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MD2 > Cardio and vasc > Flashcards

Cardio and vasc Flashcards

1
Q

Clinical presentation of lymphedema

A 
• Non-pitting edema
	• Feeling of heaviness or fullness, aching pain in limb 
	• Impaired mobility 
	• Skin changes in advanced cases
		○ Discolotation
		○ Hyperkeraosis
		○ Verrucous hyperplasia 
		○ Papillomatosis
		○ Deformity (elephantiasis)
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2
Q

Causes of lymphedema

A

Primary (congenital)
○ Milroy’s syndrome (congenital hereditary lymphedema)

Secondary
	○ Infection 
		§ Filariasis (#1 cause worldwide, developing nations)
		§ Post-op infection
	○ Malignant infiltration 
		§ Axillary, groin, intrapelvic
	○ Radiation/surgery (#1 cause in developed world)
		§ Axillary, groin lymph node removal
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3
Q

Treatment lymphedema

A

Compression bandages and sleves
Gentle exercise
Massage and manual lymph drainage therapy
Skin care (moisturisers, topical/systemic treatment of fungal and bacterial infections)

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4
Q

Risk factors for venous thrombi embolism

A 
THROMBOSIS
	○ Trauma, Travel
	○ Hypercoagulable state, history of previous VTE
	○ Recreational drugs (IVDU)
	○ Old age >60
	○ Malignancy
	○ Birth control pill (OCP)
	○ Obesity, obstetrics
	○ Surgery, smoking
	○ Immobilisation
	○ Sickness (CHF, MI, nephrotic syndrome, vasculitis)
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5
Q

PERC

A 
Old Age
Tachycardia
O2 saturation
Prior history VTE
Recent trauma/surgery
Hemoptysis
Exogenous oestrogen
clinical signs of VTE

If all are negative, can rule out PE. If any one is positive, must move onto Wells.

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6
Q

Treatment for VTE

A

Anticoagulant: LMWH or Heparin if in renal failure; start Warfarin at same time. Stop LMWH/Hep when INR in therapeutic range for 2 days.

If haemodynamically unstable: thrombolyse

If anticoag CI: IVC filter of surgical thrombectomy

Long-term Warfarin or NOAC (3-6mo or lifelong if recurrent)

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7
Q

Causes of thrombophilia

A

Genetic

  • overactivity of pro-coag factors (Factor V leiden and prothrombin mutation)
  • Deficiency of anti-coag factors (anti-thrombin III, protein C and S)

Acquired

  • Antiphospholipid syndrome (lupus anticoagulant, anticardiolipin, anti PLD antibody)
  • Heparin induced thrombocytopenia (immune reaction against heparin)
  • Sickle cell disease (prothrombotic state induced by hyper viscous blood)
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8
Q

Investigating DVT

A
  1. Well’s
  2. D-dimer: if neg and wells shows low pretest probability, exclude DVT
  3. USS of leg id D-dimer >0.5 and/or high pre-test probability
  4. Bloods
    - FBE, coag studies +/- thrombophilia screen
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9
Q

Investigating PE

A
  1. PERC. If none are positive, can rule out PE. If 1 + are positive, calculate Well’s.
  2. Well’s criteria
  3. D-dimer: if negative, along with low- pretest probability, PE can be excluded. Otherwise do CTPA
  4. CTPA first line diagnostic

CXR, ECG, ABG, FBE, blood film, procoag screen

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10
Q

Classic PE ECG changes

A

Sinus tachycardia
T wave inversion leads V1-V4 +/- II, III, aVF
RV strain pattern
Non specific ST segment changes or T wave changes
S1Q3T3: S wave lead 1, Q wave and T wave inversion in lead III
RBBB (complete or incomplete)
R axis deviation

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11
Q

Classic presentation and investigation results for polymyalgia rheumatica

A

Old (>50) white female with morning stiffness and pain (worse in evening) of shoulder, arms, hip girdle and neck and began relatively suddenly. + general malaise, fatigue, weight loss. Family HX.
Raised ESR

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12
Q

What condition is assoc in polymyalgia rheumatic?

