioprine, cyclophosphamide, rituximab
Management of systemic features - serositis - NSAIDs…

163
Q

Describe the pathophysiology of Left HF

A

Increased sympathetic activity to maintain CO through chronotropic and inotropic effects and RASS activation. Intial compesnation by maintaining BP and perfusion but places further strain on the myocardium and increases myocardial perfusion requirements which can worsen IHD. Increased sympathomimetic activity can also preispose arrhythmias.
Myocyte hypertrophy in response to stress resulting in eccentric remodelling which further reduces diastolic filling.
RAAS leads to water and Na retention, volume overload and increased preload, further increasing myocardial energy expenditure. Spiral of worsening HF due to compensation.

164
Q

What are some causes of left HF?

A

AMI
IHD
Cardiomyopathy
Valvular disease - AR, MR
HTN
Myocarditis
Pericardial disease
Infiltrative diseases - amyloidosis, haemochromatosis or sarcoidosis
CT diseases.

165
Q

What are symptoms of Left HF?

A

Dyspnoea - exertional, orhopnoea, PND
APO
Chest pain
Palpitations
Fatigue/weakness
Nocturia, oliguria
Nocturnal cough
Cool peripheries

166
Q

What are some clinical features of Left Heart failure?

A

Bibasilar rales and crackles
Cardiogenic wheeze
Weak pulse - low pulse pressure
Tachycardia
AF
Pulsus alternans
Cardiomegaly - displaced lateral, apex beat
S3 gallop
Pleural effusion signs

167
Q

How to diagnose LHF?

A

Echo - allows determination of systolic and diastolic function.
CXR - APO

168
Q

How to investigate LHF?

A

ECG
CXR
Coronary angiography
BNP (increased in HF over 200)
FBC
Electrolytes
Creatinine, BUN
Lipids
Thyroid hormones - high output HF
LFTs (right HF)
Exercise stress test

169
Q

How to treat LHF?

A

Nonpharm: Fluid and salt restriction. Lifestyle changes: exercise, diet, smoking cessation. Manage comorbidities. Cardio-pulmonary physio.
Pharm: ACEI/ARBs - vasodilation, improve Left ventricular end diastolic pressure, survival
B-blockers - Improvement in Sx and LVEF, arrhythmia prevention and survival. Atenolol, bisoprolol, carvedilol, SR metoprolol
Aldosterone antagonists - spironolactone
Diuretics
Angiotensin-Receptor Neprolysin Inhibitors - Entrest and valsartan - entresto

170
Q

Chronic management of LHF?

A

Beta blocker
ACEI
Diuretic
Aspirin
Statin

171
Q

Acute management of LHF?

A

Lasix (furosemide)
Morphine
Nitrates
Oxygen
Positive pressure (CPAP)

172
Q

What is APO?

A

Acute Cardiogenic Pulmonary oedema is due to increased capillary hydrostatic pressure secondary to elevated pulmonary pressure.

173
Q

Pathophysiology of APO?

A

Heart failure - backpressure of blood.
Increased pulmonary venous pressure
Fluid pushed from capillaries into alveoli
Failure of gaseous exchange and hypoxia

174
Q

What are the symptoms of APO?

A

SOB, orthopnoea, PND, peripheral oedema, pink frothy sputum, morning cough, decreased exercise tolerance, weight gain.

175
Q

What are clinical features of APO?

A

Expiratory crackles, worse in the base. Cardiogenic wheeze, displaced apex beat, murmurs.

176
Q

What are the causes of APO?

A

Left atrial outflow obstruction (mitral stenosis, atrial myxoma)
LV failure
Dysrhythmia
Excessive intravascular fluid administration
Other non-cardiogenic causes

177
Q

What are the CXR characteristics of APO?

A

ABCDE
Alveolar oedema (bat wing distribution)
Kerley B lines
Cardiomegaly
Dilated upper vessels
Pleural Effusion

178
Q

What is the treatment for APO?

A

Acute: CPAP or BIPAP
Diuretics - furosemide
Preload reduction: Nitrates, B-blockers
Afterload reduction: ACEIs or ARBs
Catecholamines: Dopamine - vasodilation, inotropic and chronotropic effects
Dobutamine - B1 receptor antagonist and inotropic effect and mild vasodilation
Noradrenaline - a agonist, increases aafterload and decreasesCO, used in hypotension.
Water and Na restriction
Intra-aortic balloon pump

Long term:
Diuretic and ACEI or ARB and B blocker
Na and Fluid restriction
Manage cause

179
Q

What is RHF?

A

CO inadequate to meet the bodies requirmenet due to a failure of the RV.

180
Q

What are the symptoms and signs of RHF?

A

Peripheral oedema, hepatomegaly, ascites
Peripheral oedema, increased JVP, hepatojugular reflex, parasternal heave, pulsatile hepatomegaly, ascites, S3 gallop

181
Q

What are the causes for RHF?

A

Left ventricular failure
Tricuspipd Regurgitation
Pulmonary HTN
Pulmonary Stenosis
Right AMI

182
Q

Name 3 examples and doses of ARBs

A

Candesartan 8-32 mg/qd
Irbesartan 150-300 mg / qd
Telmisartan 40-80mg/qd

183
Q

What is the MOA for ARBs?

A

Directly binds to and blocks the angiotensin I receptor, preventing its aactivation by Angiotensin II decreasing the RAAS, resulting in:
Vasodilation
Decreased Na and water reabsorption
Decreased aldosterone
ADH secretion
Net decrease in BP
Decreased myocardial workload

184
Q

What are the indication for ARBs?

A

HTN
Oedema
HF
Renal disease

185
Q

What are the adverse effects with ARBs?

A

Sudden decreased BP with first dose
Hyperkalaemia (increased risk with renal impairment)
Renal failure: fall in glomerular.perfusion pressure due to efferent arteriolar dilation
Cough and angioedema is rare.

186
Q

Contraindications to ARBs?

A

Pregnancy, hyperkalaemia, angioedema, bilateral renal artery stenosis.

187
Q

Give an example of a thiazide diuretic

A

Hydrochlorothiazide, indapamide

188
Q

How to thiazide diuretics work?

A

Inhibit the Na-Cl cotransporter in the DCT. Decreases Na and Cl reabsorption. Increases action of the Na K exchange resulting in K excretion.
Cal reabsorption
Produce diuresis and natriuresis
This transporter usually reabsorbs 5% of Na so are less efficacious than loop.

189
Q

What are the side effects of thiazide diuretics?

A

Hypokalaemia, hypercalcaemia, Gout, metabolic syndrome, Erectile dysfunction.

190
Q

What are the contraindications to thiazide diuretics?

A

Anuria.

Med (6 decks)

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