A

Temporal arteritis

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13
Q

Treatment polymyalgia rheumatica

A

Low dose corticosteroids

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14
Q

2 large vessel vasculitides and their treatment

A

Giant cell arteritis
Takayasu’s arteritis

Steroids

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15
Q

2 medium vessel vasculitides and their treatment

A

Polyarteritis nodosa
Kawasaki disease
Treatment is steroids + IV cyclophosphamide

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16
Q

an example of p-anca associated small vessel vasculitis + treatment

A

Churg-strauss syndrome.
• Granulomatous inflammation of vessels with hypereosinophilia and eosinophilic tissue infiltration
(often lung involvement)

Treatment is steroids + IV cyclophosphamide

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17
Q

an example of C-anca associated small vessel vasculitis + treatment

A

Wegener’s granulomatosis

  • Granulomatous inflammation of vessels of resp tract, lungs and kidneys

Treatment is steroids + IV cyclophosphamide

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18
Q

An example of small vessel ANCA negative vasculitis +treatment

A

Henoch-Schonlein purpura

Treatment is steroids + IV cyclophosphamide

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19
Q

Mainstays of diagnosing vasculitis?

A

Angiography
Biopsy of affected vessel

Always do ANCA as well.

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20
Q

What does an isolated systolic HTN reflect generally?

A

High pulse pressure, seen in aged and stiff arteries

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21
Q

Difference between primary and secondary HTN, which is more common?

A

Primary HTN - no specific cause identified (95%)

Secondary HTN - specific cause identified (5%). Treatable but more severe than primary.

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22
Q

What are some of the causes of secondary hypertension?

A

Chronic Renal disease (Polycystic kidneys, diabetic glomerulosclerosis, glomerulonephritis)

Vascular - Renal artery stenosis and coarctation of aorta

Endocrine - Adrenal tumours secreting aldosterone, cortisol, ACTH, catecholamines (pheochromocytoma); cushing’s

Sleep apnoea

Meds (steroids, high oestrogen states such as OCP, HRT, pregnancy)

NOT atherosclerosis (except in case of renal artery stenosis)

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23
Q

In what patients with HTN do you investigate for a secondary cause?

A

Young patients (<30 years)
Resistant HTN
Presence of certain SX

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24
Q

Examples of renal causes of secondary HTN

A

Diabetic glomerulosclerosis
Polycystic kidneys
Glomerulonephritis

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25
Q

Medications that can cause secondary HTN

A

Corticosteroids

High oestrogen states(OCP, HRT, pregnancy)

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26
Q

Vascular complications of HTN

A
  • Worsens Arteriosclerosis
  • Worsens Atherosclerosis -> aneurism / dissection
  • Hyaline arteriolosclerosis
  • Berry aneurysm
  • Acute plaque event -> thrombus formation, thromboembolism
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27
Q

Cardiac complications of HTN

A
  • IHD and infarct
  • LV concentric hypertrophy
  • Cardiac failure
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28
Q

Kidney complications of HTN

A
  • Benign nephrosclerosis (elevated BP transmitted to glomeruli which respond with tubular fibrosis, sclerosis and atrophy & hyaline arteriolosclerosis -> kidney ischaemia)
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29
Q

Brain complications of HTN

A

Ischaemic Strokes (atherosclerotic TE)

Haemmhoragic stroke (due to hyaline arteriolosclerosis in basal ganglia or SA haemmhorage due to ruptured berry aneurysm)

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30
Q

Eye complications of HTN

A

Hypertensive retinopathy

(hyalinised retinal vessels are weak and leaky, can bleed or lead to ischaemia).

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31
Q

What factors determine the treatment of HTN?

A

Degree of HTN (stage 1 SBP 140-179 & DBP 90-109; severe SBP>180 & DBP>110)

Presence of CV risk factors

Evidence of end organ damage (cardiac, arteries, kidneys)

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32
Q

How is the treatment protocol (pharm vs lifestyle modification) for different categories for HTN divided up?

A

Stage 1 SBP 140-179 & DBP 90-109 with NO CV RFs: life style modification (pharm treatment if still high after 6 months)

Stage 1 SBP 140-179 & DBP 90-109 WITH CV RFs or end-organ damage: start pharmacological treatment

Severe HTN SBP>180 & DBP>110: start pharmacological treatment

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33
Q

Pharm. treatment (order of use) for HTN

A

Step 1:
If <55yo, ACE inhibitor (or AT1Rantag)
If >55yo or afro-carribbean origin - Ca channel blocker
if >65yo - low dose thiazide

Step 2:
ACE inhibitor + Ca channel blocker

Step 3:
Add thiazide diuretic (or beta blocker only if patient has IHD and heart failure)

If BP still elevated after step 3 = RESISTANT HTN

Step 4: Refer. Consider further diuretic (thiazide-like or spironolactone) or beta or alpha blocker

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34
Q

When NOT to use Ca channel blocker in HTN

A

If patient has heart failure

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35
Q

When NOT to use ACE inhibitor in HTN

A

In severe renal impairment and pregnancy

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36
Q

What drug combinations to avoid in HTN and why? (3)

A
  1. Ace inhibitor + K-sparing diuretic (spironolactone) - risk of hyperkalaemia
  2. Ca channel blocker + beta blocker - risk of heart block
  3. ACEi + AT1R antag - not shown to be clinically effective
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37
Q

LONG-TERM Treatment protocol for CHF

A
  1. Lifestyle modification
    Smoking and alcohol cessation
    Na and fluid restriction
    Diet and exercise (weight control)
  2. Treat underlying cause and aggravating factors (valvular disease/arrhythmia; thyroid, infection, anaemia, HTN)
  3. Meds
    ACE inhibitor/ARB (slows progression, improves survival)
    + Beta blocker     (slows progression, improves survival)

+/- aldosterone antag*(spironolactone) if severe and symptomatic
+/- diuretic (furosemide) if fluid overloaded
+/- digoxin (SX control only)

+/- antiarrhythmic (if AF)
+/- Warfarin (if AF, prior TE or LV thrombus on echo)

*mortality benefit

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38
Q

ACUTE treatment of CHF (Acute pulmonary oedema)

A

LMNOPP

Lasix (furosemide)
Morphine IV
Nitroglycerin (GTN)
O2 (if hypoxaemic)
Positive airway pressure (CPAP/BiPAP)
Position

Treat underlying cause (MI/ischaemia/arrhythmia etc)

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39
Q

Precipitants/exacerbaters of heart failure

A 
MADHATTER:
MI/ischaemia
Anaemia
Drugs (NSAIDs, steroids, non-compliance)
HTN
Arrhythmias 
Thyroid
Toxic (infection)
Endocarditis/embolus
Renal failure
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40
Q

Signs/Symptoms of Heart failure

A 
Systolic (fwds) dysfunction:
S3 
Displaced apex beat 
Mitral/tricuspid regard
fatigue
syncope
systemic hypotension
cool extremities and slow cap refill w peripheral cyanosis

Diastolic (backwards) dysfunction:
Dyspnoea, orthopnoea, PND
Cough
Crackles

Peripheral edema
Incr JVP
Hepatomegaly, pulsatile liver

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41
Q

Pathophysiology of heart failure

A

Incr preload leads to incr work (septal defect or regurg)

Decr strength/contractility (IHD/cardiomyopathy)

Incr resistance leads to incr work (HTN, stenosis)

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42
Q

What conditions does IHD encompass?

A
  1. Stable angina
  2. Unstable angina
  3. MI (STEMI or NON-STEMI)
  4. Sudden cardiac death
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43
Q

Stable angina vs unstable angina

A

Stable:

  • pain comes on w exercise, cold, stress and is relieved by stress. REPRODUCIBLE.
  • due to atherosclerotic narrowing

Unstable:

  • new onset pain or pain at rest
  • accelerating pattern of pain
  • pain post MI or post-procedure
  • due to acute plaque event (plaque rupture, acute thrombus formation, partially occludes vessel)
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44
Q

STEMI vs non-STEMI

A

STEMI: Criteria for MI + ST elevation or new BBB

NON-STEMI: Criteria for MI WITHOUT ST elevation or new BBB

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45
Q

WHO Criteria for MI

A

2 of the following:

  • Classic SX of MI
  • Elevated troponin, CK
  • Typical ECG pattern (ST segment changes, T wave changes, new BBB, development of Q waves)
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46
Q

What conditions does ACS encompass and what is the underlying pathophys?

A

Acute plaque event (plaque rupture)
Unstable angina (ruptured plaque partially occludes coronary artery)
NSTEMI + STEMI (ruptured plaque completely occludes coronary artery)

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47
Q

ACUTE Management of STEMI

A

Percutaneous therapy (PCI) i.e. stent or balloon angioplasty (preferred) within 60 door to balloon time

OR Thrombolysis/Fibrinolysis (if early presentation or PCI contraindicated) with stress test before discharge

O2 
Morphine IV PRN
Aspirin (+/- clopidogrel if high risk or PCI)
Unfractioned heparin 
GTN IV 
\+/- metaclopramide
48
Q

ACUTE Management of NSTEMI or UA

A

DO NOT THROMBOLYSE!

If high risk -> PCI immediately.
If low risk with no recurrent CP -> Stress testing -> positive result -> PCI, otherwise conservative treatment (RF modification and long-term anti anginal therapy)

O2 
Morphine IV PRN 
Aspirin (+ clopidogrel if high risk or PCI)
LMWH
GTN sublingual
\+/- metaclopramide
49
Q

Long-term management of IHD post-acute ACS event (8)

A
  1. Dual anti-platelets (aspirin + clopidogrel)
  2. Beta blockers (Ca channel blocker second line)
  3. ACE inhibitors (prevent remodelling)
  4. Nitrates (GTN) PRN for symptom relief
  5. Statin (irrespective of cholesterol levels for plaque stabilisation)
  6. Modify lifestyle (exercise, diet, cease smoking, weight control, alcohol, stress)
  7. Modify CV Risk Factors (diabetes, cholesterol, HTN)
  8. Review (1 month then 6 mo thereafter)
50
Q

Complications of MI

A

Electrical instability -> Arrhythmias

Pericardial inflammation -> Pericarditis

Tissue necrosis ->

  • Cardiac tamponade or VSD (wall rupture);
  • Congestive heart failure (papillary muscle infarct -> MR)
  • Aneurysm

Impaired contractility ->

  • CHF;
  • Cardiogenic shock (hypotension -> decr perfusion)
  • Stroke, PE, DVT, organ ischaemia or infarct (ventricular thrombus -> embolism)
51
Q

Investigations for all patients w HTN

A 
FBC
UEC 
Fasting glucose
Lipid profile
12 lead ECG
Urinalysis
52
Q

What tests do you order if investigating endocrine cause of HTN?

A

plasma aldosterone and renin

53
Q

What tests do you order if investigating pheochromocytoma as cause of HTN?

A

24hour urine catecholamines

54
Q

Treatment for myocarditis

A

Supportive treatment
○ Bed rest, treat CHF, treat arrhythmias

Anticoagulation
Treat underlying cause

55
Q

What is the prognosis/outlook/comlpications for myocarditis

A
  • Usually self-limiting -> Full recovery
    • Progression to dilated cardiomyopathy (systolic heart failure)
    • Sudden death in young adults
56
Q

Causes of myocarditis

A

Idiopathic in 50%

Viral (coxsackie B, echovirus, poliovirus, HIV, mumps, flu)

Bacterial (s aureus, clostridia etc), protozoal, fungal
Drugs
Toxins
Vasculitis, SLE, RA, sarcoid
Acute rheumatic fever (strep)
57
Q

Complications of acute pericarditis

A
  • Recurrence
  • Atrial arrhythmias
  • Pericardial effusion and tamponade
  • Constrictive pericarditis
58
Q

Management of acute pericarditis

A

NSAIDs
Treat the cause
Colchicine&raquo_space; steroids if recurrent/continuing SX

59
Q

ECG pattern of acute pericarditis

A

ECG: wide-spread saddle shaped ST elevation +/- depressed PR segment

60
Q

Chest pain pattern of pericarditis

A

Central chest pain - worse on inspiration and when lying flat; relieved by leaning forwards

61
Q

Standard Management of dyslipidaemia

A

Manage modifiable risk factors

  • Smoking cessation
  • Diet (reduce saturated fats and refined sugars, incr fruit veg and fibre)
  • Reduce alcohol
  • 150min mod-intense exercise/week
  • Weight reduction

Medications

  • Statins are 1st line mono therapy
  • If severe, add Fibrates +/- fish oil

Monitoring/follow up (don’t need to know details)

  • Monitor LFTs and CK at baseline then 6 weeks after starting statin (SEs)
  • Fasting lipids at 3 mo, and if under control, monitor every 6-12 months thereafter.
62
Q

Alternate medications to Statins, for control of dyslipidaemia

A

Fibrates

Bile acid resins/sequestrates

Ezetemibe

Niacin/vitamin B3/nicotinic acid

Fish oil

63
Q

Mechanism of action - Fibrates

A

Lower TGLs by increasing synthesis of lipoprotein lipase which increases hydrolysis of TGL into FFAs which can then be taken up by tissues as an energy source

64
Q

Mechanism of action - Bile acid resins

A

Lower blood LDLs by binding to bile acids in SI so they can’t be absorbed and must be excreted.
Increase expression of hepatic LDL Rs to further decr blood LDL (must resynthesises the bile acids you have excreted)

65
Q

Mechanism of action - Ezetimibe

A

Lowers LDL by by inhibiting the cholesterol transporter in the small intestine to inhibit cholesterol absorption in gut

66
Q

Mechanism of action - niacin/vitamin B3

A

Lowers risk of abnormal lipids; decr LDL and VLDL, decr TGL incr HDL and hepatic LDL receptors. Mechanism unclear.

67
Q

What does hyperlipidaemia put you at risk of?

A

Atherosclerosis

IHD - MI, stroke

68
Q

What is the screening protocol for hyperlipidameia?

A

Full fasting lipid profile every 3 years for
○ Males > 40
○ Females > 50 (or menopausal)
○ Anyone with other CAD risk factors

69
Q

Secondary causes of hyperlipidaemia

A 
Obesity
Hypothyroid
Diabetes mellitus
Metabolic syndrome 
CKD
Nephrotic syndrome
Liver disease 
Alcoholism
70
Q

Primary causes of hyperlipidaemia

A

genetics

71
Q

What infectious agent is rheumatic fever caused by? What medical condition precedes it and by how long?

A

Strep progenies (group A beta haemolytic strep)

Pharyngeal infection precedes it 2-4 weeks earlier

72
Q

What valves are mostly affected with Rheumatic heart disease?

A

Mitral (70%)&raquo_space; Aortic (40%)&raquo_space; Tricuspid (10%)

73
Q

Treatment for Rheumatic fever

A

High dose steroids to shut down inflammatory response

Benzylpenicillin and penicillin

NSAIDs/aspirin for carditis-arthritis.

74
Q

Methods of entry for infective endocarditis

A

Blood stream

surgical and dental procedures

75
Q

Infective agents for endocarditis

A 
Staph aureus
Strep viridian's
Staph epidermis 
Enterococcus
E coli
76
Q

Classic signs and symptoms of infective endocarditis

A

Fever +/- new heart murmur
Clubbing
Anaemia
Splinter haemmhorages, osler’s nodes

77
Q

ECG findings of Premature Ventricular or atrial complexes

Management

A

Premature complex followed by a pause, then normal beat.
May be every 2 or 3 beats (bigeminy or trigemini).

MX: beta blockers/Ca channel blockers if frequently symptomatic otherwise just reassure and cut down caffeine.

78
Q

Risk factors for AF

A

CHADS2

CCF
HTN
Age >75
DM
Stroke/TIA/Thromboembolus previously
79
Q

Management of CHRONIC AF

A
  1. Evaluate stroke risk and manage -> score 0 gets aspirin; score >1 gets anticoagulation (warfarin or NOAC)
  2. Rate control if patient stable (beta blocker, diltiazem, verapamil or digoxin, or amiodarone last line)

Rhythm control (flecainide&raquo_space;> amiodarone if in HF) if patient is symptomatic, CCF, younger, or presenting for 1st time with lone AF or AF from corrected precipitant.

80
Q

Triggers of AF

A 
Heart failure/ischaemia 
HTN
MI 
PE
Valvular disease (mitral)
Hyperthyroid
Caffeine/alcohol
81
Q

Bloods when investigating AF

A

UEC
Cardiac enzymes
TFTs

82
Q

Management of Acute AF (<48 hours)

A

If very ill or haemodynamically unstable:

  1. O2
  2. Emergency cardioversion (electrical or IV amiodarone if unavailable. Flecanide)
  3. Rate control (Verapamil or Bisoprolol = Ca channel or beta blocker; digoxin or amiodarone 2nd line)
  4. Anticoagulation (LMWH)

Treat any triggering illnesses (pneumonia, MI, PE etc)

83
Q

Risk factors for PAD

A 
Smoking
Diabetes
HTN
Hypercholesterolaemia 
Family HX (hyperhomocysteinaemia)
84
Q

SX and signs of PAD

A

SX:
Claudication
Rest pain

Signs:
Rubor
Ulcers, gangrene, cellulitis
Abnormal nails

85
Q

What are the most common sites for narrowings in PAD?

in order of occurrence

A

80-90%: femoral and popliteal arteries (calf claudication, reduced popliteal, pedal pulses)

40-50%: tibial and peroneal vessels (pedal pulses absent)

30%: abdominal aorta and iliac arteries (claudication in butt, thigh, calf and reduced femoral and distal pulses)

86
Q

Why might the ABI be raised or lower than normal?

A

Diabetics - increased ABI due to stiff calcified vessels that are incompressible

Low ABI - extremely stenosed vessel, there is no blood flow distally

87
Q

what sized arteries is angiography good for? What is a draw back to this?

A

Good for large arteries (aortic, iliac,, femoral, popliteal), but requires contrast which is nephrotoxic.

88
Q

Management of intermittent claudication

A 
○ Diet and lifestyle
○ BP control
○ Aspirin
○ Statins 
○ Smoking cessation
○ Exercise (improves fitness and general pump function as well as efficiency with using O2 delivered (if they stop walking to 'control symptoms' they will lose their legs)

○ Surgical
§ End-arterectomy for short segments
§ Angioplasty and stending for short segments
□ More for proximal arteries
§ Bypass for longer blocks
□ Bigger operation with more risks and longer recovery time

89
Q

For critical limb ischaemia

A

○ HEPARIN IMMEDIATELY
○ Limb salvageable -> arteriography or duplex scanning -> endarctectomy or angioplasty

○ Limb NOT salvageable:
§ Palliation if patient unfit for surgery
§ Amputation if patient fit for surgery

90
Q

How does carotid stensois present?

A

TIA or stroke
Amaurosis (temporary monocular blindness due to CRA embolic obstruction)
Asymptomatic

91
Q

Risk factors for peripheral/chronic venous disease

A 
old age
family HX venous disease
ligamentous laxity
prolonged standing
incr BMI
Smoking
Past DVT
High estrogen states and pregnancy
92
Q

What is venous disease caused by?

A

Venous HTN and venous insufficiency

causes of venous HTN

  1. inadequate muscle pump function
  2. incompetent venous valves -> reflux
  3. venous thrombus or obstruction

Venous HTN leads to vein dilatation, skin changes and or ulceration

93
Q

Clinical presentation of chronic venous disease

A

Hyperpigmentation and haemosiderin staining

Brawny pitting oedema

Lipodermatosclerosis

Varicose veins

Ulcers

Leg heaviness, ache and fatigue at end of day

Venous eczema: Pruritis, pain, swelling, erythema, recurrent cellulitis

LEg elevation, compression alleviates pain

94
Q

How do you diagnose PVD?

A

Clinical diagnosis (typical symptoms) confirmed by DUPLEX ULTRASOUND revealing venous reflux

95
Q

Treatment of PVD

A

Initial conservative
§ Leg elevation - improves O2 delivery and reduces oedema
§ Compression - compresses dilated veins and reduces oedema; helps heal ulcers
§ Exercise - improves O2 delivery
§ Topical dermatological agents for stasis dermatitis

Vein ablation - surgical excision, sclerotherapy, thermal ablation
§ Requires a minimum of 3 months conservative therapy before proceeding w ablation.

Venous reconstruction (translocation of vein segments, transplantation of vein segments, substitution)

96
Q

Where are varicose veins commonly located?

A

Superficial veins of legs

97
Q

Signs and SX of varicose veins

A

Visibly dilated tortuous veins in legs, more obvious upon standing

Painful when standing, relieved by walking

Haemosiderin staining near affected veins

Leg cramps

Over time can lead to leg swelling and venous eczema

Lipodermatosclerosis (inverted champagne bottle legs)

Ulceration

98
Q

What is lipodermatosclerosis and what is it commonly caused by?

A

Skin thickening

Inverted champagne bottle legs - tapering of legs above ankle with reddish brown discoloration distally.

99
Q

Pathophys of varicose veins

A

Caused by incompetent venous valves -> valves fail to close so blood falls back down and pools in leg veins which accelerates valves stretching and failing, and causes veins to become dilated and tortuous due to extra blood.

100
Q

What causes a varicocoele?

What does it look like?

A

L testicular v drains into the L renal vein (must return blood at a 90deg angle which is hard to get through and so blood backs up around testicle, causing enlargement of testicular vein)

Looks like “bag of worms” which becomes larger when standing and smaller when lying flat

101
Q

What is a potential complication of a varicocoele?

A

Warm stagnant venous blood causes testicular temp to rise

-> Testicular atrophy and infertility (poor quality sperm)

102
Q

Investigations for varicose veins

A

Lower limb venous ultrasound to check for venous incompetence

103
Q

DDX for varicose veins

A

Telangiectasis
Recticular veins
both have no evidence of reflux on venous ultrasound

104
Q

Treatment varicose veins

A 
Compression stockings
Leg elevation
Injection sclerotherapy
Surgery - vein removal (Stripping, ligation)
Vein ablation
105
Q

Complications of varicose veins

A
  • Superficial thrombophlebitis
  • Venous eczema
  • Venous ulceration
  • Lipodermatosclerosis
  • Bleeding varicose vein
106
Q

Characteristics of venous ulcers

A

Commonly found in gaiter region - medial aspect of calf/ankle

Large, flat/shallow
Irregular edges
Granulomatous base (pink/beefy red)
Mild pain

Pedal pulses present

107
Q

Characteristics of arterial ulcers

A

VERY PAINFUL

Often on foot pressure point areas

Small size
Deep with punched out appearance
Regular margins
Sloughy/necrotic base

Absent pedal pulses

108
Q

Neuropathic ulcer characteristics

A

Often very large but size and shape varies
NOT PAINFUL

Appearance: Prominent hypertrophied squamous rind around edge

Often on feet -pressure point areas

109
Q

Describing ulcers

A 
○ Shape 
○ Site
○ Size
○ Edges
○ Base description (colour, slough? Etc)
○ Surrounding tissues 
○ Lymph nodes
110
Q

MX of arterial ulcer

A

Feel pulses - absent/faint indicates arterial cause

USS + ABI to confirm (ABI <0.7 indicates PAD)

Wound debridement
Wound dressing
Angiography and revascularisation

111
Q

How to intensify the MR murmur

A

get patients to roll onto L side and inspire

112
Q

How to intensify the AS murmur

A

Patient leans forwards and expires

113
Q

What is the quality of MR?

A

Pansystolic, blowing

114
Q

What is the quality of AS?

A

Crescendo Decrescendo ejection systolic

115
Q

What is AS commonly caused by?

A

Post RHD
Congenital Bicuspid valve
Calcification

116
Q

What is MR commonly caused by

A 
Congenital
					Consequence of:
◊ rheumatic heart disease
◊ Marked LV dilatation
◊ Acute infective endocarditis
◊ Papillary muscle dysfunction secondary to MI
117
Q

ECG anomalies associated w syncope (3)

A

Sinus bradycardia
Conduction block
Wolff Parkinson white syndrome

MD2 (16 decks)

